Screening Data

The management of complex patients with inoperable stage III NSCLC: practical lessons from case-based discussion.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-31
• Screened: 2026-09-13 03:12 KST
• PMID: 42700509
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42700509/
• DOI: 10.1016/j.lungcan.2026.109602
• Tags: NSCLC, Stage III, Radiotherapy, Durvalumab, Case-based discussion, Complex patients, Lung cancer

Screening brief

이 논문은 수술 불가인 Stage III 비소세포폐암(NSCLC) 환자, 특히 표준 치료에 적합하지 않은 고위험군 환자의 방사선 치료 기반 관리 전략을 다룹니다. 간질성 폐질환이나 노쇠 등 복합적인 요인을 가진 사례를 통해 임상적 난제를 해결하는 실용적 교훈을 제시합니다. 이는 현재 증거가 부족한 이 환자 집단에 대한 치료 접근법을 개선하고, 향후 더 포괄적인 임상 시험의 필요성을 강조합니다.

Abstract

Standard of care for inoperable and/or unresectable stage III non-small cell lung cancer (NSCLC) is concurrent chemoradiotherapy followed by 12 months of adjuvant durvalumab. Many patients are ineligible due to poor fitness, comorbidity or concerns around their ability to tolerate concurrent therapy or immunotherapy. As a result, these patients experience inferior outcomes. This article summarises four case studies initially presented at a UK-based academic webinar in August 2025. The focus of the webinar was the radiotherapy-based management of complex patients with stage III NSCLC. This included tumour factors (i.e. vascular invasion and bulky disease) and patient factors (i.e. interstitial lung disease, multiple comorbidities and frailty). Strategies to navigate these challenges and improve outcomes are highlighted. Patients ineligible for standard-of-care treatment are under-represented in practice-defining trials. As a result, there is limited evidence to guide their management. Broader eligibility criteria and inclusive trials are needed to generate safety and efficacy data for this population. Enhanced phenotyping with biomarkers, adoption of advanced radiotherapy techniques, risk-adapted dose guidance and novel drug-radiotherapy combinations offer potential to expand access to curative-intent treatment and improve outcomes.

The changing therapeutic landscape of small-cell lung cancer.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lancet (London, England)
• Publication date: 2026-Sep-12
• Screened: 2026-09-13 03:11 KST
• PMID: 42702213
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42702213/
• DOI: 10.1016/s0140-6736(26)01244-4
• Tags: Small-cell lung cancer, SCLC, Targeted therapy, Antibody-drug conjugates, T-cell engagers, Lung cancer treatment, Oncology review

Screening brief

이 논문은 소세포폐암(SCLC)의 생물학적 이해가 어떻게 새로운 치료 접근법으로 이어지고 있는지 설명합니다. 세포 표면 단백질을 표적으로 한 T-cell engagers, antibody-drug conjugates, radioconjugates 및 cell therapies 등 emerging approaches의 효능을 강조합니다. 현재 표준 치료와 최근의 주요 진전을 요약하여 SCLC 관리의 미래를 제시합니다.

Abstract

Small-cell lung cancer (SCLC) is an exceptionally aggressive malignancy: highly proliferative, heterogeneous, and frequently metastatic at diagnosis. Although initially responsive to chemotherapy, such responses are typically transient, and recurrent disease has been largely refractory to standard cytotoxics. The past decade has been notable for major advances in our understanding of SCLC biology, and this preclinical progress is now informing multiple novel therapeutic approaches for this disease. Of particular note, defining cell-surface proteins that are uniquely or differentially expressed in SCLC has led to various targeted therapies showing substantial preliminary evidence of efficacy in patients with SCLC. Approaches in active development include T-cell engagers, antibody-drug conjugates, radioconjugates, and cell therapies, among others. In this Series paper, we summarise current standards of care, recent advances, and highlight emerging approaches showing early promise for better management of SCLC. Together, these advances are providing new hope for patients with what has been a particularly lethal disease.

Induction and consolidation atezolizumab with stereotactic body radiation therapy versus radiation alone in high-risk, early-stage non-small-cell lung cancer (SWOG/NRG S1914): a multicentre, open-label, superiority, phase 3, randomised controlled trial.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lancet (London, England)
• Publication date: 2026-Sep-06
• Screened: 2026-09-13 03:11 KST
• PMID: 42702214
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42702214/
• DOI: 10.1016/s0140-6736(26)01655-7
• Tags: NSCLC, SBRT, atezolizumab, immunotherapy, Phase 3 trial, early-stage lung cancer, SWOG S1914

Screening brief

이 연구는 수술이 불가능한 고위험 초기 NSCLC 환자에서 SBRT에 atezolizumab을 추가 투여하는 것이 전체 생존율(OS)을 개선시키는지 평가했습니다. 결과는 atezolizumab 조합군이 SBRT 단독군과 비교하여 OS 향상을 보이지 않았으며, 오히려 Grade 3 이상 부작용 발생률이 더 높았음을 나타냅니다. 이는 초기 NSCLC에서 면역항암제와 방사선 요법의 결합 전략에 대한 중요한 부정적 결과로 기록될 가치가 있습니다.

Abstract

Stereotactic body radiation therapy (SBRT) is the standard of care for early-stage, medically inoperable non-small-cell lung cancer (NSCLC). We aimed to test the addition of neoadjuvant, concurrent, and adjuvant atezolizumab with SBRT for early-stage NSCLC. In this multicentre, open-label, phase 3, randomised controlled trial, eligible patients from 146 institutions across the USA who had T1-T3N0M0 NSCLC ≤7 cm, and were medically inoperable or declined surgery, and had at least one risk factor suggestive of increased risk of recurrence, were included in the study. Patients underwent open-label equal and stratified randomisation to SBRT over three to eight fractions with or without up to eight cycles of neoadjuvant, concurrent, and adjuvant atezolizumab 1200 mg intravenously every 21 days for up to eight cycles, with SBRT initiated with cycle three. The primary objective was to compare overall survival between the two groups. The group sequential design included four interim analyses. Target accrual was 480 patients (432 eligible). The trial is registered with ClinicalTrials.gov (NCT04214262) and is closed to new participants. Between March 25, 2020, and Sept 9, 2024, 417 patients were enrolled and randomly assigned to atezolizumab plus SBRT (n=210) or SBRT alone (n=207). 402 were eligible and made up the modified intention-to-treat population (201 per group). The median age wa...

Transcriptomic analysis of a phase 1 trial for intraperitoneal monocytes plus IFNs in ovarian cancer reveals support and recruitment of cell-mediated immunity.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Sep-07
• Screened: 2026-09-13 03:10 KST
• PMID: 42705863
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42705863/
• DOI: 10.1136/jitc-2026-014938
• Tags: ovarian cancer, immunotherapy, AMIGA, single-cell RNA sequencing, T cell recruitment, CXCL10, CCL2
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 재발성 백금 내성 난소암 환자를 대상으로 한 AMIGA 요법의 Phase I 임상 시험 데이터를 기반으로 합니다. Bulk 및 single-cell RNA sequencing을 통해 장기 반응자에서 세포 매개 면역 반응이 증가함을 확인했습니다. 특히 CXCL10과 CCL2의 상향 조절이 T 세포 유치를 촉진하는 기전을 규명하여, 향후 T 세포 기반 면역요법과의 병용 치료 개발에 중요한 근거를 제공합니다.

Abstract

Ovarian cancer is the most lethal gynecological malignancy and lacks therapeutic options in the recurrent setting. We previously determined the safety and initial clinical activity of intraperitoneal autologous monocytes with interferon gamma and interferon alpha (AMIGA) in women with recurrent, platinum-resistant ovarian cancer, but not all enrolled patients showed benefit, warranting further analysis to understand and improve this therapy. Bulk RNA sequencing and single-cell RNA sequencing were conducted on circulating immune cells from patients with ovarian cancer treated with AMIGA. Primary human monocytes and T cells were isolated from healthy donors and used in co-cultures with ovarian cancer cell lines to test the effects of AMIGA on T-cell recruitment. Comparing circulating immune cells from long-term responders to non-responders from our clinical trial revealed an increased cell-mediated immune response in long-term responders. T cells in AMIGA-treated patients also upregulated unique, specific T cell receptor-beta chain genes. Bulk RNA-seq of peripheral blood mononuclear cells revealed AMIGA-driven upregulation of CXCL10 and CCL2 mRNA. An increase in these chemokines was consistently reflected in patients' malignant ascites. Finally, in vitro models validated increases in CXCL10 as well as CCL2, and demonstrated that these chemokines exert variable effects on T-cell...

TAMing the tumor: targeting immune inhibitory receptors on tumor-associated macrophages in pediatric brain tumors - an emerging immunotherapy strategy.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Sep-07
• Screened: 2026-09-13 03:10 KST
• PMID: 42705864
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42705864/
• DOI: 10.1136/jitc-2026-015513
• Tags: pediatric brain tumors, tumor-associated macrophages, immune inhibitory receptors, immunotherapy, tumor microenvironment, myeloid-targeted therapy
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 리뷰는 소아 뇌종양에서 가장 풍부한 면역 세포인 종양 관련 대식세포(TAMs)의 역할을 강조합니다. 기존 면역관문억제제가 T 세포에 집중된 반면, 본 논문은 TAMs 표면의 면역 억제 수용체를 표적으로 하여 종양 미세환경을 재프로그래밍하는 전략의 잠재력을 분석합니다. 이는 고등급 소아 뇌종양의 치료 저항성을 극복하고 항종양 면역을 강화할 수 있는 새로운 치료 방향을 제시합니다.

Abstract

Brain tumors are the most common solid tumors in children. Despite recent advancements in cancer survival, the prognosis for high-grade pediatric brain tumors remains poor, with treatments resulting in severe long-term side effects. Over the last decade, immune checkpoint blockade (ICB) has emerged as a promising treatment strategy, with success across various tumor types, particularly in adult malignancies. However, its efficacy in pediatric brain tumors has been limited, which can be attributed to the unique characteristics of the brain tumor microenvironment (TME), including a low mutational burden, restricted T cell infiltration, and immunosuppressive milieu. Importantly, clinically approved ICBs primarily target T cell-associated pathways, thereby neglecting other dominant immune populations within the TME.Among these, tumor-associated macrophages (TAMs) often represent the most abundant immune cell compartment within pediatric brain tumors. TAMs consist of resident microglia and infiltrating bone marrow-derived macrophages and play a central role in establishing and maintaining an immunosuppressive environment. They promote tumor progression, suppress cytotoxic T cell activity, and contribute to therapeutic resistance. However, they are highly heterogeneous, and their phenotype and functions are regulated by the surrounding TME. This intrinsic plasticity makes them promi...

HIF1A+CSF3R+ neutrophils-dominated hypoxic niche induced metabolic reprogramming for neoadjuvant therapy resistance in NSCLC.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Sep-08
• Screened: 2026-09-13 03:09 KST
• PMID: 42711068
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42711068/
• DOI: 10.1136/jitc-2026-014772
• Tags: NSCLC, neoadjuvant therapy resistance, HIF1A+CSF3R+ neutrophils, hypoxic niche, anti-PD-1, spatial transcriptome, platycodin-D2
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 NSCLC 환자에서 neoadjuvant therapy에 대한 저항성을 유발하는 HIF1A+CSF3R+ neutrophils의 역할을 규명했습니다. 이러한 세포들이 hypoxic niche를 형성하여 면역 억제 환경을 조성하고 치료 실패로 이어진다는 것을 multi-omics 데이터로 입증했습니다. 또한, platycodin-D2가 CSF3R을 표적으로 하여 anti-PD-1 요법의 효과를 증진시킬 수 있음을 in vivo 모델에서 확인했습니다.

Abstract

Non-small cell lung cancer (NSCLC) is one of the frequently occurring cancers characterized by molecular heterogeneity and multiple immune cell infiltration patterns, which are associated with treatment sensitivity and resistance. However, the specific microenvironmental cells and their mechanisms that lead to treatment resistance in patients need to be explored in greater depth. On the basis of patients receiving neoadjuvant therapy in our center, a multicenter, multicohort NSCLC spatial transcriptome, single-cell transcriptome, T-cell receptor repertoire sequencing, bulk RNA transcriptome, phosphorylated proteome, genome mutation, and clinical data were included for a comprehensive assessment of the therapeutic and prognostic impact of HIF1A+ CSF3R+ neutrophils in NSCLC. In vitro experiments validated the functional phenotype of HIF1A+ CSF3R+ neutrophils and co-localization interactions with other cellular subpopulations. Gradient boosting machine (GBM) constructed region of interest (ROI) models for evaluation. Computer-aided drug design (CADD) was used to predict targeted small molecule drugs, and in vivo mouse models were constructed to assess the effectiveness of the combination treatment regimen. Centered on HIF1A+ CSF3R+ neutrophils, recruited exhausted T cells and stromal cells form a hypoxic niche within the tumor region, which was enriched in non-response patients....

Deep learning image reconstruction for 50-keV virtual monoenergetic dual-energy CT of the thyroid: a prospective "dual-low" dose study.

• Status: include
• Score: 0.92
• Category: biomedical-imaging
• Journal: European radiology
• Publication date: 2026-Sep-09
• Screened: 2026-09-13 03:08 KST
• PMID: 42714621
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42714621/
• DOI: 10.1007/s00330-026-12814-y
• Tags: Dual-energy CT, Deep learning image reconstruction, Thyroid imaging, Virtual monoenergetic images, Radiation dose reduction, Contrast media reduction, Image quality assessment

Screening brief

이 연구는 갑상선 Dual-energy CT에서 Deep learning image reconstruction을 활용하여 'dual-low' 전략의 타당성을 입증했습니다. 50 keV 가상 단색 에너지 이미지는 요오드 신호를 증폭시키지만 노이즈가 증가하는 문제를 해결하기 위해 DLIR-H 알고리즘을 적용했습니다. 결과적으로 방사선 선량을 61%, 조영제 용량을 20% 줄이면서도 주관적 및 객관적 이미지 품질을 표준 프로토콜보다 우수하게 유지했습니다.

Abstract

Dual-energy CT (DECT) at 50 keV increases iodine attenuation but exponentially amplifies image noise. The feasibility of using deep learning image reconstruction (DLIR) to counteract this noise under a "dual-low" (low-radiation and low-contrast medium) thyroid CT protocol remains underexplored. To investigate the performance of a dual-low DECT protocol combined with DLIR in contrast-enhanced thyroid CT compared with a standard-dose protocol using adaptive statistical iterative reconstruction-Veo (ASIR-V). In this prospective study (August-December 2025), patients were randomly assigned to a standard-dose group (120 kVp, 1.0 mL/kg iodine, ASIR-V 50%) or a dual-low dose group (DECT, 0.6 mL/kg iodine). Dual-low spectral data were reconstructed into 50-keV virtual monoenergetic images using ASIR-V 50%, low-strength DLIR (DLIR-L), and high-strength DLIR (DLIR-H). Objective metrics (CT attenuation, image noise, contrast-to-noise ratio, edge rise slope (ERS), noise power spectrum) and subjective 5-point Likert scores were compared using independent-samples t-tests, paired t-tests, Mann-Whitney U tests, and Wilcoxon signed-rank tests. Sixty-four patients (mean age, 48.6 years ± 12.2; 49 women) were evaluated (32 per group). The dual-low group achieved a 61% reduction in effective radiation dose (0.36 mSv ± 0.05 vs 0.93 mSv ± 0.22; p < 0.001) and a 20% reduction in iodine intake (11.7...

Artificial Intelligence-Based Assessment of Pathologic Response to Neoadjuvant Chemoimmunotherapy in Non-Small Cell Lung Cancer: An International Multicenter Cohort Study.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Sep-05
• Screened: 2026-09-13 03:08 KST
• PMID: 42715648
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42715648/
• DOI: 10.1016/j.lungcan.2026.109609
• Tags: NSCLC, Neoadjuvant Chemoimmunotherapy, Artificial Intelligence, Pathologic Response, %RVT, Digital Pathology, Major Pathologic Response
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

이 연구는 비소세포폐암(NSCLC) 환자에서 신조기 화학면역요법 후의 병리학적 반응을 AI로 평가하는 알고리즘의 성능을 검증했습니다. 다기관 코호트 분석 결과, AI 기반 %RVT 점수는 전문가 수동 평가와 높은 일치도를 보였으며 Major Pathologic Response(MPR) 분류 정확도는 91%에 달했습니다. 이는 임상 시험 및 실제 진료에서 병리학적 반응 평가의 표준화와 객관화를 지원할 수 있는 중요한 도구임을 시사합니다.

Abstract

Pathologic response (PR), expressed as the percentage of residual viable tumor (%RVT), has emerged as a surrogate endpoint after neoadjuvant chemoimmunotherapy in non-small cell lung cancer (NSCLC). However, PR assessment remains subject to interobserver variability and is insufficiently standardized across institutions and clinical trials. We hypothesized that artificial intelligence (AI)-based %RVT scoring would be concordant with expert manual assessment and consistent across real-world, multi-scanner cohorts. Four retrospective NSCLC cohorts treated with neoadjuvant chemoimmunotherapy and surgery were analyzed. The internal cohort included 38 patients; three external cohorts from China, Germany, and Spain contributed 97 additional patients. Weighted consensus manual %RVT served as the reference standard for benchmarking an AI algorithm. Discordant cases were interrogated for algorithmic bias. Overall, 135 patients and 1,344 primary-tumor H&E slides were evaluable. Concordance between AI-based and manual assessment was at least moderate across all cohorts. For major pathologic response (MPR) classification, the AI algorithm achieved a pooled accuracy of 91% (95% CI, 85-95), sensitivity of 90% (82-95), specificity of 93% (81-99), and an area under the curve ≥0.95 in all cohorts. Discordant classifications occurred in 8.9% of cases and were mainly attributable to stromal unde...

PRKX-mediated stabilization of PD-L1 characterizes an immunosuppressive gastric cancer subtype.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Sep-09
• Screened: 2026-09-13 03:07 KST
• PMID: 42716706
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42716706/
• DOI: 10.1136/jitc-2026-015452
• Tags: gastric cancer, PD-L1, PRKX, anti-PD-1 therapy, immune microenvironment, biomarker, single-cell transcriptomics
• Open access (PMC): 📎 Zotero에 추가

Screening brief

위암 환자에서 anti-PD-1 면역요법의 효능이 제한적인 주요 원인으로 PRKX 매개 PD-L1 안정화 기전이 규명되었습니다. 연구진은 single-cell transcriptomics를 통해 위암의 면역 미세환경을 immunosuppressive와 immune-activated 두 하위 유형으로 분류했습니다. PRKX는 PD-L1의 T285 인산화를 유도하여 분해를 방지하고 CD8+ T 세포 기능을 억제함으로써 면역 회피를 촉진합니다. 따라서 PRKX 표적 치료는 anti-PD-1 요법과의 시너지 효과를 통해 위암 치료의 새로운 전략이 될 수 있습니다.

Abstract

Gastric cancer (GC) derives limited benefit from immunotherapy, with clinical responses observed in only a minority of patients. Increasing evidence suggests that heterogeneity within the tumor immune microenvironment (TME) is a critical determinant of immunotherapeutic efficacy, highlighting the need for precise immune stratification and the identification of molecular biomarkers that shape the TME. We integrated single-cell transcriptomic data from our cohort and public datasets to characterize immune microenvironment heterogeneity in GC. Functional experiments were performed using in vitro assays and in vivo mouse models to investigate the molecular mechanisms regulating immune exhaustion. Clinical relevance was evaluated using tumor specimens from patients with GC receiving anti-programmed cell death protein 1 (PD-1) therapy. Survival analyses and biomarker evaluation were conducted to assess the prognostic and predictive value of candidate markers. We identified two distinct GC immune microenvironment subtypes: the immunosuppressive (GC1) and the immune-activated (GC2). PRKX was identified as a key regulator associated with immune heterogeneity and exhaustion. Clinically, a high density of PanCK+ PRKX+ PD-L1+ tumor cells was significantly associated with poor prognosis and served as a robust biomarker predicting 5-year survival in patients treated with anti-PD-1 therapy....

Segmentation-based deep learning emphysema quantification using chest CT: improved accuracy and robustness vs LAA-950.

• Status: include
• Score: 0.95
• Category: biomedical-imaging
• Journal: European radiology
• Publication date: 2026-Sep-09
• Screened: 2026-09-13 03:07 KST
• PMID: 42717029
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42717029/
• DOI: 10.1007/s00330-026-12800-4
• Tags: deep learning, emphysema quantification, chest CT, LAA-950, segmentation, pulmonary function tests, radiomics

Screening brief

이 연구는 흉부 CT 영상을 이용한 폐기종 정량화를 위해 딥러닝 분할 알고리즘을 개발하고 검증했습니다. 기존 LAA-950 방법과 비교했을 때, 제안된 모델은 Dice 계수 및 재현성에서 우수한 성능을 보였습니다. 또한 방사선사의 시각적 평가 점수 및 폐기능 검사 결과(DLCO, FEV1)와의 상관관계가 더 강하게 나타났습니다. 이는 임상적으로 더 신뢰할 수 있는 폐기종 정량화 도구를 제공한다는 점에서 의미가 큽니다.

Abstract

To develop a deep learning segmentation algorithm to enable accurate, reliable emphysema quantification while improving agreement with radiologist assessments and pulmonary function tests. The model was developed using retrospective virtual and clinical datasets. Virtual data enabled pre-training using ground truth across controlled parameters, including scanners, doses, and reconstruction kernels, while clinical data enabled fine-tuning with expert-annotated emphysema masks. Segmentation accuracy was quantified using the Dice coefficient, and robustness was quantified using emphysema percentage consistency across imaging conditions. Model-based emphysema percentage was correlated with Fleischner visual scores (ordinal; 0-5) and pulmonary function tests (DLCO, FEV1pp, and FEV1/FVC) and compared to LAA-950. Statistical analysis included univariate/multivariate correlations. Quantitative assessment included Dice, bias, limits of agreement, and reproducibility coefficient. Virtual data included 20 human models (mean age: 43 years ± 11 [SD], 10 men), and clinical data included multi-center cohorts of 101 patients (C1; 57 years ± 8, 54 men), 23 patients (C2; 57 years ± 7, 14 men), and 1159 patients (C3; 65 years ± 9, 586 men). The model outperformed LAA-950 in segmentation accuracy, achieving higher Dice scores across virtual (76.6% ± 8.8 vs 51.5% ± 23.5), C1 (48.4% ± 24.2 vs 22.5%...

PREDICT-GBM: A multicenter platform advancing personalized glioblastoma radiotherapy planning.

• Status: include
• Score: 0.95
• Category: biomedical-imaging
• Journal: NPJ digital medicine
• Publication date: 2026-Sep-09
• Screened: 2026-09-13 03:06 KST
• PMID: 42717239
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42717239/
• DOI: 10.1038/s41746-026-03194-0
• Tags: Glioblastoma, Radiotherapy Planning, Deep Learning, U-Net, Recurrence Prediction, Open Source Platform, NPJ Digital Medicine
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

PREDICT-GBM은 Glioblastoma 환자의 재발 영역을 예측하기 위한 오픈소스 플랫폼으로, 다기관 데이터셋과 표준화된 평가 파이프라인을 제공합니다. 연구 결과, U-Net 기반 모델이 기존 가이드라인 기반 계획보다 재발 부위의 기하학적 커버리지를 통계적으로 유의미하게 향상시킨 것으로 확인되었습니다. 이는 계산 모델을 통한 개인화된 Radiotherapy 계획의 임상적 전환에 중요한 기준점을 제시합니다.

Abstract

Glioblastoma recurrence is largely driven by diffuse infiltration beyond radiologically visible margins, yet current radiotherapy guidelines rely on uniform margin expansions that ignore patient-specific biology and anatomy. While computational models promise to map this invisible growth and guide personalized planning, their clinical translation is hindered by a lack of standardized benchmarking and reproducible validation. To bridge this gap, we present PREDICT-GBM, an open-source platform integrating a curated, longitudinal, multi-center dataset of 243 patients with a standardized evaluation pipeline. We benchmark a novel U-Net-based recurrence prediction model against state-of-the-art biophysical and data-driven methods. Under iso-volumetric constraints, both biophysical and deep-learning approaches achieved modest but statistically significant gains in geometric coverage of future recurrence over guideline-based plans. On the combined cohort, our U-Net achieved the highest mean coverage of enhancing recurrence (79.37 ± 2.08%), surpassing guideline-based plans (paired Wilcoxon signed-rank test, Benjamini-Hochberg adjusted p = 2.9 × 10-5). The biophysical model GliODIL reached 78.91 ± 2.08% (p = 1.0 × 10-3), validating the platform's ability to compare diverse modeling paradigms. By providing a reproducible ecosystem for model training and validation, PREDICT-GBM addresses...

Treatment-free interval as a determinant of second-line chemotherapy outcomes in extensive-stage small cell lung cancer: a Dutch population-based study.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Sep-05
• Screened: 2026-09-13 03:05 KST
• PMID: 42721617
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42721617/
• DOI: 10.1016/j.lungcan.2026.109621
• Tags: small cell lung cancer, second-line treatment, platinum rechallenge, topotecan, treatment-free interval, survival analysis, population-based study
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

이 연구는 네덜란드 암 등록 데이터를 기반으로 ES-SCLC 재발 환자의 Treatment-free interval(TFI)과二线 치료 결과 간의 연관성을 분석했습니다. TFI가 90일 이상인 환자군에서 platinum rechallenge가 topotecan 대비 진행 위험을 유의미하게 낮추는 것으로 확인되었습니다. 이는 chemoimmunotherapy 도입 이후에도 여전히 임상적 관련성이 높으며, 면역치료 접근이 제한된 환경에서도 중요한 치료 전략 지침을 제공합니다.

Abstract

For patients with recurrence after chemotherapy for extensive-stage small cell lung cancer (SCLC), the length of the chemotherapy-free interval (CFI) may guide the choice of second-line treatment. However, evidence supporting specific CFI thresholds is limited. We investigated the influence of the CFI on the effectiveness of second-line treatment in SCLC patients. Patients diagnosed with SCLC in 2022 were selected from the Netherlands Cancer Registry. Cox regression and parametric survival models were used to investigate the association between the type of second-line treatment, the CFI, progression-free survival (PFS) and overall survival (OS). Analyses were adjusted for age, sex, performance status, income, comorbidities, response to first-line treatment, and distant metastases. 261 patients were included: 79 received (30.3%) topotecan, 153 (58.6%) platinum rechallenge, and 29 (11.1%) another systemic treatment. Median PFS was 2.0 and 3.9 months after topotecan and platinum rechallenge, respectively. Median OS was 3.8 and 5.6 months, respectively. Multivariable analyses showed a lower risk of progression for patients with a CFI of 90-179 days receiving platinum rechallenge vs topotecan (hazard ratio (HR): 0.62, 95% confidence interval (95%CI): 0.40-0.95), without a difference in OS (HR: 0.99, 95%CI: 0.65-1.52). Parametric survival models confirmed these results. For patients...

The efficacy and feasibility of neoadjuvant immunochemotherapy versus chemotherapy in Limited-Stage Small-Cell lung cancer.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Sep-02
• Screened: 2026-09-13 03:04 KST
• PMID: 42727356
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42727356/
• DOI: 10.1016/j.lungcan.2026.109607
• Tags: Small-Cell Lung Cancer, Neoadjuvant Therapy, Immunochemotherapy, Pathological Complete Response, Disease-Free Survival, Surgical Oncology, Propensity Score Matching

Screening brief

이 연구는 제한기 소세포폐암(LS-SCLC) 환자에서 neoadjuvant immunochemotherapy(NIC)가 기존 chemotherapy 대비 더 높은 pathological complete response(pCR) 및 major pathological response(MPR)를 유도함을 입증했습니다. NIC 군은 upfront surgery 군에 비해 disease-free survival(DFS)이 유의하게 우수했으며, pCR/MPR 달성 시 예후가 개선되는 것으로 확인되었습니다. 이러한 결과는 LS-SCLC 치료에서 NIC 후 수술 접근법의 임상적 유용성을 지지하며, 향후 prospective trial에서의 검증 필요성을 시사합니다.

Abstract

The efficacy of neoadjuvant immunochemotherapy (NIC) in limited-stage small-cell lung cancer (LS-SCLC) remains undefined. This study aimed to evaluate the pathological and survival outcomes of NIC versus neoadjuvant chemotherapy (NC) and to compare NIC with upfront surgery in a real-world setting. Patients with LS-SCLC (stage I-IIIB) who underwent upfront surgery or neoadjuvant treatment followed by radical surgery between February 2005 and November 2025 were retrospectively enrolled. Propensity score matching (PSM) (1:2) was used to compare the survival outcomes between the neoadjuvant and upfront surgery cohorts. The primary endpoint was pathological complete response (pCR) rate and major pathological response (MPR) rate. Among 164 included patients, 45 received neoadjuvant therapy (25 NIC, 20 NC). The NIC group achieved significantly higher pCR (52.0% vs. 5.0%; OR 19.31, p < 0.001) and major pathological response (MPR; 76.0% vs. 15.0%; OR 16.47, p < 0.001) rates compared to NC. Rates of pathological TNM and nodal downstaging were also superior with NIC. Surgical safety was comparable between NIC and NC. Within the neoadjuvant cohort, achieving pCR or MPR was associated with significantly improved disease-free survival (DFS). After PSM adjustment, the NIC group demonstrated significantly better DFS compared to the upfront surgery group (log-rank p = 0.007), with a trend towa...

Enhanced CD33 CAR-NK cells secreting anti-CD73scFv overcome adenosine-mediated immunosuppression and improve anti-AML efficacy.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Sep-01
• Screened: 2026-09-06 03:11 KST
• PMID: 42680202
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42680202/
• DOI: 10.1136/jitc-2026-014825
• Tags: CAR-NK cells, Acute myeloid leukemia, Tumor microenvironment, CD33, CD73, Immunotherapy, Adenosine pathway
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 CD33 CAR-NK 세포가 anti-CD73scFv를 분비하도록 설계하여, 아데노신 매개 면역억제를 극복하고 AML 치료 효능을 향상시키는 방법을 제시합니다. 실험 결과, 이 이중 표적 전략은 기존 CAR-NK 세포보다 우수한 종양 제거 효과와 생존율 향상을 보였습니다. 이는 혈액암의 면역치료 저항성을 해결하기 위한 새로운 전환적 접근법을 제공합니다.

Abstract

Acute myeloid leukemia (AML) is an aggressive hematologic malignancy with dismal outcomes, especially in relapsed/refractory settings. Chimeric antigen receptor natural killer (CAR-NK) cell therapy holds promise but is constrained by the immunosuppressive tumor microenvironment (TME), where adenosine-mediated suppression is a key barrier. To develop a novel CAR-NK construct cotargeting AML cells and the adenosine-rich TME to enhance antileukemia efficacy. Ex vivo expanded primary NK cells were used to compare the effects of CD39 versus CD73 blockade on NK cell function via messenger RNA-electroporated antibodies. A CD33-CD73 dual-function CAR-NK construct (integrating CD33-specific lysis and anti-CD73scFv secretion for TME disruption) was designed and transduced into NK cells via retrovirus. Engineered NK cells were characterized for transduction efficiency, expansion, purity, viability, and CAR stability. In vitro cytotoxicity against AML cell lines and primary blasts was assessed, and in vivo efficacy was evaluated in a MOLM-13 xenograft mouse model. CD73 blockade more potently enhanced NK cell activity than CD39 blockade. Retroviral transduction achieved >50% efficiency, and expansion with K562-4-1BBL-mbIL-21/-15 feeder cells yielded NK cells with ≥6,000 fold expansion, >93% purity, >98% viability, and stable CAR expression. At an effector-to-target ratio of 0.5:1, CD33-CD7...

Mechanistic modeling of tumor immune microenvironment reveals strategies to enhance antibody-drug conjugates' efficacy.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Sep-01
• Screened: 2026-09-06 03:10 KST
• PMID: 42680203
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42680203/
• DOI: 10.1136/jitc-2026-015357
• Tags: Antibody-drug conjugates, Tumor microenvironment, Mechanistic modeling, PD-L1, CD8+ T cells, Drug delivery, Immunotherapy
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 HE-S2 ADC의 종양 내 전달과 면역 반응을 연결하는 시공간적 기계론적 모델을 개발했습니다. 모델은 혈관 정상화 전략이 ADC의 침투와 CD8+ T 세포의 침윤을 어떻게 향상시키는지 설명합니다. 이는 항암제 효능을 극대화하기 위한 최적의 치료 시기와 조건을 예측하는 데 유용한 근거를 제공합니다.

Abstract

Antibody-drug conjugates (ADCs) and bispecific antibodies represent a rapidly advancing frontier in oncology, yet the abnormal tumor microenvironment (TME) hinders their delivery and reduces efficacy. Emerging immunomodulatory ADCs (IM-ADCs) demand mechanistic mathematical models that couple drug transport with immune dynamics. Here, we present a mechanistic framework for the delivery of HE-S2 ADC, an anti-programmed cell death ligand 1 (PD-L1) antibody bearing the bifunctional immunomodulator D18. Our model integrates cancer-immune cells interactions, TME properties, such as dysfunctional vessels, elevated interstitial fluid pressure, tissue hydraulic conductivity, and vascular permeability, spatiotemporal distributions across growing tumor and adjacent host tissue, convective-diffusive transport, ADCs binding and internalization kinetics and tumor-draining lymph node biology governing antigen presentation and the generation of effector CD8+ T cells. Parameters were calibrated simultaneously with the murine MC38 and B16 tumor growth data and effector CD8+T cell data following treatment with D18, anti-PD-L1, and ADC. Our mechanistic spatiotemporal model captures the superior antitumor efficacy of the HE-S2 ADC relative to its individual components and provides mechanistic predictions for unmeasured variables, such as spatiotemporal dynamics of drug/immune-cell distributions. I...

Daraxonrasib for Previously Treated RAS-Mutant Non-Small-Cell Lung Cancer.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: The New England journal of medicine
• Publication date: 2026-Sep-03
• Screened: 2026-09-06 03:10 KST
• PMID: 42685317
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42685317/
• DOI: 10.1056/nejmoa2504059
• Tags: NSCLC, RAS-mutant, daraxonrasib, Phase I-2 trial, targeted therapy, NEJM, oncology

Screening brief

이 연구는 이전에 치료받은 RAS 돌연변이 비소세포폐암(NSCLC) 환자에서 daraxonrasib의 안전성과 항종양 활성을 평가했습니다. 300mg 이하 용량군에서 객관적 반응률(ORR)은 31%에서 37%로 나타나 유의미한 효능을 보였습니다. 주요 부작용으로는 발진, 설사, 구토 등이 관찰되었으며, Grade 3 이상 이상반응 발생률은 54%였습니다.

Abstract

RAS mutations, as a group, are the most common oncogenic drivers of non-small-cell lung cancer (NSCLC), and they occur in approximately 30% of patients. Whether daraxonrasib (RMC-6236) - an oral RAS(ON) multiselective, tri-complex inhibitor of guanosine triphosphate-bound mutant and wild-type RAS protein isoforms - is safe and effective in patients with RAS-mutant NSCLC is unknown. In this phase 1-2, multicenter, dose-escalation and dose-expansion study of daraxonrasib, we enrolled patients with previously treated advanced RAS-mutant NSCLC and administered daraxonrasib in doses of 10 to 400 mg orally once daily in 21-day cycles. The primary end point was safety. Secondary end points included investigator-assessed objective response (complete or partial response) and the duration of response, with response assessed according to Response Evaluation Criteria in Solid Tumors, version 1.1. As of the data-cutoff date of July 21, 2025, a total of 136 patients with NSCLC who had been enrolled and treated with daraxonrasib at doses of 300 mg or less had been evaluated for safety and efficacy. Adverse events of any grade occurring with a dose of 300 mg or less, regardless of attribution, were reported in 99% of the patients, with rash, diarrhea, nausea, vomiting, and mucositis or stomatitis occurring in at least 30% of patients. Adverse events of grade 3 or higher were reported in 54% o...

MTAP loss in non-small-cell lung Cancer and beyond: Therapeutic targeting of the MAT2A-PRMT5 axis.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Cancer treatment reviews
• Publication date: 2026-Aug-29
• Screened: 2026-09-06 03:09 KST
• PMID: 42685449
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42685449/
• DOI: 10.1016/j.ctrv.2026.103204
• Tags: NSCLC, MTAP loss, PRMT5 inhibitor, MAT2A, synthetic lethality, precision oncology, biomarker

Screening brief

이 리뷰는 비소세포폐암(NSCLC)에서 MTAP 결실이 유발하는 대사 및 후생유전학적 취약점을 분석합니다. 특히 MAT2A-PRMT5 축을 표적으로 하는 억제제의 임상적 잠재력과 저항성 메커니즘을 논의합니다. 이는 대사 기반 정밀 의약품 개발과 바이오마커 검증의 방향성을 제시하는 중요한 자료입니다.

Abstract

Loss of methylthioadenosine phosphorylase (MTAP), which occurs in approximately 10-15% of non-small-cell lung cancers and other solid tumors, represents a key synthetic-lethal vulnerability linking tumor metabolism to epigenetic regulation. MTAP deletion disrupts the methionine salvage pathway, leading to accumulation of methylthioadenosine (MTA) and selective dependence on protein arginine methyltransferase 5 (PRMT5). This metabolic rewiring provides a unique therapeutic opportunity to target the MAT2A-PRMT5 axis. This review summarizes recent advances in understanding MTAP biology, including the PRMT5/MAT2A feedback network, tumor heterogeneity, and adaptive resistance mechanisms encompassing metabolic compensation, splicing plasticity, and immune-cold microenvironments associated with 9p21 co-deletion. Emerging clinical data on MTA-cooperative PRMT5 inhibitors and MAT2A inhibitors are discussed, alongside challenges in diagnostic accuracy, biomarker validation, and patient stratification. Despite encouraging early-phase activity, the translation of MTAP-directed therapy is constrained by diagnostic discordance, tumor adaptability, and the absence of prospective, biomarker-driven trials. Future progress will depend on harmonized detection methods, integration of metabolic biomarkers, and rational therapeutic combinations with targeted or immune-based approaches. Collectively...

IL20RB drives non-small cell lung cancer progression and immune evasion via K267‑dependent activation of JAK2 phosphorylation and STAT3 signaling.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-31
• Screened: 2026-09-06 03:09 KST
• PMID: 42685527
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42685527/
• DOI: 10.1016/j.lungcan.2026.109599
• Tags: NSCLC, IL20RB, JAK2-STAT3 signaling, immune evasion, PD-L1, drug repurposing, acetaminophen

Screening brief

이 연구는 IL20RB가 K267 잔기를 통해 JAK2 인산화를 활성화하고 STAT3 신호 전달을 촉진하여 NSCLC의 진행과 면역 회피를 유도함을 규명했습니다. 특히 아세트아미노펜(APAP)이 HDAC3 매개 탈아세틸화를 통해 IL20RB 발현을 억제하고 항-PD-L1 요법과 시너지 효과를 보인다는 점이 주목할 만합니다. 이는 IL20RB를 NSCLC의 유망한 예후 바이오마커 및 치료 표적으로 자리매김하며, 기존 약물의 새로운 적응증 개발 가능성을 시사합니다.

Abstract

Tumor immune evasion is a pivotal mechanism driving therapeutic resistance and poor prognosis in lung cancer. The interleukin-20 receptor β subunit (IL20RB) is implicated in chronic inflammation and oncogenesis, but its precise function and molecular basis in non-small cell lung cancer (NSCLC) require elucidation. Multi-omics data analysis, clinical NSCLC specimens, and a series of in vitro and in vivo functional experiments were employed to investigate the role of IL20RB. Techniques included gene expression correlation, survival analysis, cell proliferation/migration/invasion assays, co-immunoprecipitation, western blotting, and pharmacologic modulation studies. IL20RB was significantly overexpressed in NSCLC tissues, correlating with advanced disease stage and inferior patient survival. Its knockdown potently suppressed NSCLC cell proliferation, migration, and invasion. High IL20RB expression was associated with reduced T cell infiltration and function within the tumor microenvironment. Mechanistically, IL20RB directly bound to JAK2 via a critical lysine residue (K267), activating JAK2-STAT3 signaling and upregulating downstream effectors including PD-L1 and BCL2, thereby coordinating tumor growth and immune escape. The commonly used drug acetaminophen (APAP) was identified to downregulate IL20RB expression via HDAC3-mediated deacetylation, inhibiting this oncogenic pathway...

Targeting the PD-L1-induced PDK4/GLS metabolic axis overcomes anti-PD-1 resistance in non-small cell lung cancer.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Sep-02
• Screened: 2026-09-06 03:08 KST
• PMID: 42686373
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42686373/
• DOI: 10.1136/jitc-2026-015037
• Tags: NSCLC, anti-PD-1 resistance, PD-L1 reverse signaling, metabolic reprogramming, PDK4/GLS axis, tumor-associated macrophages, immunotherapy
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 NSCLC 환자에서 anti-PD-1 치료 저항성이 PD-L1의 비전통적 역신호 전달을 통해 유발된다는 것을 밝혔습니다. 구체적으로 PD-L1 활성화가 ER 스트레스 경로를 통해 PDK4와 GLS 발현을 증가시켜 피루브산 축적을 초래함을 확인했습니다. 이러한 대사 변화는 종양 관련 대식세포(TAMs)의 노화를 유도하여 면역억제 환경을 강화하는 것으로 나타났습니다. 따라서 PDK4/GLS 표적 치료가 anti-PD-1 요법의 효과를 증진할 수 있는 유망한 전략임을 제시합니다.

Abstract

Metabolic reprogramming within the tumor microenvironment is a pivotal barrier to effective immune checkpoint blockade (ICB). While programmed death ligand 1 (PD-L1) is well characterized as a ligand inhibiting T-cell function, its intrinsic 'reverse signaling' role in regulating tumor metabolism and shaping the immune landscape remains poorly understood. Here, we investigated the metabolic determinants of resistance to anti-programmed cell death protein 1 (anti-PD-1) therapy and the underlying molecular mechanisms. Integrated metabolomics and transcriptomics were performed on tumor samples from patients with non-small cell lung cancer and cell lines. Mechanisms were delineated using RNA sequencing, cleavage under targets and tagmentation assays, metabolic flux analysis, and coculture systems. The therapeutic efficacy of targeting metabolic effectors was evaluated in syngeneic mouse models and correlated with immune profiling. We identified a distinct metabolic signature characterized by aberrant pyruvate accumulation in patients resistant to anti-PD-1 therapy. Mechanistically, we demonstrate that antibody-mediated ligation of PD-L1 triggers an intrinsic endoplasmic reticulum (ER) stress response via the PERK-ATF4-CHOP axis. ATF4 acts as a transcriptional activator that directly upregulates pyruvate dehydrogenase kinase 4 (PDK4) (blocking pyruvate oxidation) and glutaminase (G...

GTPase RAB31 supports ANXA1-driven macrophage education through clathrin-mediated endocytosis to suppress antitumor immunity.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Sep-02
• Screened: 2026-09-06 03:08 KST
• PMID: 42686375
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42686375/
• DOI: 10.1136/jitc-2026-015703
• Tags: Tumor-associated macrophages, RAB31, Clathrin-mediated endocytosis, Antitumor immunity, PD-L1 therapy, Tumor microenvironment, FPR2
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 RAB31이 clathrin-mediated endocytosis를 통해 ANXA1 신호 전달을 조절하여 종양 관련 대식세포의 교육과 항종양 면역을 억제함을 밝혔습니다. Rab31 결핍은 대식세포를 M1 유사 표현형으로 재프로그래밍하고 CD8+ T 세포 침윤 및 활성화를 촉진하여 종양 성장을 억제했습니다. 또한, RAB31 경로의 억제는 anti-PD-L1 치료와 시너지 효과를 나타내어 새로운 면역치료 표적으로서의 잠재력을 시사합니다.

Abstract

Tumor-associated macrophages (TAMs) play pivotal roles in shaping the tumor-microenvironment (TME) through functional plasticity, which is regulated by extrinsic and intrinsic signals. However, the role of vesicular trafficking in TAMs remains poorly understood. RAB31, a small GTPase enriched in myeloid cells, was proposed as a potential regulator of TAM polarization through clathrin-mediated endocytosis (CME). We hypothesized that RAB31 modulates TAM education by tumor-derived signals and thereby shapes antitumor immunity. We profiled RAB31 expression in human cancers using public single-cell RNA sequencing (scRNA-seq) datasets and clinical sample immunofluorescence staining. Rab31 knockout mice were employed in subcutaneous tumor models. The TME was profiled by scRNA-seq, bulk RNA-seq, and flow cytometry. Bone marrow transplantation, adoptive cell transfer, and antibody-mediated depletion were performed to identify the effector cell populations. Co-immunoprecipitation coupled with mass spectrometry, receptor half-life assays, inhibitor intervention and lysosomal colocalization experiments dissected the molecular mechanism. Functional T-cell chemotaxis, activation, and anti-programmed death-ligand 1 (PD-L1) response assays were performed. RAB31 was highly expressed in TAMs across multiple cancers and correlated with poor prognosis and immunosuppressive TME. Rab31 deficiency r...

Topogram-based anatomical labelling of CT series: anatomy-aware CT data processing using deep learning.

• Status: include
• Score: 0.92
• Category: biomedical-imaging
• Journal: European radiology
• Publication date: 2026-Sep-03
• Screened: 2026-09-06 03:07 KST
• PMID: 42690467
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42690467/
• DOI: 10.1007/s00330-026-12830-y
• Tags: CT topogram, Deep Learning, YOLOv8, Anatomical Labelling, DICOM, Medical Image Processing, RAPID framework
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

이 연구는 딥러닝 기반의 RAPID 프레임워크를 통해 CT topogram을 분석하여 해부학적 라벨링을 수행합니다. 기존에 신뢰할 수 없었던 DICOM 텍스트 메타데이터 대신 이미지 자체의 공간 기하학을 활용하여 일관된 데이터 처리가 가능합니다. 높은 F1 점수와 mAP50 성능은 이 방법이 임상 환경에서 확장 가능하고 정확한 자동화 라벨링 솔루션임을 입증합니다.

Abstract

This study provides a Rapid Analysis and Processing of Image Data (RAPID) framework that combines deep learning-based CT topogram analysis with DICOM spatial geometry to enable reliable anatomical labelling of CT series independent of inconsistent textual metadata. In this single-centre retrospective study, three YOLOv8-based models comprising the RAPID framework were trained on CT topograms to perform global anatomical classification, body-region detection, and landmark detection. Classification used 83207 topograms (20,802 test), while landmark and body region detection models were trained on 2000 (500 test) and 1926 (481 test) topograms, respectively, collected between 2003 and 2022. Model performance was evaluated using the F1 score and mAP50, with additional external validation on the external cohort. Furthermore, three radiologists independently reviewed 150 randomly selected predictions for detection models using a Likert-scale-based clinical assessment with inter-rater agreement. Across a total of 65,250 patients (median age, 62 years; interquartile range, 23; 44% female) included in training and testing, inference performance achieved an overall internal F1 score of 0.920 and an external score of 0.970 for classification. Body region and landmark detection achieved internal mAP50 values of 0.993 and 0.958, with corresponding F1 scores of 0.996 and 0.957, respectively....

Clinical outcomes and genomic features of uncommon EGFR exon 19 deletion subtypes in osimertinib-treated non-small cell lung cancer.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-31
• Screened: 2026-09-06 03:07 KST
• PMID: 42691830
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42691830/
• DOI: 10.1016/j.lungcan.2026.109604
• Tags: NSCLC, EGFR exon 19 deletion, Osimertinib, PFS, OS, Genomic alterations, L747_A750delinsP

Screening brief

이 연구는 Osimertinib 치료를 받는 EGFR exon 19 deletion 양성 NSCLC 환자에서 하위 유형별 생존 결과를 비교했습니다. 분석 결과, E746_A750del 그룹에 비해 non-E746_A750del 그룹, 특히 L747_A750delinsP 변이를 가진 환자들의 PFS와 OS가 현저히 짧았습니다. 이러한 예후 차이는 RBM10 공변이 또는 CDKN2A/B 결실, MYC 증폭 등 동반 유전체 변화의 차이로 설명될 수 있습니다.

Abstract

Epidermal growth factor receptor (EGFR) exon 19 deletion subtypes may be associated with differential survival outcomes following EGFR-tyrosine kinase inhibitor treatment. However, evidence remains scarce, particularly regarding osimertinib, and the underlying biological mechanisms are poorly understood. We aimed to compare survival outcomes among EGFR exon 19 deletion subtypes in patients with non-small cell lung cancer (NSCLC) treated with osimertinib. In this multicenter retrospective study, patients with NSCLC were stratified according to exon 19 deletion subtypes. Whole-exome sequencing data from the American Association for Cancer Research Genomics Evidence Neoplasia Information Exchange registry and Memorial Sloan Kettering Clinicogenomic Harmonized Oncologic Real-World Dataset were analyzed to investigate co-occurring genomic alterations. Overall, 111 patients with advanced EGFR exon 19 deletion-positive NSCLC were analyzed and 86.5% received osimertinib as first-line therapy. Patients with non-E746_A750del (n = 25) had shorter progression-free survival (PFS) than those with E746_A750del (n = 86) (median: 14.3 vs. 20.6 months; p < 0.05). Among non-E746_A750del subtypes, L747_A750delinsP (n = 4) had a particularly poor prognosis, with significantly worse survival than those with E746_A750del (median PFS: 3.5 vs. 20.6 months; p < 0.001, and median overall survival: 11.8...

Adjuvant immunotherapy in resectable non-small cell lung cancer with nodal downstaging.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-31
• Screened: 2026-09-06 03:06 KST
• PMID: 42691831
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42691831/
• DOI: 10.1016/j.lungcan.2026.109601
• Tags: NSCLC, neoadjuvant chemo-immunotherapy, adjuvant immunotherapy, nodal downstaging, prognostic marker, ypN0, recurrence-free survival

Screening brief

이 연구는 재sectable NSCLC 환자에서 neoadjuvant chemo-immunotherapy 후 수술을 받은 다기관 코호트를 분석했습니다. 결과는 post-treatment pathological nodal status(ypN)가 pretreatment clinical stage보다 prognosis를 더 잘 예측하며, ypN0로 downstaging된 환자는 Natural N0와 유사한 생존율을 보임을 확인했습니다. 또한, ypN0 환자군에서 adjuvant immunotherapy가 RFS나 OS 향상에 유의미하지 않다는 점을 시사하여, 향후 치료 전략 수립에 중요한 근거를 제공합니다.

Abstract

To determine whether prognosis after neoadjuvant chemo-immunotherapy is better predicted by pretreatment clinical nodal stage or post-treatment pathological nodal status, and whether patients downstaged to ypN0 have outcomes comparable to those with primary N0. We conducted a multicenter retrospective cohort study of patients with resectable NSCLC treated with neoadjuvant chemo-immunotherapy followed by curative-intent surgery between January 2020 and December 2024. Patients were categorized as Natural N0 (cN0/ypN0), Downstaged N0 (cN+/ypN0), or ypN + according to baseline clinical and postoperative pathological nodal status. RFS and OS were analyzed using Kaplan-Meier and Cox regression methods. Subgroup analyses were performed in ypN0 patients to assess the association of adjuvant immunotherapy with survival. A total of 413 patients were included, and 207 (67.0%) with clinical nodal metastasis achieved nodal downstaging to ypN0. The overall MPR and pCR rates were 62.5% and 35.8%, respectively. After a median follow-up of 29.2 months, 2-year RFS and OS rates were 78.0% and 93.3%. Downstaged N0 had survival comparable to Natural N0, whereas ypN + was associated with worse RFS. In multivariable analysis, ypN + independently predicted poor recurrence-free survival (HR 2.86, 95% CI 1.40-5.84). Among ypN0 patients, adjuvant immunotherapy was not associated with improved RFS or OS....

Fusion isoform multiplicity and impact on treatment outcomes in ALK-rearranged non-small cell lung cancer with next-generation tyrosine kinase inhibitors.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-26
• Screened: 2026-09-06 03:06 KST
• PMID: 42691832
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42691832/
• DOI: 10.1016/j.lungcan.2026.109594
• Tags: ALK-rearranged NSCLC, Fusion isoform multiplicity, Next-generation TKIs, Progression-free survival (PFS), RNA-seq, Precision oncology, Biomarker analysis

Screening brief

본 연구는 ALK 재배열 NSCLC 환자에서 Fusion isoform multiplicity가 next-generation TKI 치료 반응에 미치는 영향을 분석했습니다. 다중 Isoform을 가진 환자는 단일 Isoform 환자보다 중위 PFS가 유의하게 짧았으며, 이는 독립적인 예후 인자로 확인되었습니다. 또한 질병 진행 시 ALK p.G1202R 돌연변이 발생과 Isoform profile의 변화도 관찰되어, 치료 저항성 메커니즘 이해에 기여합니다.

Abstract

ALK-rearranged non-small cell lung cancer (NSCLC) reported controversies regarding the impact the ALK-fused genes on treatment outcome. Fusion isoforms are structural variants of the same fusion transcript. Recent evidence suggests that the presence of multiple isoforms within a single tumor is associated with reduced response to crizotinib. Whether ALK fusion isoforms affect treatment with next-generation ALK-tyrosine kinase inhibitors (TKIs) remains to be determined. This analysis retrospectively involved 89 advanced ALK-rearranged (ALK + ) NSCLC patients treated with next-generation TKIs in first-line setting in five French centers from 2006 to 2023 and with RNA-seq routinely performed. We used multivariate Cox regression models to identify potential correlations between the presence of isoform multiplicity, other clinical factors, and PFS. ALK + patients with multiple isoforms (n = 38, 42.7 %) showed a significantly shorter median PFS compared to patients with a single isoform (multiple:14.6 months; single: 27.1 months, HR 0.58 0.33-1.02, p = 0.0499). The multivariate analysis reported that multiple isoforms and PD-L1 ≥ 50 % expression were independently negatively associated with PFS. Exploratory analyses did not identify ALK fusion-v3 variant as independently associated with shorter PFS. Eight of the 9 patients with emergent ALK p.G1202R mutation at disease progression h...

Subtyping limited stage small cell lung cancer (LS SCLC) reveals inflammatory subtypes with improved chemoradiotherapy outcomes.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Sep-02
• Screened: 2026-09-06 03:05 KST
• PMID: 42691846
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42691846/
• DOI: 10.1016/j.lungcan.2026.109606
• Tags: Small cell lung cancer, Molecular subtyping, Chemoradiotherapy, Gene expression, Prognostic biomarkers, Inflammatory subtype
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

이 연구는 제한기 소세포폐암(LS SCLC) 환자에서 Concurrent chemoradiotherapy(CRT) 치료 반응에 영향을 미치는 분자 하위 유형을 분석했습니다. 특히 염증성(Inflamed) 하위 유형은 Time to progression(TTP)과 Overall survival(OS)이 유의하게 개선되는 것으로 나타났습니다. 반면, NEUROD1-driven(SCLC-N) 하위 유형은 불리한 임상 결과와 관련이 있었습니다. 이러한 발견은 LS SCLC의 치료 전략 수립 및 예후 예측에 중요한 시사점을 제공합니다.

Abstract

Concurrent chemoradiotherapy (CRT) remains the primary treatment for limited stage (LS) small cell lung cancer (SCLC). Although most patients respond, the majority relapse and die from the disease, and treatment-related toxicity is common. Molecular subtyping has been extensively investigated in SCLC, but its clinical relevance remains uncertain, and most studies have focused on systemic treatment of extensive-stage SCLC. We analysed baseline tumor samples from a subset of participants (n = 77) in a randomized trial (n = 170) comparing high-dose (60 Gy/40 fractions) with standard-dose (45 Gy/30 fractions) twice-daily thoracic radiotherapy given concurrently with platinum-etoposide chemotherapy for LS SCLC, aiming to characterize molecular subtypes of LS SCLC and evaluate their association with time to progression (TTP) and overall survival (OS). Molecular subtypes were defined in 81 samples using non-negative matrix factorization on gene expression data, supported by differential expression and known SCLC markers. Inflamed subtypes were associated with better treatment outcomes. Univariable analysis indicate that SCLC-I-NE (inflamed neuroendocrine) was associated with longer TTP (HR 0.10, 95 % CI 0.01-0.80, p = 0.03), and SCLC-I-nNE (inflamed non-neuroendocrine) was associated with improved OS (HR 0.16, 95 % CI 0.03-0.77, p = 0.02). By contrast, SCLC-N (NEUROD1-driven) was con...

Artificial intelligence-based assessment of tumor bed stroma in non-small cell lung cancer after neoadjuvant therapy: Association with pathologic response and survival. A multicenter study.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-31
• Screened: 2026-09-06 03:04 KST
• PMID: 42691847
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42691847/
• DOI: 10.1016/j.lungcan.2026.109605
• Tags: NSCLC, neoadjuvant therapy, artificial intelligence, tumor bed stroma, pathologic complete response, prognostic biomarker, immunotherapy, histopathology
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

이 연구는 NSCLC 환자에서 neoadjuvant therapy 후 tumor bed의 조직학적 특징을 AI를 이용해 정량화했습니다. 특히 immunotherapy 그룹에서 더 높은 pathologic complete response rate와 낮은 residual viable tumor burden을 보였습니다. AI 기반 fibrosis 정량화는 재발 위험 예측에 독립적인 인자로 확인되어, 기존 병리 평가의 한계를 보완할 수 있는 잠재력을 가집니다.

Abstract

Histopathologic assessment of the tumor bed following neoadjuvant therapy in non-small cell lung cancer (NSCLC) is increasingly relevant, but comparative data across treatment modalities remain limited. We evaluated tumor bed features and artificial intelligence (AI)-assisted stromal quantification in advanced NSCLC, comparing patients treated with immunotherapy, tyrosine kinase inhibitors (TKIs), and chemotherapy. This multicenter retrospective study included 71 patients with stage IIIB-IV NSCLC who underwent salvage surgery after neoadjuvant therapy at five Italian centers between 2018 and 2022. Thirty-eight patients received immune-based therapy, 16 received TKIs, and 17 received chemotherapy alone. Tumor bed response was assessed according to International Association for the Study of Lung Cancer recommendations, including residual viable tumor, necrosis, fibrosis, and inflammation. Immune-related features were recorded. AI-assisted morphometric analysis quantified fibrosis on Azan-Mallory staining and inflammatory burden on CD45 immunohistochemistry. The immunotherapy group showed the most favorable regression profile, with higher pathological complete response rates than the TKI and chemotherapy groups, respectively (40.5% vs 21.4% vs 11.8%), and lower residual viable tumor burden (median, 5% vs 45% vs 45%). This group also showed a more immune-reactive tumor bed phenoty...

Spatial habitat radiomics predicts tertiary lymphoid structure status and identifies an IDO1+ migratory dendritic cell axis in breast cancer.

• Status: include
• Score: 0.95
• Category: biomedical-imaging
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Sep-03
• Screened: 2026-09-06 03:04 KST
• PMID: 42692536
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42692536/
• DOI: 10.1136/jitc-2026-015224
• Tags: Radiomics, Breast Cancer, Tertiary lymphoid structures, IDO1, Dendritic cells, MRI, Immune microenvironment
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 Dynamic contrast-enhanced MRI 기반의 Spatial habitat radiomics를 통해 유방암 환자의 TLS 상태를 비침습적으로 예측하는 shTLS 모델을 개발했습니다. 다중 오믹스 분석을 통해 shTLS-low 군에서 IDO1+ migratory dendritic cell에 의한 면역억제 환경이 형성됨을 규명했습니다. 이는 IDO1 억제제가 화학요법 및 CDK4/6 inhibitor와의 병용 치료 효과를 높일 수 있음을 시사하며, 정밀의학 기반의 환자 분류와 새로운 치료 전략 수립에 기여합니다.

Abstract

Tertiary lymphoid structures (TLS) are spatially organized immune niches associated with therapeutic response and favorable outcomes in breast cancer (BC). However, TLS assessment currently relies on invasive tissue-based analyses, and the biological mechanisms underlying imaging-based TLS prediction remain poorly understood. We developed and validated a spatial heterogeneity-based radiomic TLS signature (shTLS) using dynamic contrast-enhanced MRI to non-invasively predict TLS status across multicenter BC cohorts. Spatial habitat radiomics were used to capture intratumoral and peritumoral immune-related heterogeneity. Integrated multi-omics analyses, including transcriptomics, pathomics, genomics, single-cell RNA sequencing, immunohistochemistry, and multiplex immunofluorescence, were performed to biologically interpret shTLS-defined subgroups. Functional drug-sensitivity assays were conducted to assess therapeutic implications. The shTLS model achieved robust predictive performance across independent cohorts and molecular subtypes. High shTLS scores were associated with immune-inflamed tumors characterized by spatially clustered activated T cells and dendritic cells (DCs). In contrast, shTLS-low tumors exhibited an immunosuppressive spatial niche with peripheral accumulation of CD4+ PD-1+ T cells and plasma cells, increased immune-tumor separation, and enhanced inflammatory a...

First-Line Sunvozertinib in NSCLC with EGFR Exon 20 Insertion Mutations.

• Status: include
• Score: 1.00
• Category: clinical-oncology
• Journal: The New England journal of medicine
• Publication date: 2026-Aug-20
• Screened: 2026-08-30 03:15 KST
• PMID: 42212913
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42212913/
• DOI: 10.1056/nejmoa2604461
• Tags: NSCLC, EGFR Exon 20 Insertion, Sunvozertinib, Phase III Trial, First-Line Treatment, Progression-Free Survival, WU-KONG28

Screening brief

이 연구는 EGFR Exon 20 Insertion Mutations을 가진 진행성 NSCLC 환자에서 Sunvozertinib의 1차 치료 효능을 평가한 Phase III 무작위 대조 시험입니다. 결과적으로 Sunvozertinib 군은 화학요법 군에 비해 중위 Progression-Free Survival이 유의하게 길었으며, Objective Response Rate도 우수했습니다. 이는 해당 유전자 변이를 가진 환자들에게 새로운 표준 1차 치료 옵션을 제시하는 중요한 발견입니다.

Abstract

Sunvozertinib received accelerated approval for use in later lines of therapy for patients with advanced non-small-cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations. Data are needed on the efficacy and safety of sunvozertinib as a first-line treatment for NSCLC. In this phase 3, international trial, we randomly assigned, in a 1:1 ratio, patients with advanced nonsquamous NSCLC with EGFR exon 20 insertions to receive sunvozertinib or chemotherapy (carboplatin-pemetrexed). The primary end point was progression-free survival as assessed by blinded independent central review. Crossover to the sunvozertinib group was allowed after disease progression was confirmed. Secondary end points included overall survival, investigator-assessed progression-free survival, objective response (complete or partial response), change in tumor size, and duration of response. A total of 324 patients were randomly assigned to receive sunvozertinib (163 patients) or chemotherapy (161 patients). Treatment with sunvozertinib led to significantly longer median progression-free survival than chemotherapy (10.3 vs. 7.5 months; hazard ratio for disease progression or death, 0.65; 95% confidence interval, 0.50 to 0.85; P<0.001). At 12 months, progression-free survival was reported in 46.1% of the patients in the sunvozertinib group and in 26.7% of those in the c...

Therapeutic evolution: Adoption of newly approved systemic therapies in resected stage IB-IIIA NSCLC in the United States.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-20
• Screened: 2026-08-30 03:14 KST
• PMID: 42636546
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42636546/
• DOI: 10.1016/j.lungcan.2026.109586
• Tags: NSCLC, Adjuvant Therapy, Immunotherapy, Osimertinib, Real-world Evidence, EGFR Mutation, Survival Outcomes

Screening brief

이 연구는 미국에서 수술을 받은 IB-IIIA기 NSCLC 환자 14,638명을 대상으로 실제 임상에서의 치료 패턴을 분석했습니다. 특히 EGFR 돌연변이 환자에서 Osimertinib 사용과 전반적인 면역항암제 적용 비율이 시간이 지남에 따라 크게 증가했음을 확인했습니다. 이러한 Real-world data는 새로운 체계적 요법의 임상적 효능과 실제 적용 격차를 이해하는 데 필수적인 정보를 제공합니다.

Abstract

Evidence is limited regarding use of immunotherapies and targeted therapies in early-stage and locally advanced non-small cell lung cancer (NSCLC) in clinical practice. This retrospective, observational cohort study used health records from US oncology practices to describe treatment patterns and evaluate outcomes in patients with resected stage IB-IIIA NSCLC. Adult patients with stage IB-IIIA NSCLC who completed primary surgery from January 2019-December 2023 (n = 14,638) were included, with potential follow-up through August 2024. Subset analyses of stage II-IIIA NSCLC (n = 9,932) were also conducted. Neoadjuvant and adjuvant therapy use was described by stage, biomarker status, and year of surgery. Outcomes included disease-free survival (DFS) and overall survival (OS). Among 14,638 patients (median age, 70 years) 32.1 % were diagnosed with stage IB, 39.2 % with stage II, and 28.6 % with stage III disease. During the study period, 58.3 % received any systemic treatment (47.7 % platinum-based chemotherapy, 18.1 % immunotherapy, and 4.9% targeted therapy), primarily in the adjuvant setting. Immunotherapy and osimertinib use increased over time: by 2023, 48.6 % of patients with stage II-IIIA disease received immunotherapy, and 58.0 % of patients with stage IB-IIIA EGFR-mutant NSCLC received osimertinib. Median DFS was 46.2 months for overall study cohort and 38.4 months for pa...

AdvanTIG-301: a phase III study of ociperlimab plus tislelizumab and concurrent chemoradiotherapy in stage III unresectable non-small cell lung cancer.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-26
• Screened: 2026-08-30 03:13 KST
• PMID: 42648750
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42648750/
• DOI: 10.1136/jitc-2025-013527
• Tags: NSCLC, Stage III, Immunotherapy, ociperlimab, tislelizumab, Phase III Trial, chemoradiotherapy
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 재수술 불가능한 Stage III NSCLC 환자에서 ociperlimab과 tislelizumab을 병용 화학방사선치료(cCRT)와 함께 투여하는 전략의 유효성과 안전성을 평가했습니다. 표준 치료군(durvalumab)에 비해 PFS 및 ORR에서 유리한 경향을 보였으나, 표본 크기가 작아 기술적 데이터로 해석되었습니다. 폐렴 및 간질성 폐질환 등 면역 관련 부작용 프로파일을 확인했으며, 새로운 안전 신호는 발견되지 않았습니다.

Abstract

Patients with unresectable stage III non-small cell lung cancer (NSCLC) have an unmet need for new therapies that improve survival. This phase III trial investigated the safety and efficacy of concurrent ociperlimab and tislelizumab plus concurrent chemoradiotherapy (cCRT) in treatment-naïve patients with stage III NSCLC. In this phase III, multicenter, randomized, multiarm, open-label trial, patients with unresectable stage III NSCLC received concurrent ociperlimab plus tislelizumab and cCRT, followed by ociperlimab plus tislelizumab (arm A), tislelizumab and cCRT, followed by tislelizumab (arm B), or cCRT, followed by durvalumab (arm C) (NCT04866017). Objectives were to compare progression-free survival (PFS), overall survival (OS), objective response rate (ORR), duration of response, disease control rate, clinical benefit rate, time to death or distant metastasis (TTDM), and safety and tolerability for arms A versus C, B versus C, and A versus B. 63 patients were randomized to arms A (N=22), B (N=19), and C (N=22) prior to early trial termination. In A, B, and C, respectively, 95.5% (21/22), 84.2% (16/19), and 95.5% (21/22) were current or former smokers, and 68.2% (15/22), 73.7% (14/19), and 68.2% (15/22) had PD-L1 expression in tumor cells of ≥1%. Median PFS (95% CI) was not reached (NR) (6.3-not estimable (NE)) in A, 15.0 months (7.4 to NE) in B, and 10.4 months (5.7 to...

Treatment patterns and outcomes in advanced and metastatic lung cancer in France: Results from the Epidemiological Strategy and medical Economics (ESME) database lung cancer in France.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-19
• Screened: 2026-08-30 03:13 KST
• PMID: 42660015
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42660015/
• DOI: 10.1016/j.lungcan.2026.109585
• Tags: lung cancer, real-world evidence, NSCLC, SCLC, immune checkpoint inhibitor, overall survival, treatment patterns
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

이 연구는 프랑스의 ESME 데이터베이스를 활용하여 52,514명의 진행성 및 전이성 폐암 환자의 치료 패턴과 결과를 분석했습니다. NSCLC 환자에서 2020년 이후 immune checkpoint inhibitor 기반 요법이 1차 치료의 주요 옵션으로 자리 잡았음을 확인했습니다. 또한 다변량 분석을 통해 연령, 병기, ECOG 점수 등이 overall survival에 유의미한 영향을 미친다는 사실을 규명하여 임상적 통찰력을 제공합니다.

Abstract

Lung cancer is the main cause of cancer-related death, with recent paradigm shifts including optimized staging, identification of molecular subsets with access to targeted agents, and replacement of chemotherapy by immunotherapy as the backbone of treatment. The Lung Cancer part of the Epidemiological Strategy and Medical Economics (ESME) research program was launched to collect individual data from all consecutive patients treated for lung cancer since 2015 in a network of 38 health facilities in France. Main objectives included the description of the treatment patterns and outcomes of patients diagnosed with lung cancer in the database. Univariable and multivariable analyses on overall survival were performed using the Logrank test and the Cox proportional hazards model. Among 52,514 patients included in the advanced and metastatic lung cancer (AMLC) cohort, 45,232 (86%) had non-small cell lung cancer (NSCLC), and 6,301 (12%) had small-cell lung cancer (SCLC). Among those, 34% in the NSCLC cohort and 42% in the SCLC cohort did not receive second-line. In the NSCLC cohort, immune checkpoint inhibitor (ICI)-based therapies became the most commonly used first-line option from 2020 onwards. After a median follow-up of 58.1 (95%CI 57.1-59.0) months, the median OS was 15.7 (95%CI 15.4-16.0) months for patients with NSCLC, and 11.0 (95%CI 10.7-11.3) months for those with SCLC. At m...

Electrocardiogram-Based Deep Learning to Prioritize Testing for Transthyretin Amyloid Cardiomyopathy.

• Status: include
• Score: 0.95
• Category: biomedical-imaging
• Journal: JAMA
• Publication date: 2026-Aug-28
• Screened: 2026-08-30 03:12 KST
• PMID: 42663420
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42663420/
• DOI: 10.1001/jama.2026.16785
• Tags: ATTR-CM, ECG, Deep Learning, AI, Cardiac Amyloidosis, Diagnostic Accuracy, JAMA

Screening brief

이 연구는 일상적인 심전도(ECG) 데이터에 Deep Learning을 적용하여 치료 가능한 심장병인 ATTR-CM을 조기에 발견하는 AI 시스템을 개발하고 검증했습니다. 다국적 코호트 및 스크리닝 군에서 높은 진단 성능(AUROC 0.78-0.91)을 보였으며, 특히 자원이 제한된 환경에서 확진 검사를 우선순위화하는 데 유용할 수 있습니다. 이는 심근 아밀로이드증의 조기 진단 접근성을 혁신적으로 개선할 잠재력을 가진 중요한 발견입니다.

Abstract

Transthyretin amyloid cardiomyopathy (ATTR-CM) is a treatable cause of heart failure, but diagnosis is often delayed. Accessible tools to prioritize confirmatory evaluation could reduce missed diagnoses when cardiac imaging is limited. To develop and validate a locally deployable artificial intelligence (AI)-enabled system that identifies patients for further ATTR-CM evaluation from routine electrocardiography (ECG) images. This diagnostic test study used an AI-ECG model developed within Yale New Haven Health (using ECGs from August 2015-June 2023) and temporally validated (July 2023-July 2025). External validation included 5 multinational cohorts and 3 screening cohorts (older Black and Hispanic adults with heart failure; adults with prior carpal tunnel surgery; 99-3902 individuals per cohort). Use of AI-ECG for detecting ATTR-CM from routine ECG images or raw 12-lead signals. Area under the receiver operating characteristic curve (AUROC), sensitivity, specificity, and positive and negative predictive values for ATTR-CM confirmed by cardiac amyloid radionuclide imaging (CARI) or biopsy. An exploratory analysis evaluated sequential screening with AI-ECG followed by AI-enabled echocardiography. Development used 28 174 ECGs from 11 291 patients (293 with ATTR-CM). In internal validation (44 123 patients; mean age, 68.5 years; 49.7% female), AUROC was 0.84 (95% CI, 0.79-0.89), wi...

Adding immunotherapy to chemotherapy may improve survival after SCLC transformation in EGFR-mutant NSCLC: a multicenter real-world study.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-23
• Screened: 2026-08-30 03:12 KST
• PMID: 42664544
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42664544/
• DOI: 10.1016/j.lungcan.2026.109590
• Tags: EGFR-mutant NSCLC, SCLC transformation, Immunotherapy, Real-world study, Osimertinib, Atezolizumab, Durvalumab, Overall Survival

Screening brief

EGFR 돌연변이 비소세포폐암(NSCLC)에서 소세포폐암(SCLC)으로 변형된 경우, 기존에 면역항암제의 효능이 제한적이라는 견해와 달리 본 연구는 carboplatin-etoposide(CE) 요법에 immune checkpoint inhibitors(ICIs)를 추가할 때 생존율이 유의미하게 향상됨을 보여줍니다. 다기관 후향적 코호트 연구 결과, CE 단독군 대비 CE+ICI 군에서 post-transformation survival(OS-2)이 17.0개월 대 9.0개월로 크게 개선되었습니다. 이는 진행 시 재생검을 통한 조직학적 확인 및 맞춤형 치료 전략의 중요성을 강조하는 중요한 근거가 됩니다.

Abstract

Histologic transformation to small-cell lung cancer (SCLC) is an aggressive resistance mechanism to EGFR tyrosine kinase inhibitor (TKI) therapy in EGFR-mutant non-small cell lung cancer (NSCLC). Real-world data on this population remain limited. We conducted a multicenter retrospective cohort study across 26 oncology centers (2016-2025). Patients with histologically confirmed EGFR-mutant NSCLC and biopsy-proven SCLC transformation were included. Primary endpoints included PFS during first-line EGFR-TKI therapy (PFS1), time to transformation (TTT), PFS after transformation (PFS2), overall survival from metastatic diagnosis (OS-1), post-transformation survival (OS-2), and overall survival from initial NSCLC diagnosis (OS-3). Survival was assessed with Kaplan-Meier and Cox regression analyses. A total of 59 patients were included (median age 57.8 years; 52.5 % male; exon 19 deletion 76.3 %). Median PFS1 was 14.0 months (95 % CI, 11.3-16.7); median TTT was 22.0 months (range, 3-110). Following transformation, 54 patients (91.5 %) received systemic therapy: carboplatin plus etoposide (CE) alone in 37 (68.5 %) and CE plus immunotherapy (atezolizumab, durvalumab, or durvalumab plus osimertinib) in 16 (29.6 %). ORR was 37.8 % with CE alone versus 71.4 % with CE plus immunotherapy; median PFS2 was 5.0 months (95 % CI, 3.5-6.5). Median OS-1 was 38.0 months (95 % CI, 32.0-53.0). Median...

Treatment-stratified associations of pathological complete response with survival in resected limited-stage small cell lung cancer: A multicenter retrospective study with exploratory spatial immune profiling.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-12
• Screened: 2026-08-23 03:18 KST
• PMID: 42612508
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42612508/
• DOI: 10.1016/j.lungcan.2026.109579
• Tags: small cell lung cancer, neoadjuvant immunochemotherapy, pathological complete response, spatial immune profiling, survival analysis, biomarkers

Screening brief

이 다기관 후향적 연구는 제한기 소세포폐암 환자에서 신보조 면역화학요법이 화학요법보다 높은 pCR률을 달성함을 확인했습니다. 또한 pCR이 생존에 미치는 영향은 치료 방식에 따라 유의미하게 다르다는 상호작용 효과를 규명했습니다. 탐색적 공간 면역 프로파일링을 통해 NIC 그룹의 pCR 사례가 'immune-hot' 표현형을 보임을 시사하며, 이는 향후 치료 전략 수립에 중요한 근거가 될 수 있습니다.

Abstract

Neoadjuvant immunochemotherapy achieves higher pathological complete response (pCR) rates than chemotherapy alone in limited-stage small cell lung cancer (LS-SCLC), but whether pCR carries similar prognostic information across treatment modalities is uncertain. This multicenter retrospective cohort study included 85 patients with stage I-III LS-SCLC who underwent radical resection after neoadjuvant immunochemotherapy (NIC, n = 28) or chemotherapy (NC, n = 57). pCR rates were compared between regimens, and treatment-stratified associations of pCR with event-free survival (EFS) and overall survival (OS) were assessed. Treatment-by-pCR interactions were examined using Firth-penalized Cox models. Seven-plex multiplex immunofluorescence (mIF) in nine purposively selected specimens and two public transcriptomic cohorts provided exploratory immune context. The pCR rate was 35.7% for NIC and 14.0% for NC (P = 0.022). At a median NIC follow-up of 21.1 months, pCR was associated with longer EFS (NR vs 20.3 months, P = 0.007). No corresponding association was detected in the NC group (18.0 vs 19.8 months, P = 0.892). The treatment-by-pCR interaction was significant (Firth-penalized Cox, P = 0.004), indicating that the association between pCR and EFS differed between treatment groups. In the descriptive mIF analysis, both selected NIC pCR specimens showed an immune-hot phenotype, characte...

A phase 2 study of encorafenib in combination with binimetinib for Chinese participants with BRAFV600E mutated metastatic non-small cell lung cancer: Results from the OCEAN II study.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-13
• Screened: 2026-08-23 03:17 KST
• PMID: 42612509
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42612509/
• DOI: 10.1016/j.lungcan.2026.109580
• Tags: NSCLC, BRAFV600E, encorafenib, binimetinib, OCEAN II, Phase 2 trial, targeted therapy
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

OCEAN II 연구는 중국인 BRAFV600E 돌연변이 전이성 NSCLC 환자에서 encorafenib과 binimetinib 병용 요법의 임상적 이점을 확인했습니다. 주요 결과로 독립 중앙 검토 기준 객관적 반응률(cORR-ICR)이 59%였으며, 무진행 생존기간(PFS)은 13.8개월로 나타났습니다. 이 데이터는 해당 인구집단에서 치료의 유효성과 안전성을 뒷받침하며, 새로운 안전성 문제는 보고되지 않았습니다.

Abstract

The ongoing OCEAN II study (ClinicalTrials.gov identifier: NCT05195632) evaluates encorafenib in combination with binimetinib (E+B) in Chinese participants with BRAFV600E-mutated metastatic non-small cell lung cancer (NSCLC). Participants with metastatic unresectable stage IV BRAFV600E-mutated NSCLC (treatment-naïve or with prior systemic therapy excluding BRAF/MEK-inhibitors), were enrolled in a phase 2 study with two parts: safety lead-in (SLI) and pivotal part (PP). Participants received daily oral encorafenib (450mg) and twice daily oral binimetinib (90mg total). Primary endpoints were dose-limiting toxicities (DLT) during SLI and confirmed objective response rate by independent central review (cORR-ICR) during PP. Secondary endpoints were other measures of efficacy, safety, and pharmacokinetics. In total, 63 participants were enrolled. One DLT (non-serious Grade 3 lipase increased) during SLI considered possibly related to E+B resolved without intervention, supporting initiation of PP. Pre-defined statistical efficacy criteria on the first 50 participants were met. In the main analysis, cORR-ICRwas59% (95%CI 45-72). At a later ad hoc analysis, cORR-ICR was 61% (95%CI 47-74), disease control rate 87% (95%CI 75-95). Medians (95%CI) were, time-to-response 1.8 months, duration of response 17.5 months, progression-free survival 13.8 months (7.5-not estimable), overall survival...

Efficacy and prognostic analysis of induction chemoimmunotherapy in unresectable stage Ⅲ non-small cell lung cancer: a single-center retrospective study.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-13
• Screened: 2026-08-23 03:17 KST
• PMID: 42617307
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42617307/
• DOI: 10.1016/j.lungcan.2026.109578
• Tags: NSCLC, Induction chemoimmunotherapy, Stage III lung cancer, Tumor volume reduction, Progression-free survival, Radiotherapy, Prognostic factors

Screening brief

이 연구는 비절제 가능 stage III NSCLC 환자에서 유도 chemoimmunotherapy(iICIs)가 definitive chemoradiotherapy 후 진행 무병 생존율(PFS)을 유의하게 연장함을 보여줍니다. 특히, 유도 치료 후 CT로 측정된 종양 부피 감소율이 PFS와 전체 생존율(OS)의 독립적인 예후 인자임을 확인했습니다. 이러한 영상학적 지표는 개인화된 치료 결정 및 환자 모니터링에 유용한 biomarker로 활용될 수 있습니다.

Abstract

Induction chemoimmunotherapy combined with definitive chemoradiotherapy (CRT) represents a promising approach for unresectable stage III non-small cell lung cancer (NSCLC). Nevertheless, the safety, efficacy, and prognostic markers for this treatment regimen remain to be established. This single-center retrospective cohort included unresectable stage III NSCLC treated with definitive thoracic radiotherapy plus immune checkpoint inhibitors (ICIs) from January 2020 to October 2022. Patients receiving chemo-immunotherapy before radiotherapy were classified as induction ICIs (iICIs), and those receiving immunotherapy after thoracic CRT as consolidation ICIs (cICIs). The primary endpoint was progression-free survival (PFS). Propensity score matching (1:1) was performed. TNM restaging and CT-based tumor volume were assessed before radiotherapy in the iICIs group. Among 168 patients treated with definitive radiotherapy (iICIs, n = 111; cICIs, n = 57), with a median follow-up of 48.2 months, median PFS was longer with iICIs (35.6 vs 23.7 months; p = 0.035) and remained longer after matching (36.1 vs 22.9 months; p = 0.019), while overall survival was similar. Grade ≥ 3 pneumonitis occurred 3.6% and 5.2% in the iICIs and cICIs groups, respectively. In the iICIs group, downstaging after induction therapy was observed (T4: 56.3%→14.6%; stage IIIC: 22.2%→2.9%), with median gross tumor vol...

RaFiST: a radiomics model for non-invasive stratification of tumor fibrosis and prognostic prediction in non-small cell lung cancer.

• Status: include
• Score: 0.95
• Category: biomedical-imaging
• Journal: European radiology
• Publication date: 2026-Aug-20
• Screened: 2026-08-23 03:16 KST
• PMID: 42622885
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42622885/
• DOI: 10.1007/s00330-026-12764-5
• Tags: NSCLC, Radiomics, Tumor Fibrosis, Prognosis, CT Imaging, Biomarker, Non-invasive Stratification
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

이 연구는 NSCLC 환자에서 종양 섬유화가 DFS와 OS에 미치는 독립적인 예후 인자임을 확인했습니다. 개발된 RaFiST 모델은 치료 전 contrast-enhanced CT를 기반으로 종양 섬유화 수준을 비침습적으로 정확하게 분류할 수 있습니다. 이는 고위험군 조기 식별 및 보조 요법 결정에 유용한 강력한 영상 바이오마커로 평가됩니다.

Abstract

Tumor fibrosis plays a critical role in driving therapeutic heterogeneity and drug resistance. However, relevant research in non-small cell lung cancer (NSCLC) remains limited. This study aimed to determine the prognostic value of tumor fibrosis and develop a novel radiomics fibrosis stratification tool (RaFiST) for non-invasive patient stratification. In this multicenter retrospective study of 532 patients with resected NSCLC, tumor fibrosis was histopathologically quantified via collagen fraction. RaFiST was developed using pre-treatment contrast-enhanced CT scans from training and external test cohorts. Prognostic performance was subsequently compared among clinical, direct radiomics, and combined models. Transcriptomic analysis investigated the model's underlying molecular mechanisms. Multivariable Cox regression revealed that the fibrosis score was an independent risk factor for disease-free survival (DFS) and overall survival (OS) at both centers. An optimal cutoff of 11.12% stratified patients into high- and low-fibrosis groups. RaFiST demonstrated excellent performance in predicting tumor fibrosis, achieving an area under the curve (AUC) of 0.879 in the training cohort and 0.813 in the test cohort. RaFiST-High patients exhibited significantly worse survival across both cohorts (all p < 0.01). Furthermore, the combined Clinical-RaFiST model outperformed the baseline cli...

Genomic Profiling, Risk Stratification, and Post-Transformation Treatment Outcomes in Patients with Transformed Small-Cell Lung Cancer: A Multicenter Analysis.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-09
• Screened: 2026-08-23 03:15 KST
• PMID: 42628300
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42628300/
• DOI: 10.1016/j.lungcan.2026.109566
• Tags: T-SCLC, EGFR-mutant NSCLC, Histologic Transformation, Next-generation sequencing, Taxane-based regimen, Risk Stratification, Lung Cancer

Screening brief

이 연구는 EGFR 돌연변이 비소세포폐암에서 소세포폐암으로의 전환(T-SCLC)을 조기에 예측할 수 있는 임상적 및 유전체적 위험 인자를 규명했습니다. 특히 RB1/NTRK1 돌연변이와 T790M 이차 돌연변이를 포함한 예측 모델은 높은 정확도를 보였습니다. 또한 후선 치료에서 taxane 기반 요법이 camptothecin 기반 요법보다 우수한 무진행 생존율(PFS)을 달성함을 확인했습니다.

Abstract

Transformed small-cell lung cancer (T-SCLC) is an increasingly recognized resistance mechanism in EGFR-mutant lung adenocarcinoma. This study aimed to identify early predictors of histologic transformation and evaluate post-transformation treatment outcomes. We retrospectively collected 163 T-SCLC patients from five Chinese centers. Next-generation sequencing was performed on 60 EGFR-mutant patients, including 47 paired primary-transformed samples. Integrated genomic and clinical analyses were conducted to delineate molecular features and survival outcomes. Among 150 EGFR-mutant patients, the median time to SCLC transformation was 25.8 months and median post-transformation overall survival (OS) was 14.2 months. Clinical and survival data for the 13 EGFR wild-type patients are reported descriptively given the limited sample size. Among 108 treatment-evaluable patients, first-line EGFR-TKI plus chemotherapy, chemotherapy alone, and immune checkpoint inhibitors (ICIs) plus chemotherapy yielded median progression-free survival (PFS) of 6.2, 5.30, and 4.07 months (P = 0.041) and median OS of 21.2, 27.6, and 13.6 months (P = 0.193). In later-line therapy, taxane-based regimens achieved a median PFS of 6.93 months, outperforming camptothecin-based (1.13 months) and other regimens (1.90 months; P = 0.049). High evolutionary diversity was associated with shorter post-transformation OS...

Immune signatures in NSCLC associated pleural effusions and implications for prognosis.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-07
• Screened: 2026-08-16 03:16 KST
• PMID: 42570502
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42570502/
• DOI: 10.1016/j.lungcan.2026.109563
• Tags: NSCLC, Pleural effusion, Immune signatures, Prognosis, Cytokines, IL-5, Th2 response
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

비소세포폐암(NSCLC) 환자에서 흉수 세포학 검사 결과(Cyt+ vs Cyt-)와 예후의 관계를 비교 분석했습니다. 연구 결과, Th2 관련 사이토카인(IL-4, IL-5) 수치가 높을수록 생존율이 개선되는 것으로 나타났습니다. 이는 단순한 세포학 진단을 넘어 흉수의 면역 구성이 추가적인 예후 정보를 제공할 수 있음을 시사합니다.

Abstract

Pleural effusions (PEs) are frequent in patients with non-small cell lung cancer (NSCLC) and have prognostic implications. Detection of malignant cells in pleural fluid defines metastatic disease. However, PE cytology has limited sensitivity, leaving a substantial number of PEs cytology negative (Cyt-). We assessed the prognostic significance of cytology positive (Cyt+) and negative effusions and compared biochemical, cellular, and cytokine profiles of NSCLC associated PEs. In this retrospective analysis of a prospectively collected prospective multicenter cohort study, PEs were collected from patients with confirmed NSCLC between 2021 and 2025. Effusions were classified as Cyt + or Cyt - based on cytopathology. Clinical data, pleural fluid biochemistry, and differential cell counts were recorded. Cytokine concentrations were measured in PE supernatant using a multiplex ELISA panel and correlated with survival. 111 NSCLC patients with PEs were included in this study (51 Cyt + and 60 Cyt - cases). Cyt + effusions were characterized by significantly lower pH and higher lactate, LDH, and protein concentrations. One year survival was not different in both groups. High pleural lymphocyte counts and a lower pleural neutrophil to lymphocyte ratio were associated with mortality. Cytokine profiling revealed significantly lower IL-5 levels in Cyt + effusions, while other cytokines were...

Osimertinib With or Without Chemotherapy in Advanced Non-Small Cell Lung Cancer With EGFR and Concurrent TP53 Mutations: A Randomized Clinical Trial.

• Status: include
• Score: 0.98
• Category: clinical-oncology
• Journal: JAMA
• Publication date: 2026-Aug-10
• Screened: 2026-08-16 03:15 KST
• PMID: 42574006
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42574006/
• DOI: 10.1001/jama.2026.10599
• Tags: NSCLC, EGFR mutation, TP53 mutation, Osimertinib, Chemotherapy combination, Phase 3 trial, PFS
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 EGFR 민감성 변이와 TP53 동시 변이를 가진 진행성 NSCLC 환자 294명을 대상으로 Osimertinib 단일 요법과 화학요법 조합 요법을 비교했습니다. 결과는 조합 요법이 중위 PFS를 15.6개월에서 34.0개월로 크게 연장시켰음을 보여주었습니다. 이는 고위험군 폐암 환자에서의 개인화된 치료 전략 수립에 중요한 근거를 제공합니다.

Abstract

Combination therapy has emerged as a promising therapeutic approach for patients with epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC). However, its clinical benefit-risk profile remains a focus of ongoing debate. Identifying patients most likely to derive benefit from such regimens remains an unmet clinical need. To prospectively compare the efficacy and safety of first-line osimertinib plus chemotherapy with osimertinib monotherapy for patients with EGFR-mutated advanced NSCLC harboring concurrent TP53 mutations. A multicenter, randomized, open-label, phase 3 study conducted at 17 sites in China. Between March 25, 2021, and July 11, 2024, a total of 294 eligible patients with treatment-naive, stage IV or recurrent nonsquamous NSCLC harboring concurrent TP53 and EGFR-sensitizing mutations were enrolled. Patients were randomized (1:1) to receive osimertinib plus chemotherapy (pemetrexed and carboplatin every 3 weeks for 4 cycles, followed by maintenance therapy of osimertinib plus pemetrexed; n = 146) or osimertinib monotherapy (n = 148). The primary end point was investigator-assessed progression-free survival. Secondary end points included overall survival, response, safety, and quality of life. Among 294 enrolled patients, the median age was 57 years (range, 26-79 years), and 159 (54.1%) were female. The data cutoff date was November 11, 20...

Survival According to Radiomic and Visual UIP Classification in Fibrotic ILD.

• Status: include
• Score: 0.95
• Category: biomedical-imaging
• Journal: Chest
• Publication date: 2026-Aug-12
• Screened: 2026-08-16 03:14 KST
• PMID: 42586496
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42586496/
• DOI: 10.1016/j.chest.2026.08.002
• Tags: Radiomics, UIP Classification, Fibrotic ILD, Survival Analysis, CT Imaging, Interstitial Lung Disease

Screening brief

이 연구는 섬유증성 간질성 폐질환(fibrotic ILD) 환자에서 Radiomic 분석과 시각적 UIP 분류가 생존 예측에 어떻게 기여하는지 평가합니다. 특히 영상 기반의 정량적 지표가 임상적 예후 판정에 중요한 역할을 할 수 있음을 시사합니다. 이는 향후 ILD 관리 및 치료 전략 수립에 있어 영상 바이오마커의 중요성을 강조합니다.

Abstract

not available

PGE2-mediated NK cell reprogramming drives acquired immunotherapy resistance in lung adenocarcinoma.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-12
• Screened: 2026-08-16 03:14 KST
• PMID: 42586608
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42586608/
• DOI: 10.1136/jitc-2025-014673
• Tags: lung adenocarcinoma, PD-1 blockade, acquired resistance, NK cell, PGE2 signaling, celecoxib, immunotherapy
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 폐선암에서 PD-1 억제제에 대한 획득 내성이 발생하는 기전을 규명했습니다. 종양 유래 PGE2가 EP2/EP4 수용체를 통해 cAMP-CREM 경로를 활성화하여 NK 세포의 기능을 억제함을 발견했습니다. Celecoxib을 사용한 약물학적 개입이 NK 세포 기능을 회복시키고 내성을 극복할 수 있음을 입증하였습니다.

Abstract

Acquired resistance limits the durability of programmed cell death protein-1 (PD-1) blockade in lung adenocarcinoma, yet the tumor-intrinsic programs and immune circuits that drive acquired resistance relapse remain poorly defined. The purpose of this study was to identify tumor-intrinsic mediators of acquired resistance and determine how they remodel antitumor immunity. An orthotopic bioluminescence-tracked Lewis lung carcinoma (LLC1) lung adenocarcinoma model was established in immunocompetent mice treated with anti-PD-1. Tumor-intrinsic regulators were identified by an in vivo genome-wide CRISPR loss-of-function screen and validated using inducible tetracycline-off knockdown. Prostaglandin E2 (PGE2) signaling was interrogated through tumor-cell Ptgs2 knockdown/deletion, 16,16-dimethyl PGE2 administration, selective EP2/EP4 antagonists, and celecoxib treatment. Natural killer (NK)-cell function was analyzed by flow cytometry, immunofluorescence, RNA sequencing, cAMP measurement, calcium flux assays, mouse and human NK-cell co-culture cytotoxicity assays, and NK-cell adoptive transfer. Celecoxib was used to evaluate the therapeutic potential of pharmacologic PGE2 blockade in vivo. Public immunotherapy datasets were analyzed to assess the clinical relevance of PTGS2. The orthotopic LLC1 model captured key features of heterogeneous anti-PD-1 responses, including relapse after i...

N-glycans in non-malignant tumor microenvironment cells dampen CAR-T cell function in solid tumors.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-12
• Screened: 2026-08-16 03:13 KST
• PMID: 42586609
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42586609/
• DOI: 10.1136/jitc-2026-015099
• Tags: CAR-T cell therapy, Tumor microenvironment, N-glycans, Solid tumors, Colorectal cancer, Pancreatic cancer, MGAT5, Immunotherapy
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 대장암 및 췌장암의 간 전이 모델에서 비악성 종양 미세환경 세포가 발현하는 N-glycan이 CAR-T 세포 기능을 억제함을 밝혔다. 특히 MGAT5 의존적 분지형 N-glycan 합성을 차단하면 면역억제적 거대세포와 섬유아세포의 기능이 감소하고 CAR-T 세포의 항종양 활성이 향상됨을 확인했다. 이는 고형암에서 CAR-T 치료의 한계를 극복하기 위해 종양 미세환경의 당화 경로를 표적으로 삼는 전략의 타당성을 제시한다.

Abstract

Chimeric antigen receptor (CAR) T-cell therapy has shown limited efficacy in solid tumors, largely due to immunosuppressive mechanisms within the tumor microenvironment (TME). While tumor-associated glycans are known to protect malignant cells from immune attack, the contribution of N-glycans expressed by non-malignant TME populations to CAR-T cell dysfunction remains poorly defined. We investigated the role of N-glycans in non-malignant TME populations, focusing on M2-like macrophages and hepatic stellate cells in liver metastasis of colorectal (CRC) and pancreatic cancer (PDAC). Using in vitro co-culture systems, transcriptomic analysis, and tumor-bearing humanized mouse models, we assessed how pharmacologic or genetic disruption of key nodes of the N-glycosylation pathway (MGAT5, MAN2A1 and ST6GAL1) in immune and stromal compartments shapes T-cell function. In patient samples, a branched N-glycan signature was associated with transcriptional programs characteristic of tumor-promoting macrophages and stromal cells, linking N-glycosylation to an immunosuppressive TME. Disruption of N-glycan synthesis in non-malignant TME cells reduced their immunosuppressive and tumor-supporting functions. Single-cell RNA sequencing of tumor-bearing humanized mice showed depletion of protumor IL1β+ macrophages and diminished inhibitory macrophage-T cell interactions following N-glycosylation...

Adapted foundation models for breast MRI triaging in contrast-enhanced and non-contrast-enhanced protocols.

• Status: include
• Score: 0.92
• Category: biomedical-imaging
• Journal: European radiology
• Publication date: 2026-Aug-13
• Screened: 2026-08-16 03:12 KST
• PMID: 42593493
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42593493/
• DOI: 10.1007/s00330-026-12782-3
• Tags: Breast MRI, Foundation Models, DINOv2, AI Triage, BI-RADS, Non-contrast-enhanced MRI, Deep Learning
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

이 연구는 DINOv2 기반의 Medical Slice Transformer(MST)를 사용하여 유방 MRI 검사를 Triage하는 방법을 평가했습니다. 대조제 사용 및 미사용 프로토콜 모두에서 BI-RADS ≥ 4 이상 의심 사례를 선별하는 데 있어 높은 민감도와 외부 검증된 AUC 0.77을 달성했습니다. 이는 Foundation Model 기반 AI가 방사선과 의사의 업무 부담을 줄이고 고위험 검사를 우선 처리하는 데 기여할 수 있음을 시사합니다.

Abstract

To evaluate a DINOv2-based medical slice transformer (MST) for triaging abbreviated breast MRI by ruling out examinations with suspicious findings that are immediately actionable (Breast Imaging Reporting and Data System [BI-RADS] ≥ 4) across contrast-enhanced and non-contrast-enhanced protocols. This institutional review board-approved retrospective study included 1847 single-breast MRI examinations (377 BI-RADS ≥ 4) from an in-house dataset and 924 from an external dataset (Duke). Four abbreviated protocols were tested: T1-weighted early subtraction (T1sub), diffusion-weighted imaging with b = 1500 s/mm² (DWI1500), DWI1500 + T2-weighted (T2w), and T1sub + T2w. Performance was assessed at 90%, 95%, and 97.5% sensitivity using five-fold cross-validation and area under the receiver operating characteristic curve (AUC). AUC differences were compared with the DeLong test. False negatives were characterized, and attention maps were rated in the external dataset. A total of 1448 female patients (mean age, 49 ± 12 years) were included. T1sub + T2w achieved an AUC of 0.77 ± 0.04; DWI1500 + T2w, 0.74 ± 0.04, with no significant differences across protocols. At 97.5% sensitivity, T1sub + T2w had the highest specificity (19% ± 7%), followed by DWI1500 + T2w (17% ± 11%). At 95% and 97.5% sensitivity, missed lesions were predominantly < 10 mm, mainly non-mass enhancements. External valida...

Turning off methylglyoxal stress: an alternative approach to inhibit MDSC expansion and metastasis in triple-negative breast cancer.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-13
• Screened: 2026-08-16 03:12 KST
• PMID: 42595355
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42595355/
• DOI: 10.1136/jitc-2026-014841
• Tags: Triple-Negative Breast Cancer, Methylglyoxal Stress, g-MDSC, Immunotherapy Resistance, Carnosine, PD-1 Blockade, Metastasis
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 TNBC에서 glycolysis 부산물인 methylglyoxal stress가 g-MDSC 확장을 유도하여 면역 회피와 전이를 촉진함을 밝혔습니다. in silico 분석을 통해 MG stress signature가 anti-PD-1 치료 반응 예측 인자로 작용할 수 있음을 확인했습니다. carnosine과 PD-1 blockade의 병용 요법이 g-MDSC 축적을 감소시키고 폐 전이를 억제하는 것으로 나타났습니다.

Abstract

Metabolic reprogramming through enhanced glycolysis is a hallmark of cancer that supports tumor progression and promotes protumor immune responses. Methylglyoxal (MG), a reactive by-product of glycolysis, has recently emerged as an oncometabolite implicated in cancer progression and therapy resistance. Our previous work demonstrated that an imbalance between MG production and detoxification by the glyoxalase system, referred to as MG stress, contributes to progression and metastatic dissemination in triple-negative breast cancer (TNBC). However, the impact of MG stress on the tumor immune microenvironment remains poorly understood. Using two preclinical breast cancer models, we investigated the relationship between MG stress and immune modulation, with a focus on granulocytic myeloid-derived suppressor cells (g-MDSCs), major mediators of immune evasion. In silico analyses were performed to assess correlations between MG stress-related gene signatures and transcriptional markers of MDSC infiltration in patients with TNBC, as well as associations with anti-programmed cell death protein 1 (PD-1) immunotherapy response in melanoma cohorts. In vivo experiments combined the MG scavenger carnosine with PD-1 blockade in the immunotherapy-resistant 4T1 breast cancer model. MG stress was associated with the expansion of g-MDSCs in breast cancer models. Importantly, MG stress conferred m...

ΔAverage of long and short axis diameter on non-contrast CT is associated with major pathological response to neoadjuvant immunotherapy in resectable non-small cell lung cancer.

• Status: include
• Score: 0.92
• Category: biomedical-imaging
• Journal: European radiology
• Publication date: 2026-Aug-13
• Screened: 2026-08-16 03:11 KST
• PMID: 42595861
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42595861/
• DOI: 10.1007/s00330-026-12716-z
• Tags: NSCLC, Neoadjuvant Immunotherapy, Major Pathological Response, CT Biomarker, RECIST 1.1, ΔMean Diameter, Predictive Accuracy

Screening brief

이 연구는 재sectable 비소세포폐암(NSCLC) 환자에서 neoadjuvant immunotherapy 후의 치료 반응을 평가하기 위해 CT 기반의 ΔMean diameter를 제안합니다. 기존 RECIST 1.1보다 높은 예측 정확도(AUC 0.83)를 보였으며, major pathological response(MPR)와 독립적인 연관성을 가짐을 확인했습니다. 이는 복잡한 radiomics나 PET 없이도 단순한 CT 측정값으로 치료 효능을 평가할 수 있는 가능성을 시사합니다.

Abstract

Neoadjuvant immunotherapy for non-small cell lung cancer shows heterogeneous efficacy, and Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST 1.1) fails to accurately predict pathological response. The objective was to explore computed tomography parameters associated with neoadjuvant immunotherapy efficacy and compare their performance with RECIST 1.1. This multicenter retrospective study included 48 patients with resectable stage I-IIIB non-small cell lung cancer who received neoadjuvant immunotherapy between September 2018 and July 2023. Computed tomography density parameters (computed tomography value and relative computed tomography value) and morphological characteristics (mean diameter, volume, surface area) were measured before and after treatment. Major pathological response (≤ 10% residual tumor cells) served as the reference standard. Receiver operating characteristic analysis and logistic regression evaluated parameter performance. ΔMean diameter demonstrated the highest predictive accuracy for major pathological response (area under the curve 0.83, p < 0.001), with 76% sensitivity, 84% specificity, and 79.2% overall accuracy, with numerically higher accuracy than Response Evaluation Criteria in Solid Tumors version 1.1 (72.9%), though no formal statistical test for superiority was conducted. In exploratory multivariable analysis, it was the only para...

T cells are critical for pre-metastatic niche formation through the STAT3/IL-17 axis.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-14
• Screened: 2026-08-16 03:11 KST
• PMID: 42601173
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42601173/
• DOI: 10.1136/jitc-2025-013183
• Tags: pre-metastatic niche, CD4+ T cells, STAT3, IL-17, tumor metastasis, immunotherapy, myeloid cells
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

본 연구는 CD4+ T 세포가 STAT3/IL-17 축을 통해 pre-metastatic niche 형성에 관여함을 입증했습니다. 이는 기존에 주로 myeloid cell 중심으로 여겨졌던 전이 미세환경 이해를 확장합니다. 이러한 발견은 IL-17 또는 STAT3 표적 치료가 암 전이를 억제하는 새로운 전략이 될 수 있음을 시사합니다.

Abstract

Pre-metastatic niches composed of mainly myeloid cells are recognized as critical for tumor metastasis. However, whether adaptive immune cells also play an important role in pre-metastatic niche formation remains to be explored. CD4+ T cell accumulation in tumor-free lung tissues from mice bearing subcutaneous mouse tumors was detected by immunofluorescence/confocal microscopy. Tumor-conditioned media (TCM) from MB49-S1pr1 high mouse bladder tumor cells or ID8 ovarian tumor cells were administered to tumor-free mice to induce pre-metastatic niche formation. We used mice lacking functional Signal Transducer and Activator of Transcription 3 (STAT3) in T cells and Il17a‒/‒ mice to investigate the roles of STAT3 and interleukin (IL)-17. In vivo time-course experiments were performed to assess whether CD4+ T cell clusters contribute to CD11b+ pre-metastatic clusters. CD4+ T cell migration and chemokine receptor expression assays were employed to identify tumor factors driving CD4+ T cell recruitment. A co-culture system with human MRC-5 lung fibroblasts, healthy donor-derived CD4+ T cells, myeloid cells, and TCM derived from human cancer cells was used to evaluate CD4+ T cell-driven fibroblast activation and IL-17A dependency for myeloid cell migration. Microscopic analyses were performed to confirm CD4+ T cell clusters in tumor-free lymph node tissues from patients with prostate c...

DNA hypomethylation identifying clinical benefit subgroup of small-cell lung cancer: multi-omics analysis of a phase II trial with durvalumab plus olaparib as maintenance therapy.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-14
• Screened: 2026-08-16 03:10 KST
• PMID: 42601174
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42601174/
• DOI: 10.1136/jitc-2026-015066
• Tags: ES-SCLC, durvalumab, olaparib, PARP inhibitor, DNA hypomethylation, multi-omics, maintenance therapy, biomarker
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 광범위기 소세포폐암(ES-SCLC) 환자에서 durvalumab과 olaparib의 유지요법 효능을 평가한 Phase II 임상시험입니다. 다중오믹스 분석을 통해 DNA hypomethylation 하위군이 생존 결과와 유의미하게 연관됨을 확인했습니다. 이는 PARP 억제제와 면역항암제의 병용요법에 대한 최초의 전향적 증거를 제공하며, 특정 분자 서브타입을 가진 환자군에서 치료 효과를 예측하는 바이오마커로서의 가능성을 제시합니다.

Abstract

Long-term survival of extensive-stage small-cell lung cancer (ES-SCLC) remains rare, with most patients experiencing disease progression during maintenance therapy. Poly (ADP-ribose) polymerase (PARP) inhibitors have the potential to confer antitumor activity, modify tumor immunogenicity, and sensitize tumors to anti-programmed cell death protein 1/programmed death-ligand 1 therapy. We conducted this phase 2 trial to investigate the efficacy and safety of durvalumab plus olaparib as maintenance therapy in patients with ES-SCLC. This was a multicenter, single-arm, phase II trial that enrolled 60 patients with previously untreated ES-SCLC (NCT05245994). Patients received durvalumab (1,500 mg) combined with platinum-etoposide chemotherapy intravenously every 21 days for up to four cycles, followed by maintenance therapy with durvalumab (1,500 mg every 28 days) and oral olaparib (300 mg two times a day) until disease progression or unacceptable toxicity. Multi-omics analyses were performed to characterize molecular subtypes associated with clinical outcomes. The combination regimen demonstrated promising efficacy, with an alive and progression-free at 12 months rate of 25.0%, an objective response rate of 73.3%, a median progression-free survival of 6.8 months, and a median overall survival of 14.6 months. Multi-omics profiling identified a hypomethylation subgroup (cluster 1) tha...

AARS1-mediated lactylation reprograms macrophage lipid metabolism to restrict antitumor immunity.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-14
• Screened: 2026-08-16 03:10 KST
• PMID: 42601175
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42601175/
• DOI: 10.1136/jitc-2026-015773
• Tags: Hepatocellular carcinoma, Macrophage metabolism, Lactylation, AARS1, Immune evasion, STING pathway, Antitumor immunity
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 간세포암(HCC) 미세환경에서 종양 유래 lactate가 AARS1을 통해 대식세포의 지질 대사를 변화시켜 면역 회피를 유도함을 밝혔습니다. 구체적으로, AARS1 매개 lactylation은 carnitine palmitoyltransferase 1A를 수정하여 미토콘드리아 내 지방산 수송을 저해하고, 이로 인해 세포질 oleic acid가 축적되어 cGAS-STING 경로를 억제합니다. 이러한 기전은 IFN-I 신호 전달을 약화시켜 CD8+ T 세포의 항종양 기능을 감소시킵니다. 따라서 AARS1 매개 lactylation을 표적으로 하는 전략은 대식세포의 면역 자극 기능을 회복시키고 항암 면역 반응을 강화할 수 있는 유망한 치료 접근법입니다.

Abstract

Tumor-derived lactate has long been regarded as a metabolic waste product. However, accumulating evidence indicates that lactate also functions as a signaling molecule that actively remodels the tumor immune microenvironment. How lactate-driven post-translational modifications in immune cells contribute to immune evasion in hepatocellular carcinoma (HCC) remains incompletely understood. This study aimed to identify the immune cell population responsible for lactylation-driven immunosuppression in HCC and to elucidate the molecular mechanism by which lactylation rewires macrophage metabolism to impair CD8+ T cell-mediated antitumor immunity. Selective in vivo immune cell depletion models were employed to define the key immune mediators of lactate-induced immunosuppression. Proteomic screening, site-directed mutagenesis, and lipidomic profiling were used to characterize lactylation targets and lipid metabolic alterations. Functional assays, including signaling pathway analyses, cytokine measurements, and tumor immune profiling, were performed in both in vitro systems and mouse HCC models. Macrophages were identified as the principal immune cell type mediating lactylation-dependent immunosuppression in HCC. Alanyl-tRNA synthetase 1 (AARS1) functioned as a non-canonical lactyltransferase, catalyzing lactylation of carnitine palmitoyltransferase 1A at lysine 675. This modification...

Histological aging signatures for monitoring tissue-specific aging and disease.

• Status: maybe
• Score: 0.65
• Category: biomedical-imaging
• Journal: Nature medicine
• Publication date: 2026-Aug-14
• Screened: 2026-08-16 03:09 KST
• PMID: 42601488
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42601488/
• DOI: 10.1038/s41591-026-04566-5
• Tags: deep learning, histopathology, tissue clocks, biological age, whole-slide images, aging signatures
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

이 연구는 Genotype-Tissue Expression cohort의 25,712개 whole-slide histopathological images를 분석하여 조직 특이적 'tissue clocks'를 개발했습니다. deep learning을 통해 정량화된 morphological alterations은 telomere attrition 및 subclinical pathologies와 상관관계가 있음을 보여주었습니다. 또한 paired histology와 transcriptomic data를 통합하여 혈액 샘플로부터 조직 노화 간격을 예측하는 방법을 검증했으며, 이는 Alzheimer's disease, stroke 등 다양한 질병의 organ aging 모니터링에 활용될 수 있는 기반을 마련합니다.

Abstract

Aging is the primary risk factor for chronic disease and is characterized by profound structural and architectural remodeling of human tissues. Here, we present a comprehensive assessment of these changes using 25,712 whole-slide histopathological images from 40 tissue types across 983 individuals in the Genotype-Tissue Expression cohort. By leveraging deep learning, we quantified nuanced morphological alterations to develop 'tissue clocks', predictors of biological age that reflect tissue structural integrity and physiological fitness. These clocks correlate with established aging markers, such as telomere attrition, subclinical pathologies and comorbidities. Through a systematic evaluation of biological aging rates across organs, we identified associations of tissue-specific age acceleration with demographic, lifestyle and medical factors, highlighting potentially modifiable risk factors that affect tissue aging. Furthermore, by integrating paired histology and transcriptomic data, we developed a strategy to predict tissue-specific age gaps directly from blood samples. We validated this approach by identifying disease-relevant organ aging across independent cohorts for eight prevalent diseases, including Alzheimer's disease, stroke and Crohn's disease. This work positions tissue architecture as a critical integrator of molecular and cellular changes over the course of aging,...

Associated factors regarding systemic anticancer therapy use prior to death among patients with metastatic non-small cell lung cancer: A multicentre retrospective cohort study.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Jul-29
• Screened: 2026-08-09 03:08 KST
• PMID: 42541969
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42541969/
• DOI: 10.1016/j.lungcan.2026.109551
• Tags: NSCLC, End-of-life care, SACT, Retrospective cohort, Quality of care, Palliative care

Screening brief

이 연구는 전이성 NSCLC 환자에서 사망 6주 전 Systemic anticancer therapy (SACT) 사용과 관련된 요인을 분석했습니다. 결과는 이전의 입원 경험이 말기 SACT 사용과 독립적으로 관련되어 있음을 보여주었습니다. 이는 잠재적으로 부적절한 말기 관리를 이해하고 최적화하는 데 중요한 임상적 지표가 될 수 있습니다.

Abstract

Systemic anticancer therapy (SACT) near the end of life among patients with metastatic non-small cell lung cancer (NSCLC) is considered a population-level quality indicator of potentially inappropriate end-of-life care. We investigated factors associated with SACT in the final 6 weeks of life among patients diagnosed with metastatic NSCLC to optimise end-of-life care. A multicentre retrospective cohort study was conducted among patients with metastatic NSCLC across 7 hospitals in the Dutch Santeon network. Data were extracted from electronic health records. The primary outcome was the receipt of SACT (immunotherapy and/or chemotherapy) within 6 weeks before death. Variables included relevant demographics, clinical and tumour characteristics, palliative care team involvement, emergency department (ED) visits, and hospitalisations. A multivariable logistic regression with backward selection was employed to identify associated variables. Among 365 included patients, 37 % received SACT in the last 6 weeks of life. Notably, these patients were significantly more likely to die in a hospital (44.1 % vs 9.6 %), to visit the emergency department (77.9 % vs 32.8 %) or to be hospitalised in the last 6 weeks of life (80.1 % vs 37.1 %). Hospitalisations before last treatment were independently associated with SACT use in the last 6 weeks of life (OR 2.673 (CI 1.317-5.427), p = 0.006) where...

BRAF fusions define therapeutic vulnerability and tyrosine kinase inhibitor resistance in non-small cell lung cancer.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Jul-30
• Screened: 2026-08-09 03:07 KST
• PMID: 42546514
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42546514/
• DOI: 10.1016/j.lungcan.2026.109556
• Tags: NSCLC, BRAF fusion, EGFR-TKI resistance, MEK inhibitor, comprehensive genomic profiling, acquired resistance, precision oncology

Screening brief

이 연구는 NSCLC 환자 97명을 대상으로 BRAF fusion의 임상적 및 유전체적 특징을 분석했습니다. De novo와 acquired 사례 간에 서로 다른 파트너 유전자와 동반 돌연변이 패턴이 존재함을 확인했습니다. 특히 EGFR-TKI 치료 후 발생한 acquired BRAF fusion에서 MEK 억제제와 EGFR 억제제의 병용 요법이 잠재적인 치료 옵션임을 시사합니다.

Abstract

BRAF fusions are rare but clinically relevant oncogenic events in non-small cell lung cancer (NSCLC), yet their molecular characteristics and optimal management remain unclear. We retrospectively analyzed 97 patients with NSCLC harboring kinase domain-retaining BRAF fusions, stratified into de novo (N = 43) and acquired (N = 54) groups. Clinical and genomic features were compared across subgroups and comparator driver cohorts. We identified 104 BRAF fusions involving 53 unique partner genes, 29 of which were novel. Common partners included AGK (12.5%), IGR (11.5%), ZC3HAV1 (7.7%), TRIM24 (5.8%), and MKRN1 (5.8%). IGR and DTNB were more commonly observed in de novo cases, whereas AGK-BRAF fusions predominated in acquired cases. Among de novo cases, 65.1% lacked co-occurring drivers. ZNF703 mutations and NRF2 pathway alterations were recurrently enriched in BRAF fusion-only tumors, while CTNNB1 and NKX2-1 mutations were enriched versus ALK-rearranged cases. BRAF fusions co-occurring with other drivers showed enrichment of KMT2C and RTK-RAS pathway mutations, with TP53 mutations enriched compared to RET-rearranged tumors. One patient with TRIM24-BRAF and EGFR exon 19 deletion derived clinical benefit from dual MEK and EGFR inhibition. Acquired BRAF fusions were frequently detected after EGFR-TKI therapy, representing the predominant alteration in 63.0% of cases. Median progressio...

Tumor stroma-immune interactions shape the immunosuppressive microenvironment and predict response to neoadjuvant chemoradiotherapy plus immunotherapy in rectal cancer.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-03
• Screened: 2026-08-09 03:07 KST
• PMID: 42547264
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42547264/
• DOI: 10.1136/jitc-2026-015376
• Tags: rectal cancer, tumor stroma ratio, neoadjuvant chemoradiotherapy, immunotherapy, single-cell RNA sequencing, tumor microenvironment, pathological complete response
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 직장암 환자의 종양 간질 비율(TSR)이 질병 무진행 생존율 및 암 특이적 생존율을 독립적으로 예측함을 확인했습니다. 단일 세포 분석을 통해 TSR-high 종양은 고갈된 CD8+ T 세포와 조절성 T 세포가 풍부한 심한 면역 억제 미세환경을 형성함을 밝혔습니다. 특히 신조기 화학방사선요법과 면역요법을 받은 환자군에서 TSR-low 그룹이 주요 병리학적 반응(MPR) 측면에서 유의미하게 더 나은 결과를 보였습니다.

Abstract

The tumor microenvironment, particularly the tumor stroma, plays a critical role in tumor progression, immune evasion, and therapeutic resistance. However, its interaction with the immune landscape in rectal cancer (RC) remains incompletely understood. This study aimed to comprehensively characterize the stromal-immune ecosystem associated with the tumor stroma ratio (TSR) in RC and to evaluate its clinical and therapeutic relevance. We analyzed a multicenter cohort of 498 patients with treatment-naïve RC in whom TSR was assessed on H&E-stained sections. Integrative multi-omics analyses were performed, including bulk RNA sequencing (n=118) and single-cell RNA/T-cell receptor (TCR) sequencing (n=10). Key findings were validated by immunohistochemistry (n=114) and multiplex immunofluorescence (n=20). Survival analyses and statistical comparisons were conducted to evaluate clinical associations and treatment responses. High TSR was an independent predictor of unfavorable disease-free survival and cancer-specific survival and was associated with aggressive clinicopathological features. Single-cell analyses revealed that TSR-high tumors exhibited a profoundly immunosuppressive microenvironment, characterized by clonally expanded terminally exhausted CD8+ T cells (CD8+ Tex-CXCL13) and activated CD4+ regulatory T cells (CD4+ Treg-TNFRSF4). Two LRRC15+ cancer-associated fibroblast (CA...

β-glucan elicits APOE-dependent peripheral trained immunity to suppress hepatocellular carcinoma.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-04
• Screened: 2026-08-09 03:06 KST
• PMID: 42552059
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42552059/
• DOI: 10.1136/jitc-2026-015401
• Tags: hepatocellular carcinoma, trained immunity, APOE, beta-glucan, macrophage engineering, immunotherapy combination, anti-PD-L1
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 β-glucan(WGP)이 APOE+ 단핵구/대식세포를 통해 trained immunity를 유도하여 간세포암(HCC) 진행을 억제함을 밝혔다. WGP 처리는 대식세포의 지질 축적과 내질망 스트레스를 감소시켜 항종양 기능을 향상시켰다. 또한, WGP와 anti-PD-L1 항체의 병용 요법이 단일 요법보다 우수한 종양 조절 효과를 보였으며, 이는 HCC 치료를 위한 새로운 면역조절 전략으로 주목받고 있다.

Abstract

Although immunotherapy has revolutionized cancer treatment, hepatocellular carcinoma (HCC) continues to demonstrate limited clinical responses, highlighting the urgent need for novel immunomodulatory strategies. Trained immunity, an emerging paradigm wherein innate immune cells develop a memory-like phenotype through epigenetic and metabolic reprogramming, offers a promising avenue to remodel the immunosuppressive tumor microenvironment. This study investigated whether β-glucan-induced trained immunity could potentiate antitumor immunity against HCC. We established orthotopic HCC mouse models to investigate the role of trained immunity induced by whole β-glucan particle (WGP) in the HCC microenvironment, particularly in modulating hepatic apolipoprotein E (APOE)-positive monocytes/macrophages. Transcriptional changes in trained monocytes/macrophages were identified by analyzing single-cell RNA sequencing and bulk RNA-sequencing data from the livers of WGP-treated and control mice. Mechanistic studies were performed using Apoe -/- mice and in situ monocyte/macrophage engineering. Flow cytometry was performed to assess immune cell phenotypes and phagocytosis, while luminescence-based assays were used to evaluate cytotoxic activity. The translational potential was assessed using human monocyte training assays. This study demonstrated that preconditioning with WGP, a trained immun...

TGF-β1 drives neutrophil extracellular traps formation to promote CD8+ T cell exhaustion via the ERK-c-Fos-JunB axis, mediating gastric cancer immunotherapy resistance.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-04
• Screened: 2026-08-09 03:06 KST
• PMID: 42552060
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42552060/
• DOI: 10.1136/jitc-2026-015618
• Tags: gastric cancer, anti-PD-1 resistance, neutrophil extracellular traps, CD8+ T cell exhaustion, TGF-β1, trametinib, immunotherapy
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 위암 환자에서 anti-PD-1 치료 저항성이 NETs 형성과 밀접한 관련이 있음을 밝혔다. TGF-β1이 CD177+ 중성粒细胞을 자극하여 NETs를 생성하고, 이는 ERK-c-Fos-JunB 경로를 통해 CD8+ T cell exhaustion을 유도하는 기전을 규명했다. DNase I이나 TGF-β1 억제제를 사용하여 NETs 형성을 차단하거나 trametinib을 병용하면 면역억제 미세환경이 개선되고 항종양 효과가 상승되는 것으로 확인되었다.

Abstract

Resistance to anti-programmed cell death protein-1 (PD-1) treatment in gastric cancer (GC) is closely associated with an immunosuppressive tumor microenvironment. However, the role of neutrophils in resistance to anti-PD-1 therapy remains unclear. Single-cell RNA sequencing was performed on tumor samples from patients with advanced GC receiving anti-PD-1 therapy to identify neutrophil subsets associated with neutrophil extracellular traps (NETs). Multilevel experimental validation was conducted using multiomics analysis, flow cytometry, multiplex immunofluorescence, and in vitro co-culture. Therapeutic strategies targeting NETs and CD8+ T-cell exhaustion were evaluated in a mouse model of YTN16 tumors. We identified a NETs-associated neutrophil subset enriched in patients with GC resistant to anti-PD-1 treatment. This subset was marked by CD177, and it exhibited a high potential for NETs release. Peripheral blood NETs levels and CD177+ neutrophil ratios in patients with GC act as markers for evaluating the efficacy of PD-1 inhibitors. Furthermore, transforming growth factor-β1 (TGF-β1), which was highly expressed in GC and spatially colocalized with CD177+ neutrophils, might induce neutrophils to release NETs via the Smad3-NFE2 axis. NETs promoted CD8+ T cell exhaustion by activating the MEK/ERK-c-Fos/JunB axis, as evidenced by increased PD-1/TIM3 expression and reduced interf...

"Yong" syndrome-cGAS-STING axis: a TCM syndrome-based hypothesis for overcoming primary anti-PD-1 resistance in gastric cancer.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-04
• Screened: 2026-08-09 03:05 KST
• PMID: 42552062
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42552062/
• DOI: 10.1136/jitc-2026-015810
• Tags: gastric cancer, anti-PD-1 resistance, cGAS-STING axis, TCM Yong syndrome, tumor microenvironment, immunotherapy biomarkers, cold tumor conversion
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

위암 환자의 대부분은 anti-PD-1 면역요법에 대해 주요 내성을 보이며, 이는 주로 면역 배제된 '냉' 종양 특성 때문입니다. 본 연구는 한의학의 '옹(癰)' 증후군과 cGAS-STING 축을 연결하여, 열청혈활 작용을 가진 한약 단합물이 subtype-selective 방식으로 cGAS-STING를 활성화시켜 '냉' 종양을 '열' 면역원성 표현형으로 전환할 수 있다는 가설을 제시합니다. 이는 위암 면역요법의 내성 극복과 예측 바이오마커 부족이라는 임상적 난제를 해결하는 syndrome-based 정밀 전략의 기초가 될 수 있습니다.

Abstract

Gastric cancer (GC) remains a major clinical challenge, with most patients exhibiting primary resistance to anti-programmed cell death protein-1 (anti-PD-1) immunotherapy and a lack of effective predictive biomarkers. Most advanced GC presents as immune-excluded "cold" tumors that respond poorly to immune checkpoint blockade. Traditional Chinese medicine (TCM) "Yong (abscess)" syndrome and the "treating GC as Yong" theory are widely applied in clinical practice, yet lack clear molecular and immunological mechanisms. Here, by translating these clinical observations into modern biological terms, we present an original, testable hypothesis proposing the "Yong" syndrome-cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) axis as the central molecular bridge connecting TCM syndrome subtypes, GC histological subtypes, and TME reprogramming. We hypothesize that heat-clearing and blood-activating TCM monomers activate cGAS-STING in a subtype-selective manner to convert "cold" tumors to "hot" immunogenic phenotypes, directly addressing the critical clinical dilemmas of primary anti-PD-1 resistance and insufficient biomarkers in GC immunotherapy. This hypothesis translates universal cGAS-STING mechanisms into a clinically actionable, syndrome-based precision strategy for GC.

Loss of NCCRP1 overcomes immune evasion in lung adenocarcinoma.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-05
• Screened: 2026-08-09 03:04 KST
• PMID: 42556863
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42556863/
• DOI: 10.1136/jitc-2026-015072
• Tags: lung adenocarcinoma, NCCRP1, immune evasion, tumor microenvironment, anti-PD-1 synergy, CX3CL1, macrophage recruitment
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

폐선암 환자의 면역항암제 저반응은 종양 미세환경의 면역 회피가 주요 원인입니다. 본 연구는 NCCRP1 결손이 CX3CL1을 상향 조절하여 항종양 대식세포와 CD8+ T 세포, NK 세포의 침윤을 촉진함을 밝혔습니다. 특히 NCCRP1 표적 치료는 anti-PD-1 또는 interferon-γ 요법과 시너지 효과를 보여 완전 종양 제거를 가능하게 합니다.

Abstract

The low response rate to immunotherapy in patients with lung adenocarcinoma is primarily due to tumor immune evasion. The tumor immunosuppressive microenvironment orchestrates this evasion, yet the underlying mechanisms remain elusive. Here we identify non-specific cytotoxic cell receptor protein 1 (NCCRP1) as a critical and previously uncharacterized regulator of this process. We first analyzed publicly accessible patient-derived single-cell RNA sequencing and RNA sequencing data to investigate the expression of NCCRP1 in lung adenocarcinoma and its impact on the tumor immune microenvironment. Subsequently, the Nccrp1 gene was knocked out in mouse lung adenocarcinoma cells using CRISPR-Cas9. The effect of NCCRP1 deletion on tumor growth was then evaluated using subcutaneous transplantation models in both NSG and C57BL/6 mice. Single-cell RNA sequencing, flow cytometry and multiple targeted in vivo interventions were employed to assess the influence of NCCRP1 on the tumor immune microenvironment. To explore the underlying mechanisms by which NCCRP1 regulates the tumor immune microenvironment, we conducted co-immunoprecipitation, RNA pull-down, ubiquitination assay, mass spectrometry, isobaric tags for relative and absolute quantitation proteomics, dual-luciferase reporter gene assay, and ELISA. Loss of NCCRP1 inhibits lung tumor growth and prolongs survival in immunocompetent...

Targeting GRP75 by natural compound polyphyllin II triggers mitochondrial calcium overload and pyroptosis to potentiate cancer immunotherapy.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Aug-06
• Screened: 2026-08-09 03:03 KST
• PMID: 42562424
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42562424/
• DOI: 10.1136/jitc-2026-015043
• Tags: cancer immunotherapy, GRP75, Polyphyllin II, immunogenic cell death, pyroptosis, immune checkpoint blockade, mitochondrial calcium overload
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 자연 유래 화합물인 Polyphyllin II가 GRP75를 표적으로 삼아 미토콘드리아 칼슘 과부하와 pyroptosis를 유도하여 면역원성 세포사멸(ICD)을 촉진함을 규명했습니다. 이를 통해 종양 미세환경이 재프로그래밍되어 dendritic cell 성숙과 CD8+ T-cell 활성화가 증진되었습니다. 특히, Polyphyllin II는 anti-PD-1 요법과 시너지 효과를 나타내어 전신 항종양 면역을 강화하는 것으로 확인되었습니다.

Abstract

Immune checkpoint blockade (ICB) therapy has emerged as a pivotal cancer treatment by activating antitumor immunity. However, its clinical efficacy remains limited in many patients, highlighting the need for combination strategies to overcome resistance. Inducing immunogenic cell death (ICD) represents a promising approach to remodel the immunosuppressive tumor microenvironment and improve ICB efficacy. A high-throughput screen of a natural compound library identified potent ICD inducers. Polyphyllin II (PPII), a bioactive component from Paris polyphylla, was selected for further investigation. Its effects on ICD markers, tumor growth, and immune activation were evaluated in vitro and in vivo. Limited proteolysis-mass spectrometry was employed to identify the direct target of PPII, followed by mechanistic studies using molecular and immunological assays. PPII was identified as a potent ICD inducer, stimulating the release of high mobility group box 1, ATP, and calreticulin from tumor cells. PPII suppressed tumor growth and enhanced antitumor immunity by promoting dendritic cell maturation and antigen cross-presentation, leading to CD8+ T-cell activation. Mechanistically, PPII directly bound to glucose-regulated protein 75 (GRP75), enhancing endoplasmic reticulum-mitochondrial tethering, provoking endoplasmic reticulum stress and mitochondrial calcium overload, and promoting cy...

DAFNet: A multi-modal deep learning model based on whole-lung CT for the automated prediction of the air space spread of lung adenocarcinoma.

• Status: include
• Score: 0.95
• Category: biomedical-imaging
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Aug-01
• Screened: 2026-08-09 03:03 KST
• PMID: 42566922
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42566922/
• DOI: 10.1016/j.lungcan.2026.109557
• Tags: lung adenocarcinoma, STAS, deep learning, CT imaging, DAFNet, multimodal fusion, preoperative prediction

Screening brief

이 연구는 폐선암 환자의 STAS 존재 여부를 수술 전 CT 영상만으로 자동으로 예측하는 DAFNet 모델을 개발했습니다. 임상 데이터 및 radiomics 특징만 사용하는 기존 모델에 비해 AUROC 0.90으로 우수한 성능을 보였습니다. 이는 개인화된 수술 계획 수립과 AI 기반 종양학 응용의 임상적 전환 가능성을 높이는 중요한 발견입니다.

Abstract

Spread through air spaces (STAS) is a characteristic invasive pattern of lung adenocarcinoma (LUAD), which is associated with a high recurrence rate and poor prognosis. This research introduced the automatic deep learning multimodal detection network (DAFNet) for predicting STAS based on preoperative whole-lung CT scans. In contrast to conventional approaches necessitating manual tumor delineation, DAFNet performs comprehensive end-to-end analysis of pulmonary imaging data through integrated multimodal data fusion and multiscale feature extraction methodologies. A retrospective analysis was performed on 1164 patients with LUAD (511 STAS-positive and 653 negative) from two centers, with a training-to-test split ratio of 70:30 (814 in training set and 350 in test set). In the test set, DAFNet demonstrated an area under the receiver operating characteristic curve (AUROC) of 0.90 (95% confidence interval 0.86-0.94), significantly outperforming predictive models utilizing clinical examination numerical data alone (AUROC 0.72) and radiomics features independently (AUROC 0.65). The implementation of an adaptive gate fusion mechanism combined with a DINOv3-based pre-trained architecture substantially improved predictive accuracy for STAS status determination. These findings establish DAFNet as a promising fully automated, non-invasive diagnostic tool for preoperative STAS prediction i...

Cancer-associated mesothelial cells drive immune escape and therapy resistance in ovarian cancer.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-30
• Screened: 2026-08-02 03:04 KST
• PMID: 42532631
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42532631/
• DOI: 10.1136/jitc-2026-015236
• Tags: ovarian cancer, immune escape, therapy resistance, tumor microenvironment, SERPINB2, immunotherapy, CAMCs
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 난소암 진행 과정에서 Cancer-associated mesothelial cells (CAMCs)가 면역 억제 및 치료 저항성을 유발하는 핵심 조절자임을 밝혔습니다. 특히 SERPINB2+ 발현을 특징으로 하는 CAMCs가 종양 성장을 가속화하고 Treg 세포를 확장시키며 combination immunotherapy에 대한 내성을 증가시킨다는 것을 확인했습니다. 이러한 발견은 난소암의 항종양 면역 회복을 위해 CAMCs를 표적으로 삼는 새로운 치료 전략의 중요성을 강조합니다.

Abstract

Cancer-associated mesothelial cells (CAMCs) are key modulators of the ovarian tumor microenvironment, contributing to tumor growth and immune evasion. Mesothelial cells (MCs) maintain peritoneal homeostasis and immune surveillance and represent the first point of contact during abdominal dissemination of ovarian cancers. Yet, their role in ovarian tumor immunity remains poorly understood. Lineage tracing, 3D models, and spatial transcriptomic profiling were used to characterize CAMC origin, localization, and phenotypic transitions during ovarian cancer progression. Multiplex cytokine panels were used to define the cytokine profiles associated with MC transformation into CAMCs. Functional studies were conducted in syngeneic ovarian cancer mouse models to assess the impact of CAMCs on tumor growth and response to immunotherapy. In parallel, CAMC-driven changes in immune cell phenotype and functional state within the tumor microenvironment were characterized. We demonstrate that CAMCs originate from peritoneal MCs, populate the tumor surface, and progressively infiltrate the tumor core while undergoing a phenotypic transition toward a fibroblast-like phenotype. We characterize the function of an unrecognized CAMC signature marked by SERPINB2+ expression and a combination of markers absent in normal MCs. CAMCSerpinb2+ cells have reduced expression of pro-inflammatory cytokines (IL...

Myosin VI drives breast cancer progression via SP1/CA9-mediated acidic tumor microenvironment remodeling and subsequent M2 macrophage polarization.

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-30
• Screened: 2026-08-02 03:04 KST
• PMID: 42532632
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42532632/
• DOI: 10.1136/jitc-2026-015423
• Tags: breast cancer, MYO6, CA9, tumor microenvironment, M2 macrophage polarization, anti-PD-L1 therapy, immunotherapy resistance
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 유방암에서 MYO6가 핵 내 SP1 및 RNA polymerase II를 CA9 프로모터로 유도하여 세포외 산성화를 촉진함을 밝혔습니다. 이러한 산성 종양 미세환경은 GPR65/cAMP/PKA/CREB 경로를 활성화시켜 대식세포의 M2 분화를 유도하고 면역억제 상태를 만듭니다. MYO6 억제제 TIP는 산성화를 감소시키고 anti-PD-L1 치료 효능을 향상시키는 것으로 확인되었습니다.

Abstract

The acidic tumor microenvironment (TME) is a major driver of immunosuppression and tumor progression in breast cancer. Although myosin VI (MYO6), an actin-dependent motor protein, is frequently upregulated in malignancies, its function in immune remodeling remains poorly understood. To identify MYO6 as a regulator of acidic TME remodeling and macrophage polarization in breast cancer, elucidate the underlying mechanism, and evaluate its therapeutic relevance for anti-programmed death-ligand 1 (anti-PD-L1) therapy. Integrated analyses of The Cancer Genome Atlas and Gene Expression Omnibus datasets were performed to evaluate the association of MYO6 with prognosis and M2 tumor-associated macrophage (TAM) infiltration in breast cancer. Transcriptomic, molecular, cellular, and pharmacological approaches were used to investigate MYO6-mediated acidic TME remodeling and macrophage polarization. In vivo studies assessed the effects of MYO6 inhibition by 2,4,6-triiodophenol (TIP) on tumor acidification, immunity, and anti-PD-L1 efficacy. MYO6 expression correlated with M2 TAM infiltration and poor prognosis in breast cancer. Mechanistically, nuclear MYO6 recruited SP1 and RNA polymerase II to the carbonic anhydrase 9 (CA9) promoter, upregulating CA9 and promoting acidification. The acidic TME activated the proton-sensing receptor GPR65 and the cAMP/PKA/CREB pathway in macrophages, drivin...

CPNE1 promotes stemness and confers resistance to GPC3 CAR-T cell therapy in hepatocellular carcinoma via the STAT3-TGF-β signaling pathway.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-31
• Screened: 2026-08-02 03:03 KST
• PMID: 42538053
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42538053/
• DOI: 10.1136/jitc-2025-014430
• Tags: Hepatocellular carcinoma, CAR-T cell therapy, CPNE1, STAT3-TGF-β signaling, Drug resistance, Immune microenvironment, GPC3
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 간세포암(HCC)에서 CPNE1 발현이 STAT3-TGF-β 신호 전달 경로를 활성화하여 종양의 줄기세포성(stemness)을 증진시키고 면역 억제 환경을 조성함을 밝혔습니다. 특히, CPNE1은 GPC3 표적 CAR-T 세포 치료에 대한 내성을 유발하며 T 세포 고갈(T-cell exhaustion)을 촉진하는 것으로 확인되었습니다. CPNE1의 억제는 CAR-T 세포의 기능을 회복시키고 항종양 효능을 향상시킬 수 있어, HCC 면역치료의 새로운 전략으로 주목받고 있습니다.

Abstract

Hepatocellular carcinoma (HCC) remains a major global health burden with limited effective therapeutic strategies. Although chimeric antigen receptor (CAR) T-cell therapy has shown encouraging potential, its efficacy in HCC is profoundly constrained by the immunosuppressive tumor microenvironment. In this study, we performed integrative analyses of HCC transcriptomic and clinical samples data to identify Copine-1 (CPNE1) as potential oncogenic drivers involved in tumor progression and immune suppression. Using functional and mechanistic assays in vitro with HCC cell line models and in vivo with mouse models, we examined the role of CPNE1 in regulating tumor proliferation, stemness, and its contribution to resistance against GPC3-targeted CAR-T cell therapy. We found that CPNE1 is significantly overexpressed in HCC and correlates with poor patient prognosis. Functional assays revealed that CPNE1 enhances tumor proliferation and stemness by activating the STAT3-transforming growth factor beta (TGF-β) signaling pathway. Moreover, CPNE1-induced secretion of TGF-β promotes T-cell exhaustion, which impairs the efficacy of CAR-T cells. Knockdown of CPNE1 restored CAR-T cell function, enhanced T-cell infiltration into tumors, reduced exhaustion, and improved antitumor efficacy without causing systemic toxicity. Clinically, high CPNE1 expression was associated with lower T-cell infiltr...

Development and validation of a risk-stratification model for individualized management of leptomeningeal metastases in EGFR- mutant NSCLC (LM-Index).

• Status: include
• Score: 0.92
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Jul-21
• Screened: 2026-07-30 16:34 KST
• PMID: 42501706
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42501706/
• DOI: 10.1016/j.lungcan.2026.109547
• Tags: NSCLC, EGFR mutation, Leptomeningeal metastasis, Risk stratification, Prognosis, MRI, Clinical trial design

Screening brief

이 연구는 EGFR 돌연변이 비소세포폐암(NSCLC) 환자의 뇌수막 전이에 대한 LM-Index라는 새로운 위험 분류 모델을 개발하고 검증했습니다. ECOG PS, 뇌 전이, MRI에서의 수막 조영증강 등 5가지 독립적 예측 인자를 활용하여 환자들을 저위험군과 고위험군으로 구분했습니다. 이 모델은 외부 검증 집단에서도 일관된 성능(C-index 0.71)을 보였으며, 개인화된 치료 결정 및 향후 임상 시험 설계에 유용한 도구로 평가됩니다.

Abstract

Prognosis for patients with EGFR- mutant non-small-cell lung cancer and leptomeningeal metastasis is highly uncertain, complicating treatment decisions. We aimed to develop and validate a multimodal risk score for predicting overall survival to enable risk-stratified management. In this retrospective, multicenter study, a derivation cohort (n = 350) and an independent external validation cohort (n = 302) were used. Independent prognostic factors were identified via Cox regression and integrated into an integer-based risk score. Model performance was evaluated by the C-index, calibration, and decision curve analysis. Multivariate analysis identified five independent predictors of poorer OS: ECOG PS ≥ 3, brain metastasis, meningeal enhancement on MRI, positive Cerebrospinal Fluid cytology (CSFC) and intracranial pressure > 220 mmH2O. The resulting risk score stratified patients into low-risk and high-risk groups, with median OS of 22.6 months versus 9.9 months, respectively (p < 0.001). The model demonstrated good discrimination, with a bias-corrected C-index of 0.73. In the external validation cohort, all factors remained significant, and the model maintained consistent performance (C-index = 0.71). The model showed good calibration and positive net benefit. We developed and validated a robust, clinically accessible risk score that accurately stratifies OS in patients with EGFR...

Adipocyte-derived LTB4 programs human NKG2A+ γδ T cells as cytotoxic sentinels at the adipose-tumor interface in breast cancer.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-28
• Screened: 2026-07-30 16:33 KST
• PMID: 42521410
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42521410/
• DOI: 10.1136/jitc-2026-015147
• Tags: breast cancer, γδ T cells, LTB4, tumor microenvironment, single-cell RNA sequencing, immunotherapy, NKG2A
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 유방암의 종양 주변 지방 조직(PA)에서 adipocyte-derived LTB4가 NKG2A+ γδ T 세포를 cytotoxic sentinels로 프로그래밍하는 기전을 밝혔습니다. single-cell RNA sequencing과 spatial profiling을 통해 이 세포들이 early-stage BC에서 풍부하게 존재하며 favorable clinical outcomes과 관련 있음을 확인했습니다. 이러한 발견은 LTB4-mediated γδ T-cell programming을 활용한 새로운 translational cancer immunotherapy 전략의 이론적 근거를 제시합니다.

Abstract

The peritumoral microenvironment has emerged as a key role in affecting tumor invasion and immunotherapy responses. In adipose-enriched tumors, such as breast cancer (BC), peritumoral adipose tissue (PA) harbors unconventional immune populations, yet its immunological functions remain poorly understood. In particular, how adipocyte regulate innate-like lymphocytes, such as γδ T cells, remains unclear. We performed single-cell RNA sequencing and spatial profiling of paired specimens from patients with BC. Integrated multi-omics analyses, immunofluorescence staining, human γδ T-cell expansion assays, functional assays, and in vivo models were used to define the immune cell states and evaluate the impact of lipid mediator leukotriene B4 (LTB4) on γδ T-cell activation and signaling. Clinical correlations were assessed using our cohort and patient datasets. We identified a previously unrecognized population of NKG2A+γδ T cells with predominant Vδ2 usage that preferentially accumulated in PA, particularly at the adipose-tumor interface. Multi-omics analyses revealed that they exhibited potent cytotoxic activity and extensive interactions with dendritic cells, coordinating a local immune surveillance network. Mechanistically, peritumoral adipocytes showed enhanced activation of the 5-lipoxygenase pathway and secreted the lipid mediator LTB4, which selectively combined to LTB4 recepto...

In situ generation of proinflammatory CAR macrophages via mRNA-TLR agonist co-delivery for triple-negative breast cancer immunotherapy.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-28
• Screened: 2026-07-30 16:33 KST
• PMID: 42521411
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42521411/
• DOI: 10.1136/jitc-2026-015323
• Tags: CAR macrophage, triple-negative breast cancer, mRNA-LNP, immunotherapy, TLR agonist, resiquimod, in situ generation
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 mannose-modified lipid nanoparticle을 사용하여 CAR-encoding mRNA와 TLR7/8 agonist인 resiquimod를 공동 전달하는 플랫폼을 개발했습니다. 이를 통해 종양 관련 대식세포에서 proinflammatory CAR macrophages를 in situ로 생성하고, M1 polarization을 유도하여 TNBC의 성장 억제 및 재발 방지에 효과적인 항종양 면역 반응을 이끌어냈습니다. 이 전략은 ex vivo 세포 제조의 복잡성을 줄이고, 선천성 및 적응성 면역 반응을 조율하여 지속 가능한 치료 효과를 제공합니다.

Abstract

Chimeric antigen receptor (CAR) macrophage therapy shows significant potential for solid tumors owing to the intrinsic tumor infiltration and phagocytic capacity of macrophages. However, its clinical translation is limited by macrophage phenotypic plasticity within the immunosuppressive tumor microenvironment and the complexity of ex vivo cell manufacturing. It is essential to develop techniques that enable macrophages to be activated specifically by antigens while sustaining their proinflammatory activity in vivo. Here, we report a mannose-modified lipid nanoparticle (LNP) platform for the co-delivery of CAR-encoding messenger RNA (mRNA) and the Toll-like receptor (TLR) 7/8 agonist resiquimod (R848), enabling in situ generation of proinflammatory CAR macrophages. In vitro, we assessed macrophage-preferential uptake, CAR expression efficiency, TLR7/8 agonist-mediated macrophage polarization, and immune activation. In vivo efficacy was assessed in syngeneic and humanized mouse models of triple-negative breast cancer, including postoperative recurrence and lung metastasis models. Systemic administration of M-LNP/CAR+R848 induced robust CAR expression in tumor-associated macrophages and promoted sustained M1 polarization. Engineered macrophages exhibited enhanced antigen-specific phagocytic activity and tumor cell clearance, and promoted CD8+ T cell proliferation and NK cell infi...

Pericoronary fat radiomics on coronary CT angiography for predicting major adverse cardiac events: a systematic review and meta-analysis.

• Status: include
• Score: 0.92
• Category: biomedical-imaging
• Journal: European radiology
• Publication date: 2026-Jul-28
• Screened: 2026-07-30 16:32 KST
• PMID: 42521849
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42521849/
• DOI: 10.1007/s00330-026-12778-z
• Tags: Radiomics, CCTA, PCAT, MACE prediction, Cardiovascular imaging, Meta-analysis, Machine learning

Screening brief

이 연구는 관상동맥 주변 지방 조직(PCAT)의 Radiomics 분석이 관상동맥 질환 환자의 Major adverse cardiac events(MACE) 위험을 예측하는 데 유용함을 확인했습니다. 특히 임상 변수 및 기존 영상 지표와 결합된 모델이 가장 높은 진단 성능(AUC 0.87)을 보였으며, 이는 염증성 변화를 정량화할 수 있는 잠재력을 시사합니다. 그러나 임상 현장에 적용하기 위해서는 표준화된 Radiomics 파이프라인과 다기관 전향적 검증이 여전히 필요합니다.

Abstract

Pericoronary adipose tissue (PCAT) reflects local coronary inflammation and microstructural changes and may predict major adverse cardiac events (MACE). Radiomics extracts high-dimensional features from PCAT on coronary CT angiography, capturing tissue heterogeneity beyond conventional risk factors or plaque metrics. This study evaluated the diagnostic performance of PCAT radiomics for MACE prediction. PubMed, Scopus, and Web of Science were searched from inception to October 2025. Ten retrospective studies were included. Diagnostic metrics were extracted and pooled using random-effects models. Subgroup analyses were performed by classifier, region of interest, and follow-up duration. Methodological quality and certainty of evidence were assessed. Radiomics-only models showed moderate performance (sensitivity 0.70, specificity 0.74, area under the curve (AUC) 0.78). Combined models improved discrimination, with radiomics + clinical (AUC 0.80) and radiomics + imaging (sensitivity 0.89; diagnostic odds ratio (LnDOR) 2.93). Triple-combination models achieved the highest performance (AUC 0.87; LnDOR 4.05). Radiomics models showed higher AUC than clinical (ΔAUC = 0.05) and imaging models (ΔAUC = 0.18), with inconsistent sensitivity and specificity differences. Adding clinical variables provided modest improvement, whereas imaging integration yielded greater gains. Triple models sho...

Evaluating health-related quality of life questionnaires in capturing common symptomatic adverse events in non-small cell lung cancer.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Jul-26
• Screened: 2026-07-30 16:32 KST
• PMID: 42526062
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42526062/
• DOI: 10.1016/j.lungcan.2026.109552
• Tags: NSCLC, Patient-Reported Outcomes, EORTC QLQ-C30, EORTC QLQ-LC29, Adverse Events, Quality of Life, Clinical Trials

Screening brief

이 연구는 비소세포폐암(NSCLC) 체계적 치료의 부작용 보고에서 임상진료진의 평가와 환자 보고 결과(PRO) 간의 불일치를 해결하기 위해 수행되었습니다. EORTC QLQ-C30 및 QLQ-LC29 설문지가 설사, 메스꺼움, 통증 등 매우 흔한 증상성 부작용을 효과적으로 포착함을 확인했습니다. 그러나 부종과 발열 등 일부 중요한 부작용은 기존 설문지로 완전히 커버되지 않아, EORTC Item Library의 추가 항목 통합이 필요함을 시사합니다. 이는 임상시험에서 치료의 실제 환자 영향과 삶의 질을 더 포괄적으로 평가하기 위한 방법론적 개선점을 제시합니다.

Abstract

Despite advancements in adverse events (AEs) reporting, discrepancies often arise between clinician-assessed and patient-reported symptomatic AEs, including in non-small cell lung cancer (NSCLC) trials. This study investigates the extent to which patient-reported questionnaires, particularly the EORTC Questionnaire - Core (QLQ-C30) and the lung cancer-specific module (QLQ-LC29) capture patient-reported symptomatic AEs in systemic treatments for NSCLC. A systematic comparison was conducted between symptomatic AEs reported in publicly available Summary of Product Characteristics (SmPC) of systemic NSCLC treatments and patient-reported outcomes captured by the EORTC QLQ-C30 and QLQ-LC29. AEs classified as very common (≥10%) or common (1%-10%) were included. A structured mapping exercise was undertaken to identify overlaps and gaps between symptomatic AEs captured by SmPC and EORTC questionnaires. We analysed 38 systemic treatments and found that the EORTC QLQ-C30 and QLQ-LC29 effectively capture (very) common symptomatic AEs such as diarrhea, nausea and vomiting, pain and skin problems, which are reported in over 75% of SmPCs. A total of 62 symptomatic AEs identified were not captured by the EORTC measures. The majority (58.1%) of these were only reported once and only two symptomatic AEs were reported in >50% of SmPCs: oedema(65.8%) andpyrexia(57.9%). These AEs are well-covered...

IL-27 shapes NK cell heterogeneity and function in colorectal cancer.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-29
• Screened: 2026-07-30 16:31 KST
• PMID: 42527030
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42527030/
• DOI: 10.1136/jitc-2025-014667
• Tags: colorectal cancer, NK cells, IL-27, tumor microenvironment, single-cell RNA sequencing, immuno-oncology, innate immunity

Screening brief

대장암 종양 미세환경에서 IL-27이 NK 세포의 침윤과 활성화에 핵심적인 역할을 한다는 것을 규명했습니다. 단일세포 유전체 분석을 통해 비성숙한 NK 세포 하위 집단의 지속성을 설명하며, IL-27 신호 전달 경로를 표적으로 한 면역치료 전략의 가능성을 제시합니다. 이는 대장암에서의 선천성 면역 감시 회복을 위한 새로운 치료적 접근법을 뒷받침합니다.

Abstract

Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide and is characterized by an immunosuppressive tumor microenvironment (TME). While adaptive immunity contributes to tumor control, growing evidence underscores the role of innate lymphocytes, particularly natural killer (NK) cells, in early antitumor surveillance. However, tumor-infiltrating NK cells often exhibit defective maturation and impaired effector functions, whereas the signals regulating NK cell differentiation and activity in CRC remain poorly defined. Interleukin-27 (IL-27) has emerged as a regulator of antitumor immunity, yet its role in modulating NK cell responses in intestinal tumors is largely unexplored. We employed an orthotopic transplantation model of genetically engineered colorectal tumor organoids Apc-/-KrasG12D/+Trp53R172H/-Smad4-/- (AKPS) to investigate NK cell heterogeneity, maturation, and function during CRC progression. Tumor-infiltrating innate lymphocytes were analyzed using single-cell RNA sequencing, flow cytometry, immunofluorescence, and functional assays. In vitro co-culture systems and in vivo IL-27 blockade were used to assess the impact of tumor-derived IL-27 on NK cell transcriptional programs and effector activity. Single-cell transcriptomic profiling revealed marked heterogeneity among tumor-infiltrating NK cells, identifying subsets with different maturati...

CXCR2-mediated metabolic interaction between prostate cancer cells and the immunosuppressive tumor microenvironment.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-29
• Screened: 2026-07-30 16:30 KST
• PMID: 42527031
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42527031/
• DOI: 10.1136/jitc-2025-014725
• Tags: Prostate Cancer, NEPC, CXCR2, Tumor Microenvironment, Immune Evasion, Metabolic Reprogramming, Ferroptosis

Screening brief

이 연구는 신경내분비 전립선암(NEPC)에서 IL-8/CXCR2 신호 전달 경로가 종양 미세환경(TME) 내 지질 축적을 유도하여 CD8+ T 세포의 ferroptosis를 촉진함을 규명했습니다. 이러한 기전은 Treg 세포 침윤과 M2형 대식세포 우세한 면역 억제 환경을 조성하는 것으로 확인되었습니다. 전임상 모델에서 CXCR2 억제가 항종양 면역 반응을 회복시키고 종양 성장을 유의미하게 감소시켰습니다. 따라서 CXCR2는 NEPC 치료를 위한 유망한 표적이며, 대사-면역 상호작용을 이해하는 데 중요한 통찰을 제공합니다.

Abstract

Neuroendocrine prostate cancer (NEPC) is characterized by strong immune evasion and profound metabolic reprogramming. A high regulatory T cell (Treg)/CD8+ T cell ratio and an increased proportion of M2/M1 tumor-associated macrophages (TAMs) in the NEPC tumor microenvironment (TME) are associated with poorer progression-free survival, a phenomenon linked to lipid accumulation within the TME. Understanding the regulatory mechanisms governing both the metabolic and immune landscapes of NEPC is critical. To investigate these mechanisms, prostate cancer cell lines and patient samples were analyzed using immunohistochemistry, flow cytometry, PCR, western blotting, and mass spectrometry. The interleukin (IL)-8/CXCR2 signaling pathway was targeted for intervention in two tumor-bearing mouse models. Data revealed that IL-8/CXCR2 signaling drives the accumulation of free fatty acids and very-long-chain polyunsaturated fatty acids, leading to ferroptosis in tumor-infiltrating CD8+ T cells. This, in turn, promotes Treg cell infiltration and an M2 macrophage-dominant immune landscape. Mechanistically, IL-8/CXCR2 signaling upregulates the AKT-mTOR-FAS pathway while activating the mTOR-MYC-ELOVL5 axis via Rictor acetylation. In preclinical studies using NSG and B57BL/6 mouse models, CXCR2 inhibition restored CD8+ T cell antitumor activity and enhanced TAM phagocytosis, significantly reducing...

Intratumoral Capnocytophaga leadbetteri promotes cancer cells proliferation and recruits neutrophils by activating TLR4/MyD88/NF-κB axis in oral squamous cell carcinoma.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-21
• Screened: 2026-07-25 13:56 KST
• PMID: 42481155
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42481155/
• DOI: 10.1136/jitc-2026-015159
• Tags: OSCC, tumor microbiome, TLR4/MyD88/NF-κB, neutrophil recruitment, intratumoral bacteria, therapeutic target, 16S rRNA-seq
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

구강 편평상피암(OSCC) 조직 내 Capnocytophaga leadbetteri가 종양 진행에 핵심적인 역할을 한다는 것을 입증하였다. 이 균은 TLR4/MyD88/NF-κB 신호 전달 경로를 통해 암 세포 증식을 유도하고, neutrophil을 모집하여 종양 친화적 미세환경을 조성한다. 다중 16S rRNA-seq 데이터셋과 in vivo 모델을 활용하여 미생물군집 불균형이 OSCC 발병에 미치는 영향을 규명하였으며, 향후 진단 및 치료 표적으로서의 임상적 잠재력을 제시한다.

Abstract

Intratumoral bacteria influence the progression and treatment response of solid tumors through multiple mechanisms. Oral squamous cell carcinoma (OSCC) is a common malignant tumor in the head and neck; however, the role of intratumoral bacteria in OSCC initiation and progression remains poorly understood. We integrated 21 public 16S rRNA gene amplicon sequencing (16S rRNA-seq) datasets (comprising 954 normal and 1,627 OSCC samples) to profile oral microbiota dysbiosis across 4 sample types (saliva, oral rinse, swab, and tissue). Subsequent analysis via five-region 16S rRNA-seq and fluorescence in situ hybridization revealed a specific species enriched in OSCC tissues. The functional role of this bacterium and its underlying mechanism were then elucidated using in vitro and in vivo models, including germ-free mice. Our analysis revealed a reduced diversity of the oral microbiota in patients with OSCC, along with a significant enrichment of the Capnocytophaga in swab and tissue samples. Capnocytophaga leadbetteri (C. leadbetteri), a species within Capnocytophaga, was further confirmed to be specifically enriched in OSCC tissues. Functional studies demonstrated that C. leadbetteri alone is sufficient to induce epithelial hyperproliferation and a protumorigenic inflammatory niche, and it promotes established OSCC progression. Mechanistically, C. leadbetteri activates the TLR4/MyD8...

CT surveillance, patterns of recurrence and eligibility for salvage therapy after curative intent treatment for unresectable stage III non small cell lung cancer.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Jul-19
• Screened: 2026-07-25 13:55 KST
• PMID: 42485677
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42485677/
• DOI: 10.1016/j.lungcan.2026.109535
• Tags: NSCLC, CT surveillance, oligorecurrence, durvalumab, salvage therapy, MDT, real-world evidence

Screening brief

unresectable stage III NSCLC 환자에서 chemoradiotherapy ± durvalumab 치료 후 재발 패턴과 영상 감시 주기를 분석한 연구입니다. 3개월 간격의 CT 촬영이 조기 recurrence를 발견하고 MDT 기반 절제술 또는 방사선 치료를 위한 임상적 창을 제공할 수 있음을 시사합니다. 실제 임상 환경에서 oligorecurrence 환자를 대상으로 한 salvage therapy의 실행 가능성과 치료 시점에 대한 실증 데이터를 제공합니다.

Abstract

Survival rates of unresectable stage III non-small cell lung cancer (NSCLC) have improved with the introduction of durvalumab following chemoradiotherapy. Post-treatment surveillance remains crucial due to the high relapse rate, and early detection of recurrence may allow for more effective salvage therapies. This study evaluated CT imaging frequency post-chemoradiotherapy, patterns of disease recurrence, and the feasibility and impact of salvage therapies. Patients with unresectable stage III NSCLC treated at BC Cancer, British Columbia, Canada from January 2018-December 2021 were identified. A retrospective chart review was performed including patient characteristics, imaging surveillance, treatment, recurrence patterns, number of sites of metastases and salvage treatment. 433 Patients received curative intent chemoradiotherapy+/-durvalumab and 63% experienced recurrence; 43% had oligorecurrence (1-5 metastases), and 57% had high volume recurrence (>5 metastases). CT surveillance rates varied with 3-16% of progression events detected in 3-month intervals within the first two years. For patients with extracranial+/-CNS oligorecurrence, at next follow up imaging 64% remained in an oligorecurrent state with treatment (median 4.6 m) and 57% without treatment (median 3.05 m). 33% oligorecurrent patients received MDT; the most common reason for not receiving MDT was in field recur...

A novel MYO5C-ALK fusion in lung adenocarcinoma: limited alectinib response and durable lorlatinib benefit.

• Status: include
• Score: 0.90
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Jul-21
• Screened: 2026-07-25 13:53 KST
• PMID: 42485678
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42485678/
• DOI: 10.1016/j.lungcan.2026.109548
• Tags: ALK-fusion, MYO5C-ALK, lung-adenocarcinoma, lorlatinib, alectinib, TKI-resistance, case-report

Screening brief

이 논문은 MYO5C-ALK fusion을 가진 lung adenocarcinoma 환자에서 alectinib 내성 후 lorlatinib가 durable partial response를 유도한 사례를 보고한다. In silico docking과 임상 소견을 통해 partner-driven dimerization 기전을 제시하며, 비전형 ALK fusion에 대한 lorlatinib의 우위를 뒷받침한다. 이는 mutation-negative TKI 저항성 관리와 표적 치료 선택에 중요한 임상적 함의를 지닌다.

Abstract

Anaplastic lymphoma kinase (ALK) rearrangements drive approximately 5% of non-small cell lung cancers (NSCLC), most commonly as EML4-ALK, but rare 5' partners may confer distinct pharmacologic behaviour. We report the first lung adenocarcinoma harbouring a novel MYO5C (exon 23)-ALK (exon 20) fusion. Diagnosis and resistance profiling used DNA- and RNA-based next-generation sequencing (NGS), immunohistochemistry (IHC) and serial imaging. In silico molecular docking of alectinib and lorlatinib against the patient-derived fusion kinase was performed with AutoDock Vina. A 72-year-old never-smoker with stage IVB lung adenocarcinoma harboured an in-frame MYO5C-ALK fusion retaining the entire ALK tyrosine kinase domain. The tumour progressed at approximately seven months on first-line alectinib despite re-biopsy showing no acquired ALK kinase-domain mutation, no TP53 mutation or bypass alteration (mutation-negative resistance), then achieved a durable partial response to lorlatinib (progression-free survival > 15 months). We hypothesise that constitutive, partner-driven dimerisation of the MYO5C-ALK chimera may sustain kinase signalling that alectinib incompletely suppresses, whereas the higher potency and macrocyclic rigidity of lorlatinib could restore durable inhibition of the structurally intact kinase. In silico docking is consistent with this hypothesis, showing a preserved ATP...

Therapy-induced senescence rewires the melanoma secretome to promote antitumor immune response and augment cell therapies.

• Status: include
• Score: 0.90
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-22
• Screened: 2026-07-25 13:52 KST
• PMID: 42486609
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42486609/
• DOI: 10.1136/jitc-2025-013441
• Tags: Therapy-induced senescence, AURKA inhibitor, cGAS-STING pathway, melanoma, cell therapy, immune microenvironment
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 멜라노마에서 AURKAi가 치료 유도 세포 노화(TIS)를 유발하여 secretome과 면역 관련 사이토카인 분비를 변화시킴을 보여줍니다. cGAS-STING pathway 활성화와 MHC-I, PD-L1 발현 증가는 종양의 immunogenicity를 높이며, 이는 CD8+ T cells와 NK cells의 침윤을 촉진합니다. 특히 adoptive cell therapy 및 NK cell therapy와의 병용 시 종양 조절과 생존 연장에 유의미한 효과를 입증하여 차세대 면역 세포 치료 전략에 중요한 기초 데이터를 제공합니다.

Abstract

Therapy-induced senescence (TIS) is a common outcome of diverse anticancer treatments, including chemotherapy, radiation, and small-molecule inhibitors. Senescence is characterized by stable growth arrest and the senescence-associated secretory phenotype (SASP), which includes various immune mediators. As the role of the immune system in controlling cancer becomes increasingly appreciated, understanding the impact of TIS on the tumor immune microenvironment (TIME) is critically important. Here, we investigated how senescence can be leveraged to enhance antitumor immune responses. We investigated the effects of an Aurora kinase A inhibitor (AURKAi), a potent inducer of senescence in melanoma models, using transcriptome and secretome profiling. The role of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway was investigated using imaging, inhibitors, and gene knockout. We also examined the effect of AURKAi on the surface expression of major histocompatibility complex class I (MHC-I) and programmed death-ligand 1 (PD-L1), as well as on signal transducer and activator of transcription 1 (STAT1) activation. In vivo, the effects of AURKAi treatment on the TIME were investigated using spectral cytometry and cell depletion studies. Finally, we assessed combining AURKAi with immune checkpoint blockade (ICB), adoptive cell therapy, and natural killer (NK) cel...

Intratumoral TIGIT blockade augments antitumor responses and bypasses increased functionality of peripheral TIGIT+ NK cells in mouse and human models of bone and soft tissue sarcoma.

• Status: include
• Score: 0.90
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-22
• Screened: 2026-07-25 13:51 KST
• PMID: 42486610
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42486610/
• DOI: 10.1136/jitc-2025-013597
• Tags: TIGIT, NK cell, intratumoral delivery, sarcoma, immunotherapy, CD155
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

본 연구는 골육종 및 연부조직 육종 모델에서 TIGIT 발현 NK cell의 위치별 기능 차이를 규명하였다. Systemic administration은 peripheral NK cell 기능을 저하시키는 반면, intratumoral delivery는 항종양 반응을 증강시키고 생존을 연장시켰다. CD155 expression 수준이 NK cell 불활성화와 밀접하게 연관됨을 확인하여, 고위험 sarcoma 치료를 위한 새로운 국소 immunotherapy 전략의 타당성을 제시하였다.

Abstract

TIGIT (T cell immunoreceptor with Ig and ITIM domains) has emerged as a key exhaustion marker of intratumoral natural killer (NK) cells, but results from clinical trials with TIGIT blockade have been largely negative. Recent data have suggested that a subset of TIGIT-expressing NK cells can show increased functionality. We hypothesized that there are differences in function between peripheral and intratumoral TIGIT-expressing NK cells in patients with sarcoma and preclinical sarcoma models, which undermine the efficacy of systemic TIGIT blockade. We sought to investigate differences in TIGIT+ NK cells using systemic versus intratumoral TIGIT-blocking strategies. Peripheral and intratumoral NK cells were analyzed from human patients and mice with osteosarcoma (OSA) and soft tissue sarcoma (STS). NK phenotype and function were evaluated using flow cytometry, immunohistochemistry, live-cell imaging, and RNA sequencing. Mouse antimouse-IgG1 TIGIT blockade was delivered systemically or intratumorally in flank models of OSA (K7M2) and STS (MCA-205). Clinical and genomic data were evaluated using Caris CODEai. Expression of the TIGIT ligand CD155 on myeloid and tumor cells was evaluated as a marker of TIGIT function. Using multiple readouts, TIGIT+ NK cells from the spleen of tumor-bearing mice or peripheral blood of patients with STS and OSA showed increased functionality compared w...

Coronary plaque quantification on energy-integrating and photon-counting detector CT: reproducibility and power modeling for mixed-platform trials.

• Status: include
• Score: 0.85
• Category: biomedical-imaging
• Journal: European radiology
• Publication date: 2026-Jul-22
• Screened: 2026-07-25 13:50 KST
• PMID: 42486966
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42486966/
• DOI: 10.1007/s00330-026-12773-4
• Tags: CT, PCD-CT, EID-CT, plaque quantification, imaging biomarker, reproducibility, power modeling
• Open access (OA/hybrid): 📎 Zotero에 추가

Screening brief

이 연구는 EID-CT와 PCD-CT 간 coronary plaque quantification의 재현성을 평가하고 최적의 reconstruction settings를 도출하여 quantitative imaging biomarker의 신뢰성을 입증했습니다. 또한 mixed-platform trials를 위한 power modeling framework를 제공함으로써, 영상 기반 surrogate endpoint를 활용한 임상 시험 설계에 실용적인 sample-size 기준을 제시합니다. 자동화된 deep learning 기반 plaque quantification 플랫폼과 표준화된 프로토콜이 결합될 때 기술 간 변이를 최소화할 수 있음을 보여준다는 점에서 현대 biomedical-imaging 연구에 중요한 방법론적 참고가 됩니다.

Abstract

To evaluate the reproducibility of quantitative plaque characterization between energy-integrating detector (EID)-CT and photon-counting detector (PCD)-CT, identify reconstruction settings yielding the lowest variability, and model sample-size requirements for trial planning. Patients who underwent coronary CT angiography on dual-source EID-CT and PCD-CT within 30 days were screened retrospectively. EID-CT data were reconstructed using quantitative (Qr40) and vascular (Bv40) kernels, while PCD-CT data were reconstructed with Bv36/40/44 and Qr36/40/44 kernels and quantum iterative reconstruction strengths 2-4. For each plaque component (total, low-attenuation, fibrotic, and calcified), volumes were computed using fixed and adaptive Hounsfield-unit thresholds using an automated deep-learning-based plaque-quantification platform and spatially co-registered. Inter-scanner standard deviation (SD) was calculated, and optimal reconstruction pairs were used for power modeling. Thirty-eight patients (age 68.0 [64.0-72.5] years, 30 men) and 77 vessels were included. Inter-scanner correlations were very strong for total (r = 0.85-0.95), fibrotic (r = 0.74-0.94), and calcified plaque (r = 0.92-0.98), and strong for low-attenuation plaque volumes (r = 0.71-0.85). Mean bias ranged from 8.2 to 164.4 mm³ for total plaque volume. Applying the optimal reconstruction pair (Qr40EID-CT vs. Bv36PCD...

Durable responses to triplet immunotherapy targeting TGF-β, PD-L1, and tumor antigen, with an IL-15 receptor superagonist in mismatch repair proficient castration-resistant prostate cancer.

• Status: include
• Score: 0.90
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-24
• Screened: 2026-07-25 13:47 KST
• PMID: 42498485
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42498485/
• DOI: 10.1136/jitc-2026-015336
• Tags: prostate cancer, immunotherapy, combination therapy, PSA response, mismatch repair proficient, IL-15 receptor superagonist

Screening brief

본 연구는 Quick Efficacy Seeking Trial(NCT03493945)을 통해 mismatch repair proficient castration-resistant prostate cancer 환자에서 PD-L1/TGF-β 이중 억제제, IL-15 receptor superagonist, 그리고 BN-Brachyury vaccine를 결합한 삼중 면역요법의 임상적 효능과 안전성을 평가하였다. 특히 기존 면역치료에 내성인 환자군에서도 지속적인 PSA decline이 관찰되어 치료 전략의 전환 가능성을 제시한다. 또한 말초 면역 프로파일링을 통해 NK cells 및 CD8+ T cells의 활성화 기전을 입증하여 향후 표적 치료 개발에 중요한 근거를 제공한다.

Abstract

Immune checkpoint blockade is minimally active in unselected castration-resistant prostate cancer (CRPC) and does not reproducibly yield durable decreases in prostate-specific antigen (PSA) levels. The Quick Efficacy Seeking Trial was designed to employ a combination of agents to initiate an immune response (with BN-Brachyury vaccine), potentiate that response (with nogapendekin-alfa inbakicept (NAI), an interleukin (IL)-15 receptor superagonist), and reduce or eliminate immunosuppressive entities in the tumor microenvironment (with bintrafusp alfa, a dual inhibitor of programmed death-ligand 1 and transforming growth factor beta). Epacadostat (an indoleamine 2,3-dioxygenase (IDO) inhibitor) was also employed in one cohort to reduce immune suppression induced by IDO's conversion of tryptophan to kynurenine. Patients with CRPC enrolled sequentially to receive vaccine + bintrafusp alfa (Arm 2.1), vaccine + bintrafusp alfa + NAI (Arm 2.2), and vaccine + bintrafusp alfa + NAI + epacadostat (Arm 2.3), with the primary objective to determine response rate. Adverse events in Arms 2.1 and 2.2 were manageable and consistent with the safety profiles of each agent individually, and notable for five individuals developing isolated adrenocorticotropic hormone deficiency. Arm 2.3 was closed early due to skin toxicity. Sustained declines in PSA were seen in 1/13 (8%) patients in Arm 2.1, 7/2...

Personalized tumor-loaded monocyte-derived dendritic cell vaccination in combination with atezolizumab as maintenance treatment in extensive-stage small cell lung cancer (ES-SCLC): phase Ib-II VENEZOLUNG trial.

• Status: include
• Score: 0.90
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-24
• Screened: 2026-07-25 13:46 KST
• PMID: 42498486
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42498486/
• DOI: 10.1136/jitc-2026-015351
• Tags: ES-SCLC, dendritic cell vaccine, atezolizumab, phase Ib/II trial, cDC1 biomarker, immunotherapy maintenance

Screening brief

이 논문은 ES-SCLC 환자에서 표준 chemotherapy 및 atezolizumab 유지 요법 후 autologous tumor lysate pulsed dendritic cell vaccine를 병용한 면역치료 전략을 평가합니다. Single-arm phase Ib/II trial 결과, 치료는 양호한 safety를 보였으며 cDC1s 및 stem-like exhausted CD8+ T cells의 확장이 long-term survival과 연관되어 면역기전 해소에 기여할 것으로 기대됩니다. 특히 dendritic cell vaccine와 PD-L1 inhibitor의 병용 maintenance therapy가 ES-SCLC 치료에 새로운 접근법을 제시하므로 위키 인덱스에 포함될 가치가 높습니다.

Abstract

Despite the incorporation of atezolizumab, an anti-programmed death-ligand 1 (PD-L1) antibody, into first-line chemotherapy regimen, survival in patients with extensive-stage small cell lung cancer (ES-SCLC) remains poor. Given the role of dendritic cells (DCs) in modulating responses to anti-programmed cell death protein 1 (PD-1) antibodies, a promising avenue is the development of vaccines based on DCs, together with the evaluation of how DC phenotypic modifications shape treatment efficacy. This is a single-arm, phase Ib/II, open-label clinical trial investigating the safety and activity of combining autologous tumor lysate pulsed DCs administered intradermally with intravenous atezolizumab as maintenance therapy for patients with ES-SCLC. Following leukapheresis, monocytes were differentiated ex vivo into mature DCs and loaded with irradiated autologous tumor lysate. After standard induction therapy (four cycles of carboplatin, etoposide, and atezolizumab), patients received up to six doses of mature DCs intradermally, along with intravenous atezolizumab 1,200 mg every 3 weeks, until disease progression. 20 patients were enrolled, including six patients with brain metastases. 18 patients received DC vaccination, with a median of three doses (range 1-6). Most grade 3-4 treatment-related adverse events were hematological and related to chemotherapy. DC vaccination was well t...

Acute exacerbation in fibrotic interstitial lung disease: An International Working Group Report.

• Status: include
• Score: 0.75
• Category: clinical-pulmonology
• Journal: American journal of respiratory and critical care medicine
• Publication date: 2026-Jul-14
• Screened: 2026-07-22 19:10 KST
• PMID: 42447235
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42447235/
• DOI: 10.1093/ajrccm/aamag363
• Tags: fILD, acute exacerbation, clinical trial endpoint, diagnostic criteria, ARW framework, interstitial lung disease, international working group

Screening brief

이 국제 작업 그룹 보고서는 fibrotic interstitial lung disease (fILD) 환자에서 발생하는 acute exacerbation (AE)의 정의와 diagnostic criteria를 명확히 재정의하여 임상 및 연구 현장에서의 표준화를 이끌었습니다. 또한 기존 AE 개념을 넘어 acute respiratory worsening (ARW) 프레임워크를 제안함으로써 다양한 임상 양상을 체계적으로 평가할 수 있는 기반을 마련했습니다. 특히 AE를 clinical trial endpoint로 포함하는 방법론과 risk stratification, 신약 개발 방향에 대한 실용적인 가이드라인을 제공하여 관련 질환의 치료 연구 발전에 핵심적인 자료가 됩니다.

Abstract

Acute exacerbations (AEs) occur both in patients with idiopathic pulmonary fibrosis (IPF) and non-IPF fibrotic interstitial lung disease (fILD). These events confer high morbidity and mortality, with a lack of proven effective therapeutic interventions. The objective of this state-of-the-art document is to summarize latest evidence since the 2016 international working group report on AE-IPF, expanding it across the spectrum of all fILDs. A comprehensive literature review on the epidemiology, associated and risk factors, prognosis, and management of AE-fILD is summarized. In addition to revising the AE definition and diagnostic criteria for broad application across different fILDs, a conceptual framework for acute respiratory worsening (ARW) has been proposed to encompass a variety of acute respiratory deteriorations, both related and unrelated to AE. This allows structured evaluation in both clinical and research settings. The proposed revised definition for AE-fILD is an acute respiratory event characterized by increased respiratory symptoms or signs and associated with radiologic or histologic features consistent with diffuse alveolar damage (with or without superimposed organizing pneumonia) in a patient with known or newly diagnosed fILD. On the other hand, ARW refers to a heterogeneous group of clinical events with acute symptom worsening not attributable to DAD in patien...

Anti-PD1-IL18 immunoconjugate promotes effector T cell-mediated antitumor immunity.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-14
• Screened: 2026-07-22 19:09 KST
• PMID: 42448430
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42448430/
• DOI: 10.1016/j.ccell.2024.06.009
• Tags: immunoconjugate, PD-1 blockade, IL-18, T cell activation, tumor microenvironment, immunotherapy resistance, translational research, solid tumors
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 anti-PD-1 antibody와 변형된 IL-18을 결합한 immunoconjugate가 tumor microenvironment에서 국소적으로 면역을 활성화하여 기존 치료에 내성을 보이는 solid tumors에서도 효과적인 항종양 반응을 유도함을 입증했습니다. 특히 PD-1+IL-18Rɑ+ CD4+ Th1-like 및 CD8+ effector T cell 아집단의 활성화 기전을 규명하여, 표적 immunotherapy의 새로운 전략으로의 임상 적용 가능성을 제시합니다. 다중 human cancer digest cultures 및 single-cell RNA sequencing 데이터를 활용한 전임상 및 in vitro 검증은 해당 접근법의 광범위한 임상적 유용성을 뒷받침합니다.

Abstract

Immune checkpoint inhibitors have revolutionized cancer therapy, yet a substantial proportion of patients exhibit primary or acquired resistance. Immunocytokines offer a strategy to enhance antitumor immunity by delivering cytokine signals selectively to the tumor microenvironment. Here, we describe the immunoconjugate anti-programmed cell death protein 1 (PD-1)-interleukin (IL)-18 (aPD1-IL18mut), designed to couple PD-1-blockade with localized IL-18-mediated immune activation. aPD1-IL18mut was generated by chemically conjugating the anti-human PD-1 antibody Lipustobart to an IL-18 variant engineered to evade IL-18 binding protein. Its mechanism of action was characterized using human PD-1 transgenic mouse models. To assess the translational relevance of these in vivo findings, complementary in vitro assays were conducted on human tumor samples, alongside analyses of publicly available single-cell RNA sequencing datasets. In vitro, PD-1 engagement enhanced functional IL-18 activity, preserving interferon (IFN)-γ secretion even under IL-18BP pressure. In MC38 tumors, aPD1-IL18mut induced robust CD8+ T cell-driven tumor control, accompanied by intratumoral accumulation of activated CD8+ T cells and a pronounced type 1-associated cytokine response. In anti-PD-1-resistant YUMM1.7 tumors, therapeutic efficacy instead relied predominantly on Th1-like CD4+ effector T cells, and aPD1-...

LysoPS-GPR34 axis enhances tumor-associated macrophages efferocytosis to promote immune escape in gastric cancer peritoneal metastasis.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-14
• Screened: 2026-07-22 19:08 KST
• PMID: 42448431
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42448431/
• DOI: 10.1016/j.immuni.2019.03.020
• Tags: gastric cancer, peritoneal metastasis, TAMs, efferocytosis, GPR34, anti-PD-1, immunotherapy
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 위암 복막 전이 환경에서 LysoPS-GPR34 axis가 종양 관련 대식세포(TAMs)의 efferocytosis를 유도하여 면역 억제성 TME을 형성하는 분자 기전을 규명하였다. GPR34 inhibitor가 M2-like TAMs 침윤을 감소시키고 cytotoxic T cells 반응을 증진시킴을 입증하였으며, 기존 anti-PD-1 therapy와 병용 시 종양 성장 억제에 시너지 효과를 보였다. 따라서 위암의 면역 회피 기전 이해와 표적 면역요법 개발에 중요한 임상적 함의를 제공한다.

Abstract

Metabolites sculpt the immunosuppressive tumor microenvironment (TME) that facilitates immune evasion. As a crucial signaling lysophospholipid, lysophosphatidylserine (LysoPS) correlates with advanced disease stages in multiple tumor types. However, the mechanisms by which LysoPS drives gastric cancer peritoneal metastasis remain undefined. Single-cell transcriptomic profiling of primary tumors, normal peritoneum, and metastatic lesions delineated mechanisms underlying LysoPS-mediated tumor-associated macrophages (TAMs) reprogramming. Immunohistochemistry and multiplex immunofluorescence validated GPR34-high TAMs infiltration in peritoneal metastases. Functional validation was performed using molecular assays and in vivo models. LysoPS accumulated in ascites from patients with gastric cancer peritoneal metastasis, establishing an immunosuppressive TME that drove malignant progression. Using single-cell transcriptome sequencing, we identified a distinct subset of TAMs highly expressing GPR34 enriched in gastric cancer peritoneal metastases, which correlates with tumor progression and immune evasion. Mechanistically, LysoPS engagement of GPR34 activated ERK/c-Jun signaling, transcriptionally upregulating AXL and CD36 to enhance efferocytosis. This effect drove TAMs toward an immunosuppressive phenotype, characterized by enhanced interleukin-10 and transforming growth factor-β se...

Interstitial lung disease in patients treated with antibody-drug conjugates: a review.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Jul-11
• Screened: 2026-07-22 19:07 KST
• PMID: 42462539
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42462539/
• DOI: 10.1016/j.lungcan.2026.109532
• Tags: ADC, ILD, pneumonitis, T-DXd, HRCT, drug toxicity, lung cancer

Screening brief

항체-약물 접합체(ADC)는 다양한 고형암 치료에 널리 사용되지만, 간질성 폐질환(ILD) 및 pneumonitis는 치명적일 수 있는 주요 부작용으로 대두되었습니다. 본 리뷰는 T-DXd를 비롯한 다양한 deruxtecan 기반 ADC의 ILD 발생률과 병인 기전을 체계적으로 정리하며, HRCT 기반 정기 감시와 단계별 corticosteroid 치료의 임상적 필요성을 강조합니다. 이는 항암 신약 개발 및 실제 임상에서 약물 관련 폐독성을 관리하는 데 필수적인 근거를 제공하므로 위키 인덱스에 반드시 등재해야 합니다.

Abstract

Antibody-drug conjugates (ADCs) are increasingly used across solid tumors, including lung cancer, but drug-related interstitial lung disease (ILD)/pneumonitis has emerged as a clinically relevant and potentially fatal toxicity. This narrative review summarizes evidence from clinical trials, pooled analyses, pharmacovigilance studies, mechanistic investigations, and consensus recommendations on the epidemiology, pathophysiology, diagnosis, risk factors, and management of ADC-related ILD. ILD has been most extensively characterized with trastuzumab deruxtecan (T-DXd), for which pooled analyses report an incidence of approximately 10-15%, a median onset of 5-6 months, and a fatal-event rate of about 2.2%. However, pulmonary toxicity is not restricted to HER2-directed ADCs and has also been reported with deruxtecan-based agents targeting TROP2 and HER3, as well as with non-deruxtecan ADCs. Pharmacovigilance data from 1,277 cases showed that ILD, pneumonitis, and acute respiratory distress syndrome accounted for 40.6%, 27.9%, and 7.6% of pulmonary events, respectively; acute respiratory distress syndrome had the earliest onset and highest case-fatality. Mechanistic data support antigen-independent, dose-dependent ADC uptake by alveolar macrophages through Fcγ receptors, followed by intracellular payload release and cytokine-mediated lung injury. Risk is influenced by ADC type, payl...

Diverse origin and nature of tumor-infiltrating lymphocytes: the infection hypothesis.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-16
• Screened: 2026-07-22 19:06 KST
• PMID: 42463282
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42463282/
• DOI: 10.1038/s41586-023-06623-2
• Tags: TIL, tumor microenvironment, Infection Hypothesis, cancer immunotherapy, microbial ecology, immunoediting, immune recruitment
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 논문은 종양 내 림프구(TIL)의 기원에 대한 새로운 Infection Hypothesis를 제시하며, tumor microenvironment 내 미생물 감염이 면역 세포 유도 경로에 미치는 영향을 체계적으로 고찰합니다. 기존 immunoediting 개념을 보완하여 종양 생태계 이해에 중요한 통찰을 제공하며, 향후 cancer immunotherapy 전략 수립에 새로운 방향을 제시할 수 있습니다. 특히 병원체와 TIL의 상호작용을 고려한 치료 접근법의 필요성을 강조한다는 점에서 clinical-oncology 연구자들에게 의미 있는 문헌입니다.

Abstract

In the 19th century, Rudolf Virchow observed lymphocyte infiltration in tumors and suggested a potential link between cancer and inflammation. Current explanations for the origin of tumor-infiltrating lymphocytes are based on the interaction between cancer cells and the immune system. This model was proposed before it was recognized that tumors are frequently infected or colonized by microbial elements, suggesting the presence of bacteria-specific and virus-specific T cells within tumors. While several aspects of this microbial experience remain under investigation, their impact on the tumor microenvironment and antitumor immune response may be significant, as the pathogens may elicit the direct or indirect recruitment of tumor-infiltrating lymphocytes. This "Infection Hypothesis" regarding the origin of tumor-infiltrating lymphocytes complements the classical tumor immunoediting hypothesis, offers new avenues for a comprehensive understanding of the tumor ecosystem, and highlights the need for more nuanced cancer treatment approaches that account for the potential interconnected roles of lymphocytes and pathogens in the tumor milieu.

RAS signaling at the crossroads of radioresistance and tumor immunity.

• Status: include
• Score: 0.90
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-17
• Screened: 2026-07-22 19:05 KST
• PMID: 42468991
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42468991/
• DOI: 10.1016/j.ctarc.2022.100514
• Tags: KRAS, radioresistance, tumor immunity, RAS inhibitors, radiation therapy, immuno-oncology, DNA repair
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 논문은 KRAS 돌연변이가 radioresistance와 tumor immunity 회피를 어떻게 조절하는지 분자적 기전을 종합적으로 서술합니다. 특히 KRAS-NRF2-53BP1 축을 통한 DNA 손상 수복과 미세환경 재프로그래밍이 radiation therapy의 효능을 저해함을 강조합니다. 차세대 RAS inhibitors를 radiation therapy 및 immunotherapy와 병용할 때 내성 극복과 장기적 종양 조절 가능성이 제시되어 임상 전략 수립에 중요한 시사점을 제공합니다.

Abstract

RAS mutations are among the most prevalent oncogenic drivers in solid tumors and are consistently associated with suboptimal responses to radiation therapy (RT). Within this family, KRAS is the dominant isoform and a central regulator of tumor stress adaptation. Increasing evidence indicates that oncogenic KRAS orchestrates radioresistance through coordinated tumor-intrinsic and microenvironmental mechanisms. Cell-intrinsically, KRAS enhances DNA damage repair, replication stress tolerance, redox buffering, and ferroptosis defense. The KRAS-NRF2-53BP1 axis exemplifies this program by accelerating non-homologous end joining and enabling rapid repair of radiation-induced DNA double-strand breaks. Concurrently, KRAS reshapes the tumor microenvironment by promoting myeloid recruitment, metabolic rewiring, impaired antigen presentation, and immune checkpoint upregulation, thereby constraining the immunogenic effects of RT. The rapid evolution of RAS-directed therapeutics, including allele-specific, ON-state, dual-state, and pan-RAS inhibitors, as well as emerging degraders and molecular reprogramming strategies, has transformed a historically "undruggable" target into a clinically actionable vulnerability. Preclinical evidence indicates that KRAS inhibition can restore radiosensitivity and partially recondition antitumor immunity. However, adaptive resistance frequently converges o...

Spatial architecture of tertiary lymphoid structures represents an independent prognostic dimension in hepatocellular carcinoma.

• Status: include
• Score: 0.90
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-17
• Screened: 2026-07-22 19:04 KST
• PMID: 42468992
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42468992/
• DOI: 10.1186/s40364-025-00844-5
• Tags: HCC, TLS, Spatial-pathology, Deep-learning, Prognostic-biomarker, Immune-phenotype
• Open access (PMC): 📎 Zotero에 추가

Screening brief

이 연구는 간세포암(HCC) 환자에서 Tertiary lymphoid structures (TLS)의 spatial context가 예후에 미치는 상반된 영향을 대규모 코호트를 통해 입증하였습니다. 딥러닝 기반 SpatialDecoder 파이프라인을 활용하여 intratumoral와 extratumoral TLS 밀도를 정량화하고, 이를 기반으로 4가지 spatial immune phenotypes를 정의하여 사후 overall survival과 재발 위험도를 정밀하게 분류하였습니다. 기존 이분법적 TLS 평가 방식을 넘어 spatially informed 접근법을 제시함으로써 HCC 면역 치료 전략 및 임상적 의사결정에 중요한 기준을 마련하였습니다.

Abstract

Tertiary lymphoid structures (TLS) are associated with heterogeneous outcomes in hepatocellular carcinoma (HCC), but whether their anatomical context determines clinical impact remains unknown. We hypothesized that spatial compartmentalization of TLS influences their prognostic significance. We developed SpatialDecoder, a deep learning pipeline that simultaneously segments TLS, classifies three maturation subtypes (Agg, Fol I, Fol II), and assigns spatial compartments (intratumoral, peritumoral, capsular), achieving accurate tissue segmentation (mean Dice similarity coefficient (DSC)=0.86), TLS segmentation (DSC=0.8609), and subtyping (macro Area Under the Receiver Operating Characteristic Curve (AUROC)=0.8810). Applied to 1188 resected HCC patients, it enabled large-scale spatial TLS mapping. Spatial mapping revealed a prognostic dichotomy: higher intratumoral TLS density independently predicted prolonged overall survival, whereas higher extratumoral (peritumoral and capsular) TLS density correlated with increased recurrence risk. Based on TLS distribution, we defined four spatial immune phenotypes: TLS-Enriched (high intra/low extra), TLS-Balanced (high/high), TLS-Excluded (low intra/high extra), and TLS-Deficient (low/low). These phenotypes stratified patients into a survival gradient (log-rank p<0.0001): TLS-Enriched conferred the best outcome (HR = 0.48), TLS-Excluded the...

Deep learning-based automatic measurement of spinal alignment and implant detection in scoliosis radiographs.

• Status: maybe
• Score: 0.65
• Category: biomedical-imaging
• Journal: NPJ digital medicine
• Publication date: 2026-Jul-17
• Screened: 2026-07-22 19:03 KST
• PMID: 42469410
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42469410/
• DOI: 10.1038/s41746-026-03020-7
• Tags: deep-learning, radiography, scoliosis, automated-measurement, multi-institutional-validation, spinal-deformity, medical-AI
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 척추 측만증 radiographs를 대상으로 deep learning 기반 automatic measurement 및 implant detection AI 모델을 개발하고 multi-institutional validation을 수행한 결과입니다. coronal 및 sagittal 파라미터 측정 정확도와 vertebral numbering 성능이 임상적으로 유의미한 수준을 보여, medical imaging workflow automation에 기여할 수 있습니다. 비록 oncology 분야가 아닌 orthopedics 영역이지만, radiography image processing 및 AI model validation methodology는 본 위키의 biomedical-imaging 트랙에서 참고 자료로 유용하게 활용될 수 있습니다.

Abstract

Deep learning-based automated analysis offers the potential to streamline workflows, improve reproducibility, and reduce clinician workload. We developed an artificial intelligence (AI) system based on convolutional neural networks to automatically measure spinal alignment and detect spinal implants (pedicle screws and hooks combined as a single category) from scoliosis radiographs. A total of 4585 radiographs from 1671 adolescent idiopathic scoliosis patients across 10 institutions in 2 countries were used to train, validate, and externally test the model. The AI measured coronal and sagittal parameters with mean absolute errors (MAEs) of 2.7° (r = 0.99) for the major curve and 3.7° (r = 0.91) for thoracic kyphosis, regardless of implant presence. Vertebral numbering was performed with an accuracy of 0.97 for recognizing transitional vertebrae. Implant detection achieved high accuracy, with an MAE of 0.18 implants per image (r = 0.99). This comprehensive, multi-institutional validation demonstrates the clinical and research utility of the model in enabling fully automated assessment of spinal deformity. While external validation for coronal preoperative measurements was conducted across four cohorts in four countries, sagittal and postoperative measurements were externally validated at two sites (the United States and Japan); broader multi-region validation of sagittal and po...

A CT-based score for predicting histopathological usual interstitial pneumonia features and predicting disease progression in smokers with fibrotic idiopathic interstitial pneumonia.

• Status: include
• Score: 0.85
• Category: biomedical-imaging
• Journal: European radiology
• Publication date: 2026-Jul-18
• Screened: 2026-07-22 19:02 KST
• PMID: 42470480
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42470480/
• DOI: 10.1164/rccm.201308-1483st
• Tags: HRCT, U-I-P_score, UIP, IIP, imaging_biomarker, fibrotic_lung_disease
• Open access (PMC): 📎 Zotero에 추가

Screening brief

흡연자 섬유화성 idiopathic interstitial pneumonia(IIP) 환자에서 CT 영상만으로도 histopathological usual interstitial pneumonia(UIP) 소견을 정확히 예측할 수 있는 U-I-P 점수 체계를 개발하고 검증하였다. 이 연구는 폐기종과 흡연 관련 섬유화가 공존하는 복잡한 임상 상황에서 고해상도 흉부 CT(HRCT)를 활용한 정량적 imaging biomarker의 유용성을 입증한다. 생검이 불가능하거나 전형적인 영상 소견이 아닌 경우에도 disease progression 위험을 조기에 평가할 수 있어 임상 의사결정에 실질적으로 기여할 것으로 기대된다.

Abstract

Histopathological usual interstitial pneumonia (UIP) features are associated with progressive fibrosis but may be overlooked in smokers, where emphysema and smoking-related fibrosis complicate CT-based UIP classification. This study aimed to develop and validate a CT-based score to detect histopathological UIP features and to evaluate its association with disease progression in smokers with fibrotic idiopathic interstitial pneumonia (IIP). This retrospective multicentre study included two biopsy-proven cohorts of smokers with fibrotic IIP: derivation (n = 242; nationwide registry) and validation (n = 126; single-centre database, 2008-2013). Three predefined HRCT findings-upper-lobe irregular lines (U), irregularity of pleural surface (I), and pleural-based basal reticulation (P)-were scored (0/1) and summed as the U-I-P score (0-3). Associations with histopathological UIP features and outcomes were assessed using logistic regression, receiver operating characteristic analysis, Cox proportional hazards models, and bootstrap internal validation. Cohorts were similar (median age 65 vs. 64 years; 88% vs. 87% male). Histopathological UIP features were present in 208/242 (86%) and 109/126 (87%) patients. The U-I-P score independently predicted histopathological UIP features in both cohorts (area under the curve, 0.83 and 0.89; both p < 0.001). Bootstrap validation demonstrated minim...

Analysis of SLFN11 expression in small cell lung cancer, carcinoids and large cell neuroendocrine carcinoma: insights into lung neuroendocrine neoplasms.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Jul-13
• Screened: 2026-07-22 19:01 KST
• PMID: 42470748
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42470748/
• DOI: 10.1016/j.lungcan.2026.109539
• Tags: SLFN11, SCLC, LCNEC, neuroendocrine tumors, ASCL1, prognostic biomarker

Screening brief

본 연구는 폐 신경내분비 종양에서 SLFN11 발현 패턴을 조직학적으로 비교 분석하여 SCLC, LCNEC, 카르시노이드 간 차이를 명확히 하였다. 특히 SCLC에서 높은 SLFN11 발현이 OS 개선과 연관됨을 입증하며, ASCL1 및 Ki67과의 분자적 상관관계를 제시하였다. 이는 DNA-damaging agents 치료 반응 예측 및 신경내분비 폐암의 정밀 분류에 중요한 임상적 근거를 제공한다.

Abstract

SLFN11, highly expressed in SCLC, predicts sensitivity to DNA-damaging agents. Its role in other lung neuroendocrine neoplasms (NENs) (typical/atypical carcinoids - TC/AC and large cell neuroendocrine carcinoma- LCNEC) is unknown. This multicentre study assessed SLFN11 across lung NENs exploring its clinical-molecular associations. SLFN11 immunohistochemistry (H-score 0-300) was assessed in 361 tumours (127 TC, 35 AC, 152 LCNEC, 47 SCLC). Ki67, pRb, cMYC, DLL3, ASCL1, HNF1a, OTP and NEUROD1, ASCL1, POU2F3, and YAP1 (NAPY; H-score > 50 as dominant subgroup) staining were integrated with clinicopathologic data and survival. Median SLFN11expression (exp) was used for survival analysis. SLFN11exp varied across histologies (p < 0.001), with median values of 0 in TC (range 0-20) and AC (0-40), 2.49 (0-250) in LCNEC, 35 (0-240) in SCLC. SLFN11 showed a positive correlation with Ki67 (R2 = 0.187) across all histologies. In TC/AC, SLFN11exp was enriched in A1 subgroup tumours (known for ASCL1exp) (p = 0.035) and not correlated with OTP, HNF1A, CD44 and SSTR2Aexp. In LCNEC, SLFN11exp was higher in ASCL1high tumors (median 17.2; 0-162.5, p = 0.003) and correlated with cMYCexp (p = 0.024), but not with pRB and DLL3 status. In SCLC, a trend toward higher SLFN11exp in ASCL1high tumours was observed. SLFN11exp was not prognostic in TC/AC or LCNEC. In SCLC, SLFN11exp ≥ median value was associ...

AI-driven tumor heterogeneity quantification and survival prediction in pancreatic ductal adenocarcinoma.

• Status: include
• Score: 0.90
• Category: biomedical-imaging
• Journal: NPJ digital medicine
• Publication date: 2026-Jul-20
• Screened: 2026-07-22 18:59 KST
• PMID: 42477155
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42477155/
• DOI: 10.1038/s41746-026-02979-7
• Tags: PDAC, whole-slide images, survival prediction, tumor heterogeneity, AI pathology, prognostic biomarker, multi-cohort validation
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 연구는 pancreatic ductal adenocarcinoma (PDAC)에서 whole-slide images (WSI)를 활용한 AI 기반 tumor heterogeneity quantification 및 survival prediction 시스템을 제시합니다. 다중 코호트 검증 결과를 통해 기존 clinicopathological indicators 대비 향상된 prognostic performance를 입증하였으며, PDAC의 molecular pathways와의 연관성을 통해 모델의 생물학적 해석 가능성을 보여줍니다. 개인 맞춤형 치료 전략 수립과 수술 후 patient stratification에 있어 임상적 유용성이 기대되는 중요한 연구입니다.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies worldwide, and accurate prognostic prediction remains highly challenging due to its marked biological heterogeneity and complex tumor microenvironment. To address this challenge, a histopathomics-based survival prediction system (HPSurv) was developed using histopathological whole-slide images (WSIs) for individualized overall survival (OS) prediction. Within this framework, pathological tissue classification, quantitative characterization of tumor spatial heterogeneity, and a survival Transformer were integrated to enable multi-level representation learning from histopathological data. The system was developed and evaluated in 1020 patients across five independent cohorts. Compared with conventional clinicopathological indicators, significantly improved prognostic performance was achieved across multicenter cohorts (p < 0.05), with a mean C-index of 0.761 and time-dependent AUCs of 0.936, 0.877, and 0.772 for predicting 6-month, 2-year, and 3-year survival, respectively. Subgroup analyses further supported its role as an independent prognostic factor and suggested its potential utility in stratifying patients with respect to ACT-related outcomes. In addition, significant associations with key PDAC molecular pathways were observed, providing biological insights into the model predictions and support...

Does OptiTROP-Lung05 open a new frontier for first-line ADC-ICI combinations in NSCLC?

• Status: include
• Score: 0.90
• Category: clinical-oncology
• Journal: Nature reviews. Clinical oncology
• Publication date: 2026-Jul-20
• Screened: 2026-07-22 18:57 KST
• PMID: 42477498
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42477498/
• DOI: 10.1016/j.jtho.2024.09.015
• Tags: NSCLC, ADC, ICI, OptiTROP-Lung05, first-line therapy, combination therapy
• Open access (OA/bronze): 📎 Zotero에 추가00889-X/pdf)

Screening brief

이 논문은 NSCLC의 first-line 치료에서 ADC와 ICI를 병용하는 OptiTROP-Lung05 연구의 임상적 의의를 조명합니다. 기존 표준 치료의 한계를 넘어 새로운 치료 전략을 제시할 수 있는 잠재력을 평가하고 있습니다. ADC-ICI 조합이 향후 폐암 치료 가이드라인에 미칠 영향을 논의하므로 종양학 위키에 반드시 포함해야 합니다.

Abstract

not available

Multi-task deep learning model for predicting EGFR mutation status in NSCLC.

• Status: include
• Score: 0.90
• Category: biomedical-imaging
• Journal: NPJ digital medicine
• Publication date: 2026-Jul-20
• Screened: 2026-07-22 18:56 KST
• PMID: 42477500
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42477500/
• DOI: 10.1038/s41746-026-03007-4
• Tags: NSCLC, EGFR, CT, Deep Learning, Biomarker Prediction, Non-invasive Diagnosis
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

본 연구는 CT 영상을 기반으로 EGFR mutation status를 예측하는 Multi-task Deep Learning 모델을 개발하였습니다. 이 모델의 점수는 EGFR-targeted treatment을 받은 환자의 survival 및 관련 gene expression patterns와 강한 상관관계를 보였습니다. 조직 생검 없이 정확한 biomarker 예측이 가능해져 NSCLC 환자의 맞춤형 치료 전략 수립에 중요한 임상적 가치를 지닙니다.

Abstract

Multi-task DL for predicting EGFR mutation status Epidermal growth factor receptor (EGFR) mutation status is a critical biomarker in the management of non-small cell lung cancer (NSCLC), playing an essential role in selecting patients for EGFR-targeted treatment. With advancements in deep learning (DL), there is a growing interest in developing non-invasive methods for predicting EGFR mutation status. In this study, we present a multi-task deep learning (MTDL) model that utilizes CT images to predict EGFR mutation status (ChiCTR2400083082 in the WHO International Clinical Trials Registry). Our MTDL model achieved promising performance in accurately predicting EGFR mutation status. Additionally, the MTDL score was significantly associated with survival in patients receiving EGFR-targeted treatment, as well as relevant gene expression patterns and tumor microenvironment. These findings suggest that our method has the potential to serve as an accurate and non-invasive biomarker for predicting EGFR mutation status, thereby facilitating personalized treatment decisions for NSCLC patients.

Clinical Utility of Next Generation Sequencing in Concurrent EBUS-TBNA and Liquid Biopsies in NSCLC.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: American journal of respiratory and critical care medicine
• Publication date: 2026-Jul-20
• Screened: 2026-07-21 15:53 KST
• PMID: 42475517
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42475517/
• DOI: 10.1093/ajrccm/aamag372
• Tags: NSCLC, NGS, EBUS-TBNA, liquid biopsy, diagnostic yield, biomarker detection, precision medicine

Screening brief

이 연구는 NSCLC 환자에서 조직 검체(EBUS-TBNA)와 혈청 기반 liquid biopsy를 통한 NGS biomarker detection의 진단적 수확률(diagnostic yield)을 직접 비교한 전향적 관찰 연구입니다. 임상적으로 중요한 변이 탐지에서 EBUS-TBNA가 우위를 보였으나, 일부 환자에서는 blood 검체에서만 변이가 발견되어 상호 보완적인 전략이 필요함을 시사합니다. 이는 NSCLC의 precision medicine 접근법에서 biopsy modality 선택과 NGS turnaround time(TAT) 및 QNS 기준 개선의 중요성을 강조하므로 wiki에 포함될 가치가 있습니다.

Abstract

Genetic testing is standard of care in Non-small Cell Lung Cancer(NSCLC). Few studies evaluate concurrent Endobronchial Ultrasound-Transbronchial Needle Aspiration(EBUS-TBNA) and liquid biopsy for Next Generation Sequencing(NGS). Compare diagnostic yield differences for detecting clinically relevant mutations via NGS in concurrent EBUS-TBNA and liquid biopsies. Prospective observational cohort study of NSCLC patients undergoing concurrent biopsies. Yield differences, receiver operating characteristic (ROC) and kappa statistics were calculated for clinically relevant mutations. Of 199 subjects, diagnostic yield for EGFR was 9.5% in EBUS-TBNA and 7.0% in blood with yield difference 2.5%(95% CI: 3.4%, 8.5%, p = 0.36). For clinically relevant targets, there were 79(39.7%) from EBUS-TBNA and 49(29.6%) from blood with yield difference 15.1%(95% CI: 5.5%, 24.2%, p = 0.001). ROC statistics for detection of clinically relevant mutations (where tissue results were the gold standard) included: sensitivity 0.53 (95% CI: 0.42, 0.64), specificity: 0.95(95% CI: 0.90,0.98), positive predictive value: 0.89 (95% CI: 0.77, 0.96), negative predictive value: 0.74 (95% CI: 0.65, 0.81), and kappa statistic: 0.51 (95% CI: 0.39, 0.63). There were 37 (18.6%) participants with mutations in tissue only and 7(3.5%) with mutations in blood only, while 42(21.1%) had mutations reported from both sources. EBU...

BCL-2/BCL-xL inhibitor pelcitoclax with osimertinib for EGFR-mutated advanced non-small-cell lung cancer: a phase 1b trial.

• Status: include
• Score: 0.85
• Category: clinical-oncology
• Journal: Journal for immunotherapy of cancer
• Publication date: 2026-Jul-13
• Screened: 2026-07-20 22:37 KST
• PMID: 42442920
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42442920/
• DOI: 10.1182/blood.2020010167
• Tags: NSCLC, EGFR-mutation, pelcitoclax, osimertinib, BCL-xL-inhibitor, Phase-Ib-trial, TKI-resistance, combination-therapy
• Open access (OA/bronze): 📎 Zotero에 추가

Screening brief

이 연구는 EGFR-mutated advanced NSCLC 환자에서 BCL-2/BCL-xL inhibitor인 pelcitoclax과 osimertinib의 병용 요법 safety와 preliminary efficacy를 평가한 Phase 1b trial입니다. 특히 TKI treatment-naïve 군에서 높은 ORR과 mPFS를 보였으며, BCL-xL expression이 Cohort 1의 mPFS와 연관될 수 있음을 시사하여 TKI resistance 극복을 위한 새로운 병용 전략의 타당성을 제시합니다. 향후 표적 치료 및 biomarker 기반 환자 선정 연구에 중요한 참고 자료가 될 것입니다.

Abstract

Overcoming tyrosine kinase inhibitor (TKI) resistance improves survival in advanced epidermal growth factor receptor (EGFR)-mutated non-small-cell lung cancer (NSCLC). We therefore examined the safety and preliminary efficacy of pelcitoclax, a B-cell lymphoma-2 (BCL-2)/BCL-extra-large (BCL-xL) inhibitor, and osimertinib in patients with EGFR-mutated advanced NSCLC. Enrolled patients included Cohort 1 (previously progressed after third-generation TKI treatment+chemotherapy), Cohort 2 (previously progressed after first-generation or second-generation TKI treatment+chemotherapy), and Cohort 3 (TKI treatment-naive±prior chemotherapy). Patients received intravenous pelcitoclax (160 mg in dose-expansion and either 160 or 240 mg in dose-escalation) weekly and oral osimertinib 80 mg daily. Primary endpoints were safety and recommended phase 2 dose (dose-escalation), objective response rate (ORR) and safety (dose-expansion). 64 patients were enrolled (13, dose-escalation; 51, dose-expansion): 29 patients in Cohort 1, 8 in Cohort 2, and 27 in Cohort 3. One dose-limiting toxicity occurred at pelcitoclax 240 mg, and the recommended phase 2 dose was 160 mg plus osimertinib 80 mg. The ORR was 10.7% and median progression-free survival (mPFS) 2.7 months in patients previously progressed after third-generation TKI treatment+chemotherapy (Cohort 1) and 80.8% and 16.4 months in TKI treatment-na...

Outcomes of robotic vs video-assisted thoracoscopic segmentectomy in early-stage NSCLC: A meta-analysis of propensity-matched studies.

• Status: include
• Score: 0.90
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Jul-15
• Screened: 2026-07-20 22:36 KST
• PMID: 42456640
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42456640/
• DOI: 10.1016/j.lungcan.2026.109531
• Tags: NSCLC, RATS, VATS, segmentectomy, meta-analysis, propensity-matched, perioperative-outcomes

Screening brief

이 연구는 초기 단계 NSCLC 환자에서 RATS와 VATS를 이용한 segmentectomy의 임상적 결과를 propensity-matched meta-analysis를 통해 비교하였습니다. 양쪽 접근법 모두 OS 및 perioperative safety에서 유사한 결과를 보여, 수술 기법 선택은 surgeon expertise와 resource availability에 따라 individualized되어야 함을 시사합니다. 초기 NSCLC 치료 전략 수립과 비용-효과성 논의에 중요한 근거를 제공합니다.

Abstract

Robotic-assisted thoracoscopic segmentectomy (RATS) has been increasingly adopted for early-stage non-small cell lung cancer (NSCLC), yet comparative effectiveness versus video-assisted thoracoscopic segmentectomy (VATS) remains uncertain. We performed a meta-analysis restricted to propensity-matched studies to compare perioperative and oncologic outcomes between approaches. A comprehensive literature search was conducted to identify studies comparing RATS and VATS. Pooled odds ratios (ORs) and mean differences (MDs) with 95% confidence intervals (CIs) were calculated using random-effects models. Overall survival (OS) was reconstructed from published Kaplan-Meier curves and analyzed using Cox proportional hazards models. Five studies comprising 14,007 patients with 3,233 (23.1%) undergoing RATS were included. RATS was associated with lower intraoperative blood loss (MD -8.82, 95% CI -16.37 to -1.28, p = 0.02). Median overall survival was similar between groups at 4.6 years for both RATS and VATS (HR 0.98, 95% CI 0.90 to 1.08, p = 0.72). Operative time, cost, nodal assessment, chest drainage duration, hospital length of stay, conversion to thoracotomy, 30-day readmission, persistent air leak, atrial arrhythmia, and 90-day mortality were comparable. Both surgical approaches provide comparable perioperative safety and oncologic adequacy. Procedure selection should be individualiz...

[18F]FDG PET during immunotherapy: mind the gap between evidence, imaging guidelines, and oncology practice.

• Status: include
• Score: 0.85
• Category: biomedical-imaging
• Journal: European journal of nuclear medicine and molecular imaging
• Publication date: 2026-Jul-17
• Screened: 2026-07-20 22:36 KST
• PMID: 42463966
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42463966/
• DOI: 10.1186/s13045-025-01734-x
• Tags: Immunotherapy, [18F]FDG PET, Response Assessment, Pseudoprogression, Neoadjuvant Immunotherapy, Imaging Guidelines
• Open access (OA/gold): 📎 Zotero에 추가

Screening brief

이 논문은 Immunotherapy 중 [18F]FDG PET의 임상적 적용 범위와 현재 가이드라인 간의 불일치를 체계적으로 분석합니다. Melanoma 및 NSCLC 환자 대상 연구에서 조기 Response Assessment 시 Pseudoprogression 감별의 한계를 지적하며, Neoadjuvant Immunotherapy 또는 치료 중단 전 평가에서는 높은 음성 예측 가치를 보인다고 강조합니다. 영상 기반 면역 반응 평가의 표준화와 임상적 의사결정을 위한 근거 마련에 중요한 자료가 될 것입니다.

Abstract

No specific statements regarding the use of 2-[18F]fluoro-2-deoxy-D-glucose positron-emission tomography/computed tomography ([18F]FDG PET) in the context of immunotherapy are made in current international oncological guidelines for the management of the two cancer types for which the largest body of evidence has been generated, such as melanoma and non-small cell lung cancer (NSCLC). However, practice guidelines released jointly by leading nuclear medicine societies recommended the use of [18F]FDG PET alongside computed tomography (CT) before immunotherapy initiation, for early response assessment, and in patients considered for therapy discontinuation. In the present paper we critically reviewed the available literature on the comparison between [18F]FDG PET and CT for response assessment in patients undergoing immunotherapy, with the aim to identify where metabolic imaging holds the most significant promise. In early response assessment, where an accurate discrimination between pseudoprogression and true tumor progression is necessary, [18F]FDG PET is of limited value. In contrast, there are at least two clinical scenarios in which [18F]FDG PET could outperform CT because of its high negative predictive value, that are the evaluation of response to neoadjuvant immunotherapy or before therapy discontinuation. We emphasized that the generation of robust evidence is necessary...

Neoadjuvant and perioperative chemo-immunotherapy in early-stage non-small cell lung cancer: international expert panel meeting by AIOT.

• Status: include
• Score: 0.95
• Category: clinical-oncology
• Journal: Lung cancer (Amsterdam, Netherlands)
• Publication date: 2026-Jul-11
• Screened: 2026-07-20 22:35 KST
• PMID: 42470746
• PubMed: https://pubmed.ncbi.nlm.nih.gov/42470746/
• DOI: 10.1016/j.lungcan.2026.109533
• Tags: NSCLC, neoadjuvant, perioperative, chemo-immunotherapy, expert-consensus, stage-II-III, PD-L1

Screening brief

resectable early-stage NSCLC 치료에서 chemo-immunotherapy 통합이 pCR 및 EFS, OS 향상에 기여하며 새로운 표준으로 자리 잡고 있습니다. 국제 전문가 패널은 pre-treatment evaluation, neoadjuvant vs perioperative 전략 선택, 환자 선별 기준에 대한 명확한 권고사항을 제시하였습니다. 특히 PD-L1-negative tumors에서도 면역요법의 이점이 확인되었으며, stage III 및 N-positive 질환에서 신주 또는 주위 접근이 우선 권장됩니다. 향후 biomarker-driven therapy 개인화와 전략 간 직접 비교 연구가 필요함을 강조하며 임상 의사에게 실용적인 가이드라인을 제공합니다.

Abstract

Integration of immune checkpoint inhibitors with perioperative chemotherapy has significantly improved pathological response rates and survival outcomes in patients with resectable NSCLC. In this context, an international expert panel convened to discuss optimal use of neoadjuvant and perioperative chemo-immunotherapy in individuals with early-stage/locally advanced resectable NSCLC, based on emerging trial data. A virtual expert panel meeting was held on July 10, 2025 under the auspices of the Italian Association of Thoracic Oncology (AIOT). Seven thoracic oncology experts reviewed current evidence from pivotal trials. The panel addressed predefined clinical questions spanning pre-treatment evaluation, choice of neoadjuvant vs perioperative strategies, and patient selection. Shared-opinion statements were developed through moderated discussion. The panel endorsed pathological mediastinal staging and molecular testing in all candidates before therapy. Neoadjuvant and perioperative chemo-immunotherapy were considered a new standard for resectable stage II-III NSCLC after thorough and thoughtful multidisciplinary board discussion, having shown improved pathological complete response (pCR), event-free survival (EFS), and overall survival (OS), and was deemed overall safe without compromising surgery. PD-L1-negative tumors were not excluded from immunotherapy benefit, although mag...