Translational lung cancer research最新文献

{"title":"XPO1 inhibition in KRAS-mutant cancers: time for clinical trials but how?","authors":"Misako Nagasaka, Husain Y Khan, Faustine Luo, Mohammed Najeeb Al-Hallak, Muhammad Wasif Saif, Ramzi M Mohammad, Asfar S Azmi","doi":"10.21037/tlcr-2025-432","DOIUrl":"10.21037/tlcr-2025-432","url":null,"abstract":"","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":"14 8","pages":"2895-2899"},"PeriodicalIF":3.5,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>STK11</i>/<i>KEAP1</i> co-mutations in <i>SMARCA4</i>-mutant advanced non-small cell lung cancer: genetic characteristics and impact on immunotherapy efficacy.","authors":"Ziyi Dong, Ran Zuo, Yaoyang Guo, Xinyi Wen, Gang Zhao, Zhansheng Jiang","doi":"10.21037/tlcr-2025-305","DOIUrl":"10.21037/tlcr-2025-305","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;The impact of &lt;i&gt;STK11/KEAP1&lt;/i&gt; co-mutations on the efficacy of immunotherapy in patients with &lt;i&gt;SMARCA4&lt;/i&gt;-mutant advanced non-small cell lung cancer (NSCLC) remains incompletely understood. Our aim was to investigate the effects of &lt;i&gt;STK11/KEAP1&lt;/i&gt; co-mutations on the clinical prognosis of patients with &lt;i&gt;SMARCA4&lt;/i&gt;-mutant advanced NSCLC receiving immunotherapy.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We obtained 2,098 patients with stage IIIB-IV NSCLC from the cBioPortal database. Patients harboring &lt;i&gt;EGFR&lt;/i&gt;, &lt;i&gt;ALK&lt;/i&gt;, &lt;i&gt;ROS1&lt;/i&gt; and &lt;i&gt;RET&lt;/i&gt; mutations were excluded. The impacts of &lt;i&gt;SMARCA4&lt;/i&gt; and &lt;i&gt;STK11/KEAP1&lt;/i&gt; co-mutations on the efficacy of chemoimmunotherapy were analyzed, along with their associations with tumor mutational burden (TMB), programmed cell death ligand 1 (PD-L1) expression, and patient prognosis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Among 2,098 patients with NSCLC, &lt;i&gt;SMARCA4&lt;/i&gt;-mutant patients accounted for 7.7% (162/2,098), and wild-type patients accounted for 92.3% (1,936/2,098). &lt;i&gt;SMARCA4&lt;/i&gt; mutations are more common in elderly patients, smokers, and patients with adrenal metastasis. Compared with &lt;i&gt;SMARCA4&lt;/i&gt; wild-type patients, &lt;i&gt;SMARCA4&lt;/i&gt;-mutant patients had significantly greater TMB (P&lt;0.001) and poorer median overall survival (mOS) (10.6 &lt;i&gt;vs.&lt;/i&gt; 17.5 months, P&lt;0.001). Further analysis revealed that patients with &lt;i&gt;SMARCA4&lt;/i&gt; class I alterations had significantly shorter mOS (8.7 &lt;i&gt;vs.&lt;/i&gt; 14.1 months, P=0.008) and median first-line treatment progression-free survival (mPFS1) (3.7 &lt;i&gt;vs.&lt;/i&gt; 6.6 months, P=0.003) than those with class II alterations. Multivariate regression analysis confirmed that &lt;i&gt;SMARCA4&lt;/i&gt; mutations significantly increased the risk of death [hazard ratio (HR) =1.329, 95% confidence interval (CI): 1.106-1.596, P=0.002]. Compared with chemotherapy, chemoimmunotherapy significantly prolonged mPFS1 (5.6 &lt;i&gt;vs.&lt;/i&gt; 3.9 months, P=0.01) but not mOS (10.8 &lt;i&gt;vs.&lt;/i&gt; 9.5 months, P=0.91) in patients with &lt;i&gt;SMARCA4&lt;/i&gt; mutations. Among patients receiving first-line chemoimmunotherapy, TMB levels had no significant effect on mPFS1 (5.6 &lt;i&gt;vs.&lt;/i&gt; 6.6 months, P=0.83) or mOS (8.5 &lt;i&gt;vs.&lt;/i&gt; 10.8 months, P=0.38), but PD-L1-positive patients had significantly longer mPFS1 (8.3 &lt;i&gt;vs.&lt;/i&gt; 5.1 months, P=0.02) and mOS (18.9 &lt;i&gt;vs.&lt;/i&gt; 9.3 months, P=0.03). &lt;i&gt;SMARCA4&lt;/i&gt; and &lt;i&gt;STK11/KEAP1&lt;/i&gt; co-mutations were not significantly correlated with TMB (P=0.85) or PD-L1 expression (P=0.08). However, the patients with &lt;i&gt;SMARCA4&lt;/i&gt; and &lt;i&gt;STK11/KEAP1&lt;/i&gt; co-mutations had significantly shorter mPFS1 (4.5 &lt;i&gt;vs.&lt;/i&gt; 13.3 months, P&lt;0.001) and mOS (8.7 &lt;i&gt;vs.&lt;/i&gt; 20.1 months, P=0.005) in the chemoimmunotherapy group. Among &lt;i&gt;SMARCA4&lt;/i&gt;-mutant patients, those without &lt;i&gt;STK11/KEAP1&lt;/i&gt; co-mutations derived longer mPFS1 (13.3 &lt;i&gt;vs.&lt;/i&gt; 5.6 months, P=0.01) benefits from immunotherapy. In contrast, this benefit markedly reduced mPFS1 (4.5 &lt;i&gt;vs.&lt;/i&gt; 2.9 months, P=0.16) ","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":"14 8","pages":"3024-3041"},"PeriodicalIF":3.5,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Positioning amivantamab and lazertinib in the therapeutic sequence for <i>EGFR</i>-mutant NSCLC: insights from CHRYSALIS-2 cohort A.","authors":"Faith Abodunrin, Dillon E Berlin, Christine M Bestvina","doi":"10.21037/tlcr-2025-461","DOIUrl":"10.21037/tlcr-2025-461","url":null,"abstract":"","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":"14 8","pages":"2906-2911"},"PeriodicalIF":3.5,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432654/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in the research of leptomeningeal metastases in non-small cell lung cancer: a narrative review.","authors":"Jiaojiao Hong, Yue Hao, Jiangxia Yuan, Xianzi Dai, Chengyu Chen, Zhengxing Huo, Jia Zhu, Qian Wang","doi":"10.21037/tlcr-2025-163","DOIUrl":"10.21037/tlcr-2025-163","url":null,"abstract":"<p><strong>Background and objective: </strong>Lung cancer is among the malignant tumors with the highest morbidity and mortality rates, with approximately 80-85% of cases being non-small cell lung cancer (NSCLC). The incidence of central nervous system metastases is notably high, and about 3-5% of NSCLC patients develop leptomeningeal metastases. As the survival rates for NSCLC patients improve, the incidence of leptomeningeal metastases (LMs) continues to rise. This article reviews the mechanisms of leptomeningeal metastases, diagnostic and therapeutic achievements, and ongoing challenges, providing insight into the diagnosis and management of NSCLC with LM and the development of related clinical strategies.</p><p><strong>Methods: </strong>We searched PubMed, MEDLINE, EMBASE, Cochrane Library, and major international conferences for all types of articles published in English up to December 31, 2024.</p><p><strong>Key content and findings: </strong>Patients with LM face significant challenges in diagnosis and treatment due to the low sensitivity of current diagnostic methods, the nonspecific nature of clinical symptoms, and the unique anatomical location of the leptomeninges. While recent exploratory studies have identified sensitive molecular markers and potential therapeutic strategies, large-scale prospective studies are still needed for validation.</p><p><strong>Conclusions: </strong>In conclusion, a multidisciplinary approach with individualized treatment plans is essential for LM patients. For LM patients with driver gene-positive, targeted therapy is the mainstay, supplemented by local therapy or anti-angiogenic agents. For LM patients with driver gene-negative, chemotherapy combined with immunotherapy is the mainstay. If treatment is not effective, means such as sequential therapy and higher drug doses provide new treatment ideas and options for LM patients.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":"14 8","pages":"3216-3232"},"PeriodicalIF":3.5,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The OPEN trial-from the darkness, comes light.","authors":"Richard Pham, Surein Arulananda","doi":"10.21037/tlcr-2025-363","DOIUrl":"10.21037/tlcr-2025-363","url":null,"abstract":"","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":"14 8","pages":"2912-2917"},"PeriodicalIF":3.5,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145064849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complex uniportal robotic-assisted sleeve resections under spontaneous ventilation and with double lumen intubation: a case series and a narrative review of the literature.","authors":"Diego Gonzalez-Rivas, Pablo Gomes-da Silva de Rosenzweig, Luis Fernando Arana Bolaños, Adriana Simoneta Pimienta Ibarra, Hasanali David Walji, Patricio Santillan Dohetty, Jun Zhao, Chang Li, Mugurel Bosinceanu, Francina Valezka Bolaños Morales","doi":"10.21037/tlcr-2025-498","DOIUrl":"10.21037/tlcr-2025-498","url":null,"abstract":"<p><strong>Background and objective: </strong>Sleeve lobectomy (SL) has evolved into the preferred surgical option for centrally located non-small cell lung cancer (NSCLC) and other complex thoracic tumors, offering superior functional and oncological outcomes compared to pneumonectomy. The recent advent of robotic-assisted thoracic surgery (RATS), including its uniportal approach (uRATS), has extended the feasibility of SL to minimally invasive approaches. The objective of this study is to present our experience with uRATS sleeve resections, highlighting five complex cases, involving four sleeve lobectomies and one tracheal resection, performed using two different robotic platforms (da Vinci and ShuRui). Additionally, we aim to provide an up-to-date review of SL as a treatment strategy for NSCLC and centrally located tumors.</p><p><strong>Methods: </strong>We performed a narrative review covering publications from 2010 to 2025. The search was conducted across PubMed, EMBASE, and Scopus databases.</p><p><strong>Key content and findings: </strong>Although data on RATS SL remains limited, several publications have highlighted the potential benefits of this approach. Comparative studies evaluating different operative approaches for SL have shown that RATS offers advantages over both open and video-assisted thoracic surgery. uRATS SL represents a novel and evolving technique that combines technical precision with favorable perioperative outcomes. However, its adoption is often slow due to the inherent complexity and steep learning curve associated with the procedure.</p><p><strong>Conclusions: </strong>uRATS SL carinal and tracheal reconstructions have emerged as promising treatment strategies for centrally located tumors. However, there remains an urgent need for further comparative studies assessing both short- and long-term outcomes, as well as evaluating oncologic outcomes and their impact on patients' quality of life.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":"14 8","pages":"3170-3182"},"PeriodicalIF":3.5,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432592/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deep learning enhances precision diagnosis and treatment of non-small cell lung cancer: future prospects.","authors":"Xinran Zhang, Jia Liu, Wen Zhou, Junfei Lu, Liqin Wu, Yan Li, Yiyuan Wang, Zhichao Wang, Jun Cai","doi":"10.21037/tlcr-2025-187","DOIUrl":"10.21037/tlcr-2025-187","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC), a major form of pulmonary malignancy and a leading global cause of cancer-related mortality, highlights the urgent need for advanced precision treatment approaches. This article comprehensively reviews the significant progress and future directions of deep learning techniques in revolutionizing the precise diagnosis and therapeutic management of NSCLC. It demonstrates how deep learning methods have the potential to surpass traditional tumor treatment paradigms, significantly enhancing diagnostic accuracy, personalizing treatment selection, and predicting patient outcomes with greater precision. The article traces the evolution of deep learning models in this field, from basic analyses relying on single data modalities, such as imaging or genomics alone, to more sophisticated architectures capable of multimodal data fusion. It emphasizes the crucial role of integrating radiological, pathological, genomic, and clinical data in uncovering deeper biological insights. Furthermore, it outlines the typical workflow involved in developing and deploying deep learning applications for NSCLC and lists some currently used models, including convolutional neural networks for image analysis and complex architectures for multi-omics data integration. These models show considerable potential for improving diagnostic accuracy and optimizing therapeutic interventions. However, translating these computational tools into routine clinical practice faces several challenges. The review candidly addresses key issues, including the need for large-scale, high-quality, and standardized datasets; the \"black box\" nature of complex models, which requires improved interpretability to gain clinicians' trust and provide actionable insights; and profound ethical considerations regarding data privacy, algorithmic bias, and equitable access. Despite these obstacles, deep learning has emerged as a powerful instrument in the oncological arsenal, significantly enhancing the precision and efficiency of NSCLC care. Finally, the article offers a dialectical perspective on the future of deep learning in NSCLC, exploring emerging trends and providing recommendations to overcome current limitations, with the goal of maximizing its potential to improve patient survival and quality of life.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":"14 8","pages":"3196-3215"},"PeriodicalIF":3.5,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanisms and clinical insights in transformed small cell lung cancer: a narrative review.","authors":"Xianzi Dai, Yue Hao, Jiaojiao Hong, Jiangxia Yuan, Chengyu Chen, Zhengxing Huo, Jia Zhu, Qian Wang","doi":"10.21037/tlcr-2025-165","DOIUrl":"10.21037/tlcr-2025-165","url":null,"abstract":"<p><strong>Background and objective: </strong>In recent years, the application of targeted therapies has significantly improved survival rates in patients with driver gene-positive non-small cell lung cancer (NSCLC). However, one mechanism underlying acquired resistance is the histological transformation from NSCLC to small cell lung cancer (SCLC). NSCLC-to-SCLC transformation is thought to occur due to selective pressure from targeted therapies, yet this shift has also been observed in patients receiving non-targeted treatments, raising questions about its underlying mechanisms. This review aims to identify key molecular biomarkers predictive of this transformation to optimize clinical management strategies for transformed SCLC (T-SCLC).</p><p><strong>Methods: </strong>We systematically searched PubMed, EMBASE, the Cochrane Library, and major international conference proceedings for all English-language articles published up to December 31, 2024. This review synthesizes current evidence on the mechanisms of T-SCLC transformation, its genomic and transcriptomic alterations, and related therapeutic approaches.</p><p><strong>Key content and findings: </strong>T-SCLC is hypothesized to involve tumor heterogeneity and lineage plasticity. Key molecular players include dysregulation of the phosphatidylinositol 3-kinase (<i>PI3K</i>)/protein kinase B (<i>AKT</i>)/mammalian target of rapamycin (<i>mTOR</i>) pathway, <i>NOTCH-ASCL1</i> signaling, mothers against decapentaplegic homolog 4 (<i>SMAD4</i>), SRY-related HMG-box 2 (<i>SOX2</i>), and epigenetic abnormalities such as histone modifications (methylation, acetylation, ubiquitination). Tumor protein p53 (<i>TP53</i>) and retinoblastoma 1 (<i>RB1</i>) inactivation may serve as predictive biomarkers, though causal relationships require validation. Post-transformation, chemotherapy remains the first-line treatment, while combining chemotherapy with epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) improves progression-free survival.</p><p><strong>Conclusions: </strong>Current T-SCLC research is limited by retrospective designs and small sample sizes, leaving transformation mechanisms incompletely understood. This phenotypic shift highlights lung cancer plasticity as a novel resistance mechanism rooted in lineage plasticity and tumor heterogeneity. Personalized therapies guided by molecular profiling may represent a future direction for improving outcomes.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":"14 8","pages":"3233-3248"},"PeriodicalIF":3.5,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432677/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term survival with adaptive dual-targeted therapy in an epidermal growth factor receptor (<i>EGFR</i>)-mutant non-small cell lung cancer patient with mesenchymal-epithelial transition (<i>MET</i>) amplification guided by minimal residual disease (MRD) assessments: a case report and literature review.","authors":"Xinyin Liu, Shidai Jin, Jun Li, Jiali Xu, Lei Song, Wen Gao, Jun Wang, Zhihong Zhang, Renhua Guo","doi":"10.21037/tlcr-2025-850","DOIUrl":"10.21037/tlcr-2025-850","url":null,"abstract":"<p><strong>Background: </strong>Epidermal growth factor receptor-tyrosine kinase inhibitors (<i>EGFR</i>-TKIs) have achieved great success in the treatment of non-small cell lung cancer (NSCLC) with activating <i>EGFR</i> mutations. However, acquired resistance is a major obstacle to long-term disease remission in clinical practice. Mesenchymal-epithelial transition (<i>MET</i>) gene amplification has been identified as a key resistance mechanism to first- and second-generation <i>EGFR</i>-TKIs.</p><p><strong>Case description: </strong>We report the case of a 65-year-old female patient with advanced lung adenocarcinoma (LUAD) who developed bone and adrenal gland metastases following treatment with gefitinib. Next-generation sequencing (NGS) of a biopsy specimen revealed the co-occurrence of <i>MET</i> amplification and <i>EGFR</i> exon 19 deletion mutation. The combined treatment of savolitinib and gefitinib effectively controlled the disease, resulting in a favorable long-term clinical outcome. With continued follow-up through April 2025, the patient has maintained progression-free survival (PFS) over 8 years. However, monitoring revealed the patient had grade 4 peripheral edema, and negative circulating tumor DNA (ctDNA), which necessitated a savolitinib dose reduction. Subsequent minimal residual disease (MRD) assessments and radiological scans revealed a remarkable therapeutic response with sustained efficacy.</p><p><strong>Conclusions: </strong>We report the first case of a LUAD patient with <i>MET</i> amplification and <i>EGFR</i> exon 19 deletion mutation who achieved a durable response with targeted therapy. ctDNA monitoring enabled precise dose modulation that balanced therapeutic efficacy with toxicity management. This case establishes a paradigm for chronic cancer management, demonstrating that integrating molecular diagnostics with dynamic treatment optimization can effectively convert aggressive malignancies into manageable chronic conditions while preserving the quality of life of patients.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":"14 8","pages":"3270-3279"},"PeriodicalIF":3.5,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding the immune landscape: <i>KRAS</i> and <i>STK11</i> genes mutations shape CD8⁺ T cell response in resectable non-small-cell lung cancer after neoadjuvant therapy.","authors":"Kamila Wojas-Krawczyk, Magdalena Knetki-Wróblewska, Maciej Krzakowski","doi":"10.21037/tlcr-2025-442","DOIUrl":"10.21037/tlcr-2025-442","url":null,"abstract":"","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":"14 8","pages":"2918-2921"},"PeriodicalIF":3.5,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432620/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}