Thoracic Cancer最新文献

{"title":"Correlation Between Distance From Lesions to Pleura and Complications in CT-Guided Lung Biopsy: A Cross-Sectional Study in Vietnam.","authors":"Thanh Dinh Le, Thuan Nguyen Huynh, Thanh Chi Nguyen, Hau Thi Tran, Nguyen Vo Cong Do, Khang Quang Le, Son Thai Tran, Thanh Toan Vo","doi":"10.1111/1759-7714.70286","DOIUrl":"https://doi.org/10.1111/1759-7714.70286","url":null,"abstract":"<p><strong>Introduction: </strong>CT-guided transthoracic needle biopsy (CT-TTNB) is an essential diagnostic procedure but is associated with complications such as pneumothorax and pulmonary hemorrhage. The distance from the lesion to the pleura (traversed parenchymal distance) is widely recognized as a major risk factor. This study aims to evaluate the correlation between the traversed lung parenchymal distance and post-CT-TTNB complications, and to identify independent predictors for these complications.</p><p><strong>Methods: </strong>A retrospective cross-sectional study was conducted on 226 patients who underwent CT-TTNB. Data on demographics, lesion characteristics, and procedure-related factors (traversed parenchymal distance, number of biopsy samples) were collected. Multivariable logistic regression analysis was used to identify independent predictors for pneumothorax and pulmonary hemorrhage.</p><p><strong>Results: </strong>The overall complication rate was 47.35%, with pneumothorax at 29.2% and pulmonary hemorrhage at 32.74%. Multivariable analysis showed that statistically significant independent predictors for pneumothorax were male gender (adjusted odds ratio [aOR] = 3.78; 95% confidence interval [CI]: 1.81-7.89; p < 0.001) and the number of biopsy samples (aOR = 0.65; 95% CI: 0.45-0.94; p = 0.022). The traversed lung parenchymal distance was not a statistically significant independent predictor for either pneumothorax (p = 0.251) or pulmonary hemorrhage.</p><p><strong>Conclusions: </strong>In this study population, male gender and the number of biopsy samples were significantly associated with the risk of pneumothorax. The traversed lung parenchymal distance did not emerge as an independent predictor in the multivariable model. These findings challenge the traditional view and emphasize the need for a multifactorial risk assessment model rather than relying on a single parameter.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 8","pages":"e70286"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13112177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147782335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BMAL1 Drives Cisplatin Resistance in Non-Small Cell Lung Cancer Via Lactate-MRP1 Signaling Pathway.","authors":"Zixin Shi, Ziniu Qin, Chuantao Chen, Xiaolin Yang, Yunhan Hu, Xiaohui Meng, Yuxiang Cao, Xiang Tao, Zhijian Zhang, Tiancheng Xie, Huijun Wei, Zhihao Wu","doi":"10.1111/1759-7714.70279","DOIUrl":"https://doi.org/10.1111/1759-7714.70279","url":null,"abstract":"<p><p>Lung cancer, the leading cause of cancer-related mortality, faces significant therapeutic challenges due to chemoresistance. While metabolic reprogramming and circadian disruptions are implicated in tumor progression, their interplay in driving resistance remains unclear. This study identifies BMAL1, a core circadian regulator, as a key driver and potential initiator of cisplatin resistance in non-small cell lung cancer (NSCLC) through metabolic and oxidative stress pathways. We demonstrate that BMAL1 upregulates multidrug resistance protein MRP1 via HIF-1α-driven glycolysis, amplifying lactate production. Lactate activates the TAZ/c-Jun/Snail complex to increase MRP1 expression, establishing a feedforward loop that sustains chemoresistance. Furthermore, cisplatin and etoposide induce BMAL1 expression through AKT signaling in response to oxidative stress, creating a self-reinforcing resistance mechanism. Critically, targeting AKT or MRP1 reverses BMAL1-mediated resistance. These findings reveal BMAL1 as a metabolic orchestrator linking circadian dysfunction to chemoresistance and propose actionable strategies-such as AKT inhibition or chronotherapy-to circumvent therapeutic failure. This work underscores the necessity of targeting circadian-metabolic crosstalk to improve outcomes in NSCLC.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 8","pages":"e70279"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13108231/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147782298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Delayed Tumor Shrinkage Beyond Progressive Disease in Small-Cell Lung Cancer Receiving Immunochemotherapy: A Case Report.","authors":"Takahisa Kawamura, Kiyohide Komuta, Shun Futamura, Akito Miyazaki, Tsunehiro Tanaka, Kei Kunimasa, Takako Inoue, Motohiro Tamiya, Kazumi Nishino","doi":"10.1111/1759-7714.70276","DOIUrl":"10.1111/1759-7714.70276","url":null,"abstract":"<p><p>Small-cell lung cancer (SCLC) is an aggressive malignancy with a poor prognosis. Although SCLC initially responds rapidly and drastically to platinum-based chemotherapy, it quickly develops resistance and recurs shortly thereafter. Recently, immunochemotherapy has achieved better survival outcomes than traditional chemotherapy alone, as demonstrated in pivotal trials such as IMpower133 and CASPIAN. However, delayed or atypical tumor responses under immunotherapy remain poorly understood, especially in SCLC. Herein, we present a case of extensive-disease SCLC that showed a delayed tumor shrinkage following transient progression and prolonged elevation of tumor volume and ProGRP levels during immunochemotherapy. This case highlights the potential for delayed response beyond progressive disease even in SCLC, emphasizing the importance of careful evaluation before changing treatment in selected patients receiving immune checkpoint inhibitors.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 7","pages":"e70276"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147575509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Radiological, Molecular, and Pathological Factors Unite: A Model for Predicting Recurrence-Free Survival in Pathological Stage I Lung Adenocarcinoma.","authors":"Hui Zeng, Yufei Huang, Zehao Song, Zhenlong Yuan, Jingyu Ren, Jiaxi Xu, Fangzhou Ren, Wenbin Li, Jianming Ying, Changyuan Guo, Wei Tang, Ming Liang, Yuanjie Zhang, Qin Xu, Qi Xue, Fengwei Tan","doi":"10.1111/1759-7714.70291","DOIUrl":"https://doi.org/10.1111/1759-7714.70291","url":null,"abstract":"<p><strong>Background: </strong>The tumor and node metastasis (TNM) staging and pathological grading systems are currently insufficient for accurately predicting recurrence-free survival (RFS) in patients with pathological stage (p-stage) I lung adenocarcinoma (LUAD). Therefore, there is an urgent need for a more economical and applicable clinical prediction model to assess the risk of recurrence and guide clinical postoperative care.</p><p><strong>Methods: </strong>This retrospective study included 544 patients with p-stage I LUAD who were randomly allocated to development (272 patients) and validation (272 patients) cohorts. Cox regression and backward model selection were used to develop the prediction model. The predictive performance of the model was then compared with that of the current TNM staging system and two major pathological grading systems. The primary endpoint was RFS.</p><p><strong>Results: </strong>A total of 79 out of 544 patients with p-stage I LUAD experienced recurrence after surgery. Four risk factors were incorporated into a weighted risk index-high-grade patterns ratio, epidermal growth factor receptor mutation status, spread through air spaces status and consolidation tumor ratio-to establish the \"CEHS\" RFS prediction model. This model demonstrated superior predictive accuracy compared with existing staging and grading systems. High-risk patients had significantly shorter RFS than low-risk patients did. An online algorithm based on the CEHS model was also developed.</p><p><strong>Conclusion: </strong>We established and validated a novel model that integrates radiological, molecular and pathological features to predict RFS in patients with p-stage I LUAD. This new model exhibited excellent discriminatory power for classifying early-stage LUAD patients at different risks of recurrence.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 8","pages":"e70291"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13104728/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147782445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quality and Reliability of Lung Cancer Treatment Short Videos on Chinese Social Media: A Cross-Sectional Analysis for Cancer Education Improvement (January 1, 2020-October 30, 2025).","authors":"Zengrui Wang, Zhuang Luo, Le Wang, Jiefu Tang, Zhi Zhang, Xinli Fan","doi":"10.1111/1759-7714.70273","DOIUrl":"10.1111/1759-7714.70273","url":null,"abstract":"<p><strong>Background: </strong>Short-form videos have become the common source of cancer information for Chinese patients and caregivers. We evaluated the content, quality, and reliability of lung cancer treatment videos on TikTok, Bilibili, and Kwai and generated evidence-based recommendations for cancer health education.</p><p><strong>Methods: </strong>We conducted a cross-sectional study of lung cancer treatment short videos on TikTok, Bilibili, and Kwai. The top 200 most-liked videos per platform posted between January 1, 2020 and October 30, 2025, were retrieved on November 1, 2025. After screening, 300 videos (100 per platform) were analyzed. Two oncologists rated quality using GQS (1-5) and DISCERN (1-5); creator identity was classified. Comment sentiment (SnowNLP) and engagement metrics were analyzed.</p><p><strong>Results: </strong>TikTok had the highest engagement and quality (GQS 3.0, DISCERN 3.0) versus Bilibili/Kwai (2.0) (p < 0.001). Professionals achieved the highest quality (GQS 3.0) versus institutions (1.0) (p < 0.001). However, absolute quality was low across all platforms: only 6% of videos met high-quality criteria (GQS ≥ 4), and 5% met DISCERN ≥ 4. Engagement showed a weak negative correlation with quality (ρ = -0.13 to -0.21).</p><p><strong>Conclusions: </strong>Overall quality is low; professional content is more reliable but less viral. Embedding quality indicators in algorithms and promoting certified creators could improve patient cancer education.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 8","pages":"e70273"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13084701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147692300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study on the Modes of Cell Death in Lung Cancer Epithelial Cells During Acute EBV Infection Using a Co-Culture Model.","authors":"Xinyue Zhang, Chenpeng Li, Shuilian Zhang, Wenqing Yan, Yu Chen, Danxia Lu, Zhi Xie, Pai Zhang, Xue Pan","doi":"10.1111/1759-7714.70281","DOIUrl":"10.1111/1759-7714.70281","url":null,"abstract":"<p><strong>Objective: </strong>Pulmonary lymphoepithelial carcinoma is an EBV-associated malignancy; however, the pathogenesis of virus-associated cancers remains incompletely elucidated. In particular, the early pathological changes and fate decisions of pulmonary epithelial cells following acute EBV infection have yet to be fully elucidated. This study aimed to investigate cell death modes of lung epithelial cells upon acute EBV infection.</p><p><strong>Methods: </strong>An acute infection model was established by co-culturing EBV-positive Akata cells with lung cancer cells. Following infection, we evaluated morphological alterations and modes of cell death using immunofluorescence staining and confocal laser scanning microscopy.</p><p><strong>Results: </strong>The co-culture system successfully established a 72-h acute EBV infection in lung cancer cells, with ~10.3% of epithelial cells exhibiting EBV-associated GFP fluorescence. Under these conditions, the majority of epithelial cells underwent cell death. More than half of the epithelial cells died by day 5 of co-culture, and mortality progressively increased. At 72 h post-infection, immunofluorescence analysis of pMLKL, cGSDMD, and cCASP3 revealed a significant upregulation of pMLKL protein expression (p < 0.001), whereas no significant differences were observed in cGSDMD (p > 0.05) or cCASP3 (p > 0.05) levels. ~15.1% of the remaining epithelial cells following B-cell removal exhibited \"cell-in-cell\" structures. The internalized B cells underwent various forms of death, including apoptosis, pyroptosis, and necroptosis.</p><p><strong>Conclusion: </strong>Acute EBV infection drives lung cancer epithelial cell death through pMLKL-mediated necroptosis, without significant involvement of apoptosis or pyroptosis. Internalized B cells within \"cell-in-cell\" structures exhibit multiple death modalities. These findings provided novel insights into cellular fate decisions in EBV-infected epithelium prior to latency.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 7","pages":"e70281"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13076187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147677016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined Robotic Morgagni-Larrey Hernia Repair and Lobectomy for Lung Cancer.","authors":"Alfonso Fiorelli, Salvatore Tolone, Francesca Capasso, Vincenzo Di Filippo, Alessia Guarino, Francesco Coppolino, Ludovico Docimo","doi":"10.1111/1759-7714.70260","DOIUrl":"https://doi.org/10.1111/1759-7714.70260","url":null,"abstract":"<p><p>Herein, we reported a combined robotic surgery approach used to manage pre-existing ipsilateral Morgagni-Larrey hernia and early-stage lung cancer concurrently. The reduction of the colon into the abdominal cavity facilitated robotic lobectomy and prevented life-threatening postoperative complications from the presence of a hernia after lobectomy.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 8","pages":"e70260"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13105831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147782260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Danshensu Ethyl Ester Induces Ferroptosis Through Targeted Inhibition of SLC7A11 Transport Function in NSCLC.","authors":"Rui Yan, Sen Xu, Meng Yan, Dongyang Wu, Jingwen Zhang, Chunsheng Zhang, Jiale Liu, You-Jie Li, Jiankai Feng, Gui-Wu Qu, Shu-Yang Xie","doi":"10.1111/1759-7714.70283","DOIUrl":"https://doi.org/10.1111/1759-7714.70283","url":null,"abstract":"<p><strong>Background: </strong>Ferroptosis is a novel research avenue for cancer therapy. The roles of Danshensu derivatives remain unclear. This study investigated the effect of Danshensu Ethyl Ester (DEE) on ferroptosis in non-small cell lung cancer (NSCLC) cells.</p><p><strong>Methods: </strong>NSCLC cells were treated with DEE to assess ferroptosis markers, including reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), and mitochondrial membrane potential (MMP), along with related protein expression. Molecular docking and dynamics simulations predicted the DEE-SLC7A11 interaction. Intracellular cysteine levels were quantified by ELISA. The functional involvement of SLC7A11 was further verified through its knockdown and overexpression. The in vivo antitumor activity of DEE was assessed using a nude mouse xenograft model.</p><p><strong>Results: </strong>DEE treatment dose-dependently promoted cell death in A549 and H1299 cells, accompanied by increased levels of ROS and MDA, reduced GSH and MMP, and downregulated expression of SLC7A11 and GPX4. These effects were reversed by ferroptosis inhibitor Ferrostatin-1 (Fer-1), confirming ferroptosis involvement. Mechanistically, DEE directly inhibited the transport function of SLC7A11 in a p53-independent manner and also decreased p53 protein levels in wild-type A549 cells. Consistently, DEE reduced intracellular cysteine content. Genetic silencing of SLC7A11 enhanced DEE-induced ferroptosis, whereas its overexpression attenuated the effect. In vivo, DEE significantly suppressed tumor growth in a xenograft model, exhibiting efficacy comparable to that of paclitaxel.</p><p><strong>Conclusions: </strong>DEE inhibits NSCLC progression by inducing ferroptosis through the targeted inhibition of SLC7A11 transport function via a p53-independent pathway, highlighting its potential as a novel therapeutic agent for NSCLC.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 8","pages":"e70283"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13109045/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147782327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) Mutation Testing Trends, Prevalence, and Outcomes in Metastatic, Non-Squamous Non-Small Cell Lung Cancer (Non-SQ NSCLC) Patients in Queensland, Australia From 2014-2023.","authors":"Navin Niranjan, Tracey Guan, Nitin Niranjan, Atefeh Taherian Fard, Danny R Youlden, Robert Mason, Bryan A Chan, Jasotha Sanmugarajah","doi":"10.1111/1759-7714.70274","DOIUrl":"10.1111/1759-7714.70274","url":null,"abstract":"<p><strong>Background: </strong>Kirsten rat sarcoma viral oncogene homolog (KRAS) is the most commonly mutated oncogene in solid tumors, detected in up to 30% of lung adenocarcinomas. This study aimed to address gaps in the literature by analyzing KRAS mutations (KRASM) in a large Australian population.</p><p><strong>Methods: </strong>A total of 3982 patients with metastatic nonsquamous nonsmall cell lung cancer diagnosed via public hospitals were retrospectively analyzed from January 1, 2014 to December 31, 2023. Records were reviewed for evidence of KRASM testing, KRAS results, biopsy type, and programmed death-ligand 1 (PD-L1) status. KRASM testing rates were also compared to that of other commonly tested oncogenic mutations.</p><p><strong>Results: </strong>KRASM testing was performed in 52.9% of eligible patients, improving from 1.9% in 2014 to 86.3% in 2023. KRASM was identified in 830 patients (39.4% of KRASM tested patients, 20.8% overall). The most common KRASM seen was 12th codon substitution of KRAS glycine to cysteine (G12C) followed by substitutions of glycine to valine (G12V) and glycine to aspartate (G12D). Patients harboring KRASM were significantly more likely to have smoked, be female, and have higher PD-L1 expression than their KRAS wild type (wt) counterparts. All-cause survival was higher at the 1-year (43.9% vs. 35.3%) and 5-year (12.4% vs. 8.9%) marks in KRAS wt patients compared to KRAS mt.</p><p><strong>Conclusion: </strong>This study is the largest longitudinal analysis of KRASM testing conducted in Australia, with significant improvement in testing rates seen over the time period. Rates of KRASM and characteristics of Australian KRAS mt patients correspond with published literature.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 7","pages":"e70274"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147575530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pleural-Based GLI1-Altered Mesenchymal Tumor With ACTB-GLI1 Fusion: A Rare Pulmonary Entity Mimicking Synovial Sarcoma.","authors":"Marco Lizwan, Li Xiao, Chun Yuen Chow, Hiu Yeung Lau, Boon-Hean Ong","doi":"10.1111/1759-7714.70271","DOIUrl":"10.1111/1759-7714.70271","url":null,"abstract":"<p><p>GLI1-altered mesenchymal tumors are exceptionally rare mesenchymal tumors, with recent molecular studies implicating GLI1 gene fusion or amplification. We report a 39-year-old nonsmoking woman who presented with an incidentally detected right pleural-based mass. Cross-sectional imaging identified a paraspinal pleural lesion at the T5-T6 level without intraspinal extension. Video-assisted thoracoscopic resection revealed a biphasic tumor and next-generation sequencing confirmed an ACTB-GLI1 fusion. The diagnosis of GLI1-altered mesenchymal tumor was established. After multidisciplinary discussion, the patient opted for radiologic surveillance instead of adjuvant therapy. She remains disease-free at 1-year follow-up. This case expands the anatomic spectrum of GLI1-altered tumors and underscores the value of molecular testing in distinguishing them from other pleural neoplasms.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 7","pages":"e70271"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13070735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147521729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}