Thoracic Cancer最新文献

{"title":"RETRACTION: Delanzomib, a Novel Proteasome Inhibitor, Sensitizes Breast Cancer Cells to Doxorubicin-Induced Apoptosis.","authors":"","doi":"10.1111/1759-7714.70346","DOIUrl":"10.1111/1759-7714.70346","url":null,"abstract":"<p><strong>Retraction: </strong>M. Wang, L. Liang, J. Lu, Y. Yu, Y. Zhao, Z. Shi, H. Li, X. Xu, Y. Yan, Y. Niu, Z. Liu, L. Shen and H. Zhang, \"Delanzomib, a Novel Proteasome Inhibitor, Sensitizes Breast Cancer Cells to Doxorubicin-Induced Apoptosis,\" Thoracic Cancer 10, no. 4 (2019): 918-929, https://doi.org/10.1111/1759-7714.13030. The above article, published online on 18 March 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Tateaki Naito; China Lung Oncology Group; and John Wiley & Sons Australia, Ltd. The retraction has been agreed upon following concerns raised by a third party. An investigation identified a duplication between the MDA-MB-231 α-tubulin bands and the MDA-MB-361 bands in Figure 2a. An additional duplication was identified between the MCF7 p53 bands and the MDA-MB-361 PUMA bands in Figure 6. Further duplications were identified between some MCF7 JNK bands in Figure 6 and bands published earlier in another article. The MDA-MB-231 JNK bands were also previously published in that same article by the same author group. The authors acknowledged the duplications and explained that the errors occurred inadvertently during figure preparation; they also provided some supporting data. However, due to the extent and nature of the duplications, the editors have lost confidence in the results and conclusions presented in this article.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 13","pages":"e70346"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13351320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148424594","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":"The Impact of Immunotherapy on Hair Repigmentation in Patients With Thoracic Tumors: A Clinical Observation Based on Trichoscopy.","authors":"Sitong Jiang, Bo Li, Fan Yang, Haozhen Lv, Xin Nie, Hui Wang, Jianmin Chang, Lin Li","doi":"10.1111/1759-7714.70338","DOIUrl":"10.1111/1759-7714.70338","url":null,"abstract":"<p><strong>Objective: </strong>Whether hair repigmentation during cancer therapy is driven by immune checkpoint inhibitors (ICIs) or chemotherapy remains unclear. This study aimed to quantitatively identify the primary driver using a controlled design.</p><p><strong>Methods: </strong>In this prospective study, 29 patients with thoracic malignancies were divided into an immunotherapy group (n = 18) and a chemotherapy group (n = 11). Standardized dermoscopic images were captured before and after treatment. Hair pigmentation was quantified via grayscale analysis.</p><p><strong>Results: </strong>Grayscale values decreased significantly posttreatment in the immunotherapy group (p = 0.0008) but not in the chemotherapy group (p = 0.1427). The magnitude of change (ΔGrayscale) was significantly greater with immunotherapy than with chemotherapy alone (23.5 ± 24.67 vs. 4.32 ± 9.01; p = 0.0065), representing a large effect size (Cohen's d = 0.90).</p><p><strong>Conclusion: </strong>This controlled study provides quantitative evidence suggesting that immunotherapy, rather than chemotherapy, is closely associated with hair repigmentation. It establishes an objective methodological framework for future investigation of this phenomenon.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 13","pages":"e70338"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13322987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148370036","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":"Overall Survival With Pyrotinib Plus Capecitabine Versus Lapatinib Plus Capecitabine in HER2-Positive Metastatic Breast Cancer: A Single-Center Pooled Analysis.","authors":"Jialin Lin, Qiao Li, Pin Zhang, Ying Fan, Ruigang Cai, Yang Luo, Bo Lan, Shanshan Chen, Jiani Wang, Hongnan Mo, Fei Ma, Jiayu Wang, Binghe Xu","doi":"10.1111/1759-7714.70362","DOIUrl":"10.1111/1759-7714.70362","url":null,"abstract":"<p><strong>Background: </strong>Phase II and III trials have demonstrated progression-free survival (PFS) benefits of pyrotinib plus capecitabine over lapatinib plus capecitabine in HER2-positive metastatic breast cancer (MBC). However, long-term overall survival (OS) data from a single-center cohort remain limited. This pooled analysis compared OS between the two regimens and explored outcomes across prespecified subgroups.</p><p><strong>Methods: </strong>We included patients with HER2-positive MBC from our center enrolled in a Phase Ic study, a Phase II study, or the Phase III PHOEBE trial. The primary endpoint was OS. OS was analyzed using Kaplan-Meier estimates, log-rank tests, and a multivariable Cox model adjusted for ECOG performance status, pathological grade, prior anti-HER2 therapy, trastuzumab exposure duration, trastuzumab resistance, and prior chemotherapy lines. The proportional hazards assumption was assessed using Schoenfeld residuals. Exploratory subgroup analyses used prespecified categories.</p><p><strong>Results: </strong>At data cutoff, 82 patients were included; 53 received pyrotinib plus capecitabine and 29 received lapatinib plus capecitabine. Baseline characteristics were comparable between groups. Median OS was 74.61 months (95% CI 41.10-not reached) with pyrotinib plus capecitabine and 30.98 months (26.12-50.76) with lapatinib plus capecitabine (log-rank p = 0.0053). Cox models suggested a reduced risk of death with pyrotinib plus capecitabine. Subgroup analyses were exploratory and should be interpreted cautiously because several subgroup estimates were imprecise.</p><p><strong>Conclusion: </strong>In this single-center pooled analysis, pyrotinib plus capecitabine was associated with significantly longer OS than lapatinib plus capecitabine in patients with HER2-positive MBC. These exploratory results are consistent with prior Phase II/III trials and provide evidence supporting the OS benefit of pyrotinib.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 15","pages":"e70362"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13448148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685929","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":"Comparing Complications Between Shape-Sensing Robotic-Assisted Bronchoscopy and Trans-Thoracic Needle Pulmonary Biopsy Approaches: Insights From a Large Nationally Representative Administrative Database.","authors":"David Abia-Trujilo, Sebastian Fernandez-Bussy, Erik E Folch, Bryan C Husta, Gediwon Milky, Sam E Wing, Adam Gaertner, Scott S Oh","doi":"10.1111/1759-7714.70324","DOIUrl":"10.1111/1759-7714.70324","url":null,"abstract":"<p><strong>Background: </strong>Shape-sensing robotic-assisted bronchoscopy (ssRAB) is a navigation platform for biopsy of indeterminate pulmonary lesions. Large-scale, real-world evidence confirming the safety profile of ssRAB compared to transthoracic needle biopsy (TTNB) is needed.</p><p><strong>Study design and methods: </strong>A retrospective cohort study was performed using the PINC AI healthcare database among patients who underwent ssRAB or TTNB lung lesion biopsy at participating hospitals between April 2019 and March 2023. Outcomes were rates of pneumothorax and pneumothorax requiring chest-tube intervention within 3 days, and rates of in-hospital bleeding or all-cause death. Quasi-binomial logistic regression analysis was performed after one-to-five propensity score matching (PSM) accounting for patient- and hospital-related characteristics.</p><p><strong>Results: </strong>A total of 119 424 patients (5121 ssRAB, 114 303 TTNB) were identified with 4554 ssRAB and 14 319 TTNB patients after PSM. Relative to ssRAB, TTNB had significantly higher risk of pneumothorax (18.4% vs. 2.6%, OR = 7.10, p < 0.001) and pneumothorax requiring chest-tube (10.8% vs. 1.4%, OR = 7.62, p < 0.001). TTNB was associated with a higher risk for bleeding (1.5% vs. 0.6%, OR = 2.20, p < 0.001) and all-cause death (0.48% vs. 0.15%, OR = 2.47, p = 0.023); however, rates for both outcomes were relatively low.</p><p><strong>Interpretation: </strong>In this large-scale, real-world database analysis with diverse patient populations, physician experience, and health care settings, ssRAB demonstrated a better safety profile compared to TTNB. Superior safety combined with a potentially comparable performance profile and known advantages of bronchoscopy, including concurrent staging, support ssRAB as an optimal choice for non-surgical biopsies for suspicious pulmonary lesions.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 13","pages":"e70324"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13349657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148424582","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":"Histone Variant H2A.Z2 Hyper-Transcription Induced by E2F1 Accelerates Lung Adenocarcinoma Progression via the JAK-STAT Signaling Pathway.","authors":"Wenxing Jin, Yongmeng Li, Kai Jin, Shuai Wang, Rongyang Li, Dingxin Wang, Haiming Li, Hui Tian","doi":"10.1111/1759-7714.70351","DOIUrl":"10.1111/1759-7714.70351","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD) is among the most common cancers and a leading cause of cancer-related deaths. The histone variant H2A.Z has two isoforms (H2A.Z1 and H2A.Z2) encoded by distinct paralogs. Increasing numbers of evidence have demonstrated that H2A.Z1 and H2A.Z2 play a critical role in the pathogenesis of various cancers. Nevertheless, the precise biological functions and underlying mechanisms of H2A.Z in LUAD remain unclear.</p><p><strong>Methods: </strong>The levels of H2A.Z expression in LUAD were evaluated using immunohistochemistry (IHC) and western blot assays. To investigate the biological role of H2A.Z2 in LUAD cells, both in vitro and in vivo experiments were conducted. To evaluate gene expression alterations and predict downstream pathways, transcriptome sequencing was performed. To validate that E2F transcription factor 1 (E2F1) regulates H2A.Z2 expression, dual luciferase reporter assays and chromatin immunoprecipitation (ChIP) assays were used.</p><p><strong>Results: </strong>Herein, we demonstrated high expression pattern of H2A.Z in LUAD tissues and its correlation with adverse clinical outcomes. Functionally, we indicated that H2A.Z2 exerts an oncogenic function in driving LUAD cell proliferation and metastasis. Mechanistically, analysis based on transcriptome sequencing suggested the influence of H2A.Z2 on the JAK-STAT pathway. Rescue experiments revealed that H2A.Z2 promotes LUAD progression by modulating STAT5B. Furthermore, we identified E2F1 as an activator that binds to the H2A.Z2 promoter to drive its transcription, thereby providing a novel mechanism of H2A.Z2 dysregulation.</p><p><strong>Conclusions: </strong>In conclusion, our findings revealed a novel E2F1/H2A.Z2/STAT5B axis accelerating LUAD malignance, suggesting its potential as a promising target for diagnostic and therapeutic interventions in LUAD.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 13","pages":"e70351"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13358377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148430988","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":"PACIFIC-5 Trial: Refining Patient Selection for Consolidation Durvalumab in Unresectable Stage III NSCLC.","authors":"Shiqiong Zhou, Qinghua Ke","doi":"10.1111/1759-7714.70305","DOIUrl":"10.1111/1759-7714.70305","url":null,"abstract":"","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 14","pages":"e70305"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13402098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148593395","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":"Importance of Multimodal Testing for Novel ALK Fusions: A Case of MTHFD1L-ALK Positive Lung Squamous Cell Carcinoma With Negative IHC.","authors":"Huiwen Yang, Shuqiao Zheng, Jiaohui Pang, Jinming Yu, Linlin Wang","doi":"10.1111/1759-7714.70348","DOIUrl":"10.1111/1759-7714.70348","url":null,"abstract":"<p><p>Anaplastic lymphoma kinase (ALK) rearrangements are rare in lung squamous cell carcinoma (LSCC), with the clinical efficacy of ALK tyrosine kinase inhibitors (TKIs) in patients harboring uncommon ALK fusions remaining poorly characterized. We report here the first identification of a novel MTHFD1L-ALK fusion in a 63-year-old male with a heavy smoking history diagnosed with stage IIIC LSCC. The patient initially received induction therapy with the ALK TKI iruplinalkib, achieving a best response of stable disease (SD). Although subsequent chemoradiotherapy yielded a partial response (PR), disease progression occurred after four cycles of maintenance iruplinalkib, with a progression-free survival (PFS) of 8.28 months. Subsequent lorlatinib provided limited benefit, with disease progression at 5.3 months following treatment self-discontinuation. Retrospective immunohistochemical staining of ALK (D5F3) was negative despite the positive genomic finding. This case demonstrates limited clinical benefit from ALK inhibitors in LSCC with this novel fusion, expands the known mutational spectrum in non-small cell lung cancer (NSCLC), and underscores the critical importance of confirming novel fusions at the protein expression level through multimodal testing.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 14","pages":"e70348"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13382346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148521104","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":"Correction to \"Effects of Autophagy Inhibition by SAR405, a Selective VPS34 Inhibitor, on Pleural Mesothelioma Cells\".","authors":"","doi":"10.1111/1759-7714.70336","DOIUrl":"10.1111/1759-7714.70336","url":null,"abstract":"","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 13","pages":"e70336"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13335087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148391750","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":"Perioperative Aspirin Continuation in Patients Requiring Secondary Prevention Undergoing Anatomical Lung Resection: A Propensity Score-Weighted Analysis.","authors":"Junichi Murakami, Sota Yoshimine, Mototsugu Shimokawa, Toshiki Tanaka","doi":"10.1111/1759-7714.70364","DOIUrl":"10.1111/1759-7714.70364","url":null,"abstract":"<p><strong>Background: </strong>Managing perioperative aspirin for secondary prevention during lung resection balances major bleeding against catastrophic thromboembolism. Evidence guiding this scenario, especially for real-world strategies involving switches from other antiplatelets, remains limited for anatomical resections.</p><p><strong>Methods: </strong>This retrospective study (2018-2025) included 625 patients undergoing anatomical lung resection. We compared aspirin continuation (Group 1, n = 94; chronic users or clopidogrel switchers) with no-therapy controls (Group 3, n = 468). Inverse probability of treatment weighting (IPW) was used to balance 16 predefined covariates. The discontinuation group (Group 2, n = 63) served as a descriptive clinical reference. Primary endpoints were major bleeding (reoperation, ≥ 4 units RBC transfusion, or death) and major adverse cardiac and cerebrovascular events (MACCEs) within 30 days.</p><p><strong>Results: </strong>After IPW adjustment, all covariates achieved satisfactory balance (SMD < 0.1). Group 1 showed a potential trend toward increased major bleeding (odds ratio [OR], 5.87; 95% confidence interval [CI], 0.80-42.91; p = 0.08), but no significant difference in MACCE (OR, 1.51; 95% CI, 0.35-6.45; p = 0.58) compared to Group 3. In adjusted linear regression, aspirin was not an independent predictor of intraoperative blood loss (p = 0.25). Notably, Group 2 (discontinuation) exhibited alarmingly high rates of MACCE (7.9%) and 90-day mortality (4.8%). Analyses for rare events were statistically underpowered.</p><p><strong>Conclusion: </strong>Continuing aspirin showed a nonsignificant trend toward increased major bleeding, so its overall safety remains uncertain. However, the high event rates after stopping therapy highlight the significant risk of thromboembolism. Clinical judgment must carefully balance individual thrombotic benefits with potential bleeding risks.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 14","pages":"e70364"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389234/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148550509","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":"Sequential EGFR T790M, MET c.3010C>G-Associated Exon 14 Alteration, and RET-CCDC6 Fusion in EGFR-Mutant NSCLC: A Case Report.","authors":"Yan Zhu, Chan Wang, Nan-Lin Hu, Dan-He Wang, Shi-Kai Wu","doi":"10.1111/1759-7714.70322","DOIUrl":"10.1111/1759-7714.70322","url":null,"abstract":"<p><p>Acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in EGFR-mutant non-small-cell lung cancer (NSCLC) is heterogeneous, and serial re-biopsy may uncover actionable mechanisms. We report a 55-year-old man with stage IVB lung adenocarcinoma harboring EGFR L858R and TP53 R282W. First-line icotinib produced a partial response (PR) with progression-free survival (PFS) of 7 months. Rebiopsy at progression identified acquired EGFR T790M together with a MET c.3010C>G exon 14-related alteration. Almonertinib induced a second PR lasting 7 months. After renewed progression, almonertinib plus savolitinib achieved another PR for 8 months, supporting MET-dependent bypass resistance. Biopsy of a newly progressive iliac metastasis then showed emergence of RET-CCDC6 fusion, whereas T790M and the MET alteration were no longer detected. Because selective RET inhibition was initially unaffordable, the patient received pemetrexed-carboplatin plus continued almonertinib, followed by selpercatinib plus almonertinib. Local radiotherapy to oligoprogressive bone and lung lesions prolonged benefit from systemic therapy. At the latest follow-up in January 2026, the patient remained alive nearly 50 months after diagnosis. This case illustrates clonal evolution under treatment pressure and highlights three practical lessons: repeat molecular testing at each clinically meaningful progression, matched combination targeted therapy for actionable bypass alterations, and local ablative radiotherapy for oligoprogression.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":"17 14","pages":"e70322"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13402097/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148593405","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}