Cancer lettersPub Date : 2026-10-10Epub Date: 2026-08-26DOI: 10.1016/j.canlet.2026.218792
Alexander Rühle, Dai Ping, Ramon Lopez Perez, Maren Strack, Stephan Brons, Qin Yijia, Jürgen Debus, Patrick Wuchter, Anca-Ligia Grosu, Peter E Huber, Nils H Nicolay
{"title":"Corrigendum to \"Human mesenchymal stromal cells maintain their stem cell traits after high-LET particle irradiation - Potential implications for particle radiotherapy and manned space missions\" [Cancer Lett. (2022), 524, 172-181].","authors":"Alexander Rühle, Dai Ping, Ramon Lopez Perez, Maren Strack, Stephan Brons, Qin Yijia, Jürgen Debus, Patrick Wuchter, Anca-Ligia Grosu, Peter E Huber, Nils H Nicolay","doi":"10.1016/j.canlet.2026.218792","DOIUrl":"10.1016/j.canlet.2026.218792","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218792"},"PeriodicalIF":11.8,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer lettersPub Date : 2026-10-10Epub Date: 2026-08-14DOI: 10.1016/j.canlet.2026.218779
Yen-Dun Tony Tzeng, Jui-Hu Hsiao, Chia-Jung Li
{"title":"Targeting ferroptosis dependency as a new senolytic frontier.","authors":"Yen-Dun Tony Tzeng, Jui-Hu Hsiao, Chia-Jung Li","doi":"10.1016/j.canlet.2026.218779","DOIUrl":"10.1016/j.canlet.2026.218779","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218779"},"PeriodicalIF":11.8,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer lettersPub Date : 2026-10-10Epub Date: 2026-08-17DOI: 10.1016/j.canlet.2026.218776
Zifan Zhao, Ze-Yi Zheng, Jonathan T Lei, Matthew J Baik, Yi-Hsuan Wu, Lauren K Somes, Andres F Mosquera Paternina, Omar A Harb, Owen A Chang, Fengshuo Liu, Matthew V Holt, Junkai Wang, Igor Bado, Hai Wang, George Miles, Zbigniew Gugala, Meenakshi Anurag, Ahmed Elkhanany, Yi Li, Valentina Hoyos, Xiang H-F Zhang, Eric C Chang
{"title":"Corrigendum to \"NF1 loss in estrogen receptor-positive breast cancer induces osteoclast formation and immunosuppression to promote bone metastasis\" [Cancer Lett. 655 (2026) 218636].","authors":"Zifan Zhao, Ze-Yi Zheng, Jonathan T Lei, Matthew J Baik, Yi-Hsuan Wu, Lauren K Somes, Andres F Mosquera Paternina, Omar A Harb, Owen A Chang, Fengshuo Liu, Matthew V Holt, Junkai Wang, Igor Bado, Hai Wang, George Miles, Zbigniew Gugala, Meenakshi Anurag, Ahmed Elkhanany, Yi Li, Valentina Hoyos, Xiang H-F Zhang, Eric C Chang","doi":"10.1016/j.canlet.2026.218776","DOIUrl":"10.1016/j.canlet.2026.218776","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218776"},"PeriodicalIF":11.8,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer lettersPub Date : 2026-09-05DOI: 10.1016/j.canlet.2026.218833
Peng Ji, Huai-Liang Wu, Li-Hua He, Han Wang, Chao You, Li Chen, Yin Liu, Ming-Liang Jin, Yu-Ling Xiao, Xin Hu, Yi-Zhou Jiang, Zhi-Ming Shao, Yue Gong
{"title":"Integrated analysis reveals the impact of obesity on triple-negative breast cancer.","authors":"Peng Ji, Huai-Liang Wu, Li-Hua He, Han Wang, Chao You, Li Chen, Yin Liu, Ming-Liang Jin, Yu-Ling Xiao, Xin Hu, Yi-Zhou Jiang, Zhi-Ming Shao, Yue Gong","doi":"10.1016/j.canlet.2026.218833","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218833","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is a highly aggressive and heterogeneous breast cancer subtype with limited therapeutic options. While the prevalence of overweight/obese (OW/OB) women continues to rise, the impact of obesity on molecular features of TNBC remains incompletely understood. We investigated clinicopathological and molecular data (including genomic, transcriptomic, proteomic and metabolomic profiling) using our largest original multi-omics database of TNBC (N = 465) for associations with patient body mass index (BMI). Multi-omics profiling revealed that OW/OB patients exhibited worse survival as well as elevated inflammation of tumor microenvironment, higher expression of immune checkpoints, and dysregulated lipid metabolism. Our in vivo experiments demonstrated that tumors in obese mice displayed faster growth rates, a higher proportion of PD-1<sup>+</sup>CD8<sup>+</sup> T cells and enhanced responsiveness to anti-PD-1 treatment. In addition, we analyzed data from four independent clinical trials and discovered that OW/OB patients demonstrated higher pathological complete response rates and longer progression-free survival following anti-PD-1-based immunotherapy. In conclusion, our study systematically revealed that obesity is associated with coordinated immune-metabolic remodeling in TNBC, characterized by checkpoint enrichment and lipid dysregulation, which may help explain the enhanced anti-PD-1 responsiveness and should be taken into account in the field of precision medicine.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218833"},"PeriodicalIF":11.8,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"ACSL5 drives pancreatic ductal adenocarcinoma by suppressing mitophagy and enhancing ferroptosis resistance via the JAK1-STAT1-OASL axis.","authors":"Jingjing Dong, Mengting Dai, Yiming Zhou, Mengde Wu, Wei Wu, Linling Zhou, Zhaoyang Ji, Tongtong Ye, Jiaying Qin, Jialu Luo, Chenhuan Yu, Mingzhi Xu","doi":"10.1016/j.canlet.2026.218809","DOIUrl":"10.1016/j.canlet.2026.218809","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy with limited therapeutic options. Here, we identify long-chain acyl-CoA synthetase 5 (ACSL5) as a key oncogenic driver and prognostic biomarker in PDAC. Combined transcriptomic analysis of 51 PDAC samples and three public databases (GSE183795, GSE28735, GSE62452) reveals that ACSL5 is markedly upregulated in PDAC, and its overexpression is significantly associated with shorter patient survival and high diagnostic accuracy (AUC = 0.899), suggesting robust diagnostic potential. Functional assays demonstrate that ACSL5 promotes PDAC cell proliferation, migration, and tumor growth while inhibiting apoptosis. Mechanistically, ACSL5 activates the JAK1-STAT1 signaling pathway, leading to transcriptional upregulation of oligoadenylate synthetase-like protein (OASL). The ACSL5-OASL axis concurrently suppresses PINK1/Parkin-mediated mitophagy and enhances ferroptosis resistance by modulating GPX4, SLC7A11, and ACSL4 expression. Notably, the mitophagy activator CCCP effectively reverses ACSL5-driven tumor progression and restores ferroptosis sensitivity. Our findings establish ACSL5 as a promising diagnostic and therapeutic target and reveal that targeting mitophagy represents a potential strategy for ACSL5-high PDAC.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218809"},"PeriodicalIF":11.8,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Patient-derived organoids for hepatobiliary cancers: Molecular mechanisms, translational applications and precision therapeutics.","authors":"Senyan Wang, Yixuan Liu, Qi Liu, Mengzhen Zhang, Xinhan Bai, Xinze Li, Chongwei Jin, Xiaoyan Sun, Jing Xu, Xiaofang Zhao, Jing Fu, Hongyang Wang","doi":"10.1016/j.canlet.2026.218810","DOIUrl":"10.1016/j.canlet.2026.218810","url":null,"abstract":"<p><p>Hepatobiliary cancers are highly heterogeneous malignant tumors, and the drug resistance frequently emerges at advanced stages. Patient-derived organoids (PDOs) are three-dimensional ex vivo cultures. They can reproduce essential biological aspects of primary tumors, and play a key role in personalized oncology. With advances in methodology and technology, PDOs are increasingly being used in hepatobiliary cancer research at both the fundamental and translational levels. This review summarizes recent advances in patient-derived organoids, including culture matrices, microenvironment reconstruction, and organoid-on-chips. We also discuss the applications of PDOs in hepatobiliary cancer modeling and organoid biobank construction. Hepatobiliary cancer organoids hold promise for drug development and may serve as complementary tools for preclinical prediction. Integrating in vitro drug testing, resistance mechanism identification and combination regimen screening, organoid-based workflows can provide platforms for treatment stratification and personalized treatment optimization in hepatobiliary cancers. The incorporation of artificial intelligence may further expand the capabilities of organoid-based platforms. Overall, hepatobiliary cancer organoids represent clinically promising models for overcoming therapeutic resistance and developing personalized treatment strategies. They are powerful tools for precision oncology and clinical translation.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218810"},"PeriodicalIF":11.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Epitranscriptomic silencing of STK25 promotes ferroptosis evasion via the METTL3-YAP-GPX4 axis in osteosarcoma.","authors":"Zhuochao Liu, Zhusheng Zhang, Fangqiong Hu, Junxiang Wen, Yucheng Fu, Qi Liu, Tao Liang, Jun Wang, Yuhui Shen, Qiyuan Bao, Weibin Zhang","doi":"10.1016/j.canlet.2026.218807","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218807","url":null,"abstract":"<p><p>Osteosarcoma (OS) is an aggressive bone malignancy with poor outcomes in recurrent and metastatic disease. Although ferroptosis represents as a promising therapeutic strategy, its regulation in OS remains incompletely understood. Here, we identified STK25 as a regulator of ferroptosis susceptibility and tumor growth in OS. Transcriptomic analysis of paired parental and multidrug-resistant OS cell lines identified lower STK25 expression in the resistant derivatives. In a retrospective tissue microarray, low tumor STK25 expression was associated with a lower histological tumor necrosis rate after neoadjuvant chemotherapy and shorter survival. Mechanistically, METTL3 overexpression reduced STK25 reporter activity and accelerated STK25 mRNA decay in an m<sup>6</sup>A-site-dependent manner. STK25 depletion was accompanied by reduced Hippo pathway activity, increased YAP nuclear localization, and increased GPX4 expression, whereas STK25 restoration increased LATS1 and YAP phosphorylation, reduced GPX4 expression and sensitized OS cells to ferroptosis. GPX4 re-expression partially rescued cell viability and oxidative-stress phenotypes induced by STK25 overexpression, supporting GPX4 as a functional downstream effector. In xenografts, STK25 overexpression significantly suppressed tumor growth and increased ferroptosis-associated changes. These findings support an METTL3-STK25-YAP-GPX4 regulatory model that links epitranscriptomic control to ferroptosis susceptibility in OS and warrants further preclinical and prospective clinical validation.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218807"},"PeriodicalIF":11.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
