Cancer letters最新文献

Corrigendum to “PA28γ acts as a dual regulator of IL-6 and CCL2 and contributes to tumor angiogenesis in oral squamous cell carcinoma” [Cancer Lett. 428 (2018) 192–200] “PA28γ作为IL-6和CCL2的双重调节因子，有助于口腔鳞状细胞癌的肿瘤血管生成”的更正[癌症杂志]. 428 (2018)192-200]

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-17 DOI: 10.1016/j.canlet.2025.217787

Sai Liu , Dongjuan Liu , Xin Zeng , Jiongke Wang , Jiajia Liu , Junxin Cheng , Kexin Lei , Hetian Bai , Ning Ji , Min Zhou , Lu Jiang , Hongxia Dan , Jing Li , Qianming Chen

引用次数: 0

Molecular profiling reveals the malignant potential in solid pseudopapillary neoplasms of the pancreas 分子图谱显示胰腺实性假乳头状肿瘤的恶性潜能

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-15 DOI: 10.1016/j.canlet.2025.217788

Jiayi Li , Huaijin Zheng , Xiang Zhang , Boju Pan , Junliang Lu , Liangrui Zhou , Taiping Zhang , Menghua Dai , Junchao Guo , Weibin Wang , Xianlin Han , Qiang Xu , Yuze Hua , Jorg Kleeff , Huanwen Wu , Zhiyong Liang , Qiaofei Liu , Quan Liao

{"title":"Molecular profiling reveals the malignant potential in solid pseudopapillary neoplasms of the pancreas","authors":"Jiayi Li , Huaijin Zheng , Xiang Zhang , Boju Pan , Junliang Lu , Liangrui Zhou , Taiping Zhang , Menghua Dai , Junchao Guo , Weibin Wang , Xianlin Han , Qiang Xu , Yuze Hua , Jorg Kleeff , Huanwen Wu , Zhiyong Liang , Qiaofei Liu , Quan Liao","doi":"10.1016/j.canlet.2025.217788","DOIUrl":"10.1016/j.canlet.2025.217788","url":null,"abstract":"<div><div>Solid pseudopapillary neoplasm of the pancreas (SPN) is a rare tumor primarily affecting middle-aged women, typically characterized by indolent behavior but occasionally demonstrating malignant potential through invasive growth and metastasis. To elucidate the molecular mechanisms driving this heterogeneity, a multi-omics approach was applied to analyze paired metastatic lesions, primary tumors, and normal pancreatic tissues. Methylation profiling via the Illumina Infinium Methylation EPIC BeadChip identified 2425 differentially methylated positions (DMPs) in metastatic versus primary lesions, with 798 DMPs conserved across both lesion types. Tyrosine kinases and cGMP-PKG signaling pathway were the most significantly enriched KEGG pathways involved in the DMPs. Transcriptomic analysis of invasive and non-invasive SPNs using NanoString revealed 99 differentially expressed genes (DEGs). Immunohistochemical validation confirmed elevated protein expression of LY96, IFI16, and GLUD1 in invasive cases. Circulating free DNA (cfDNA) sequencing did not detect genetic mutation in non-metastatic SPN, in contrast, 42.9 % positivity of genetic mutations were detected in metastatic SPNs. Tumor microenvironment analysis by using the GEO database, 850 K methylation sequencing, NanoString transcriptome, highlighted enriched immune-suppressive stromal components in aggressive tumors. These findings establish a molecular signature linking methylation dysregulation, transcriptomic alterations, liquid biopsy, and immune evasion to SPN progression, offering potential biomarkers for risk stratification and therapeutic targeting.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"625 ","pages":"Article 217788"},"PeriodicalIF":9.1,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144072669","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}

引用次数: 0

Corrigendum to “Selective degradation of FGFR1/2 overcomes antiestrogen resistance in ER+ breast cancer with FGFR1/2 alterations” [619 1 (2025) 217668 1–13]

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-14 DOI: 10.1016/j.canlet.2025.217782

Yasuaki Uemoto , Chang-Ching A Lin , Bingnan Wang , Dan Ye , Yisheng V. Fang , Emmanuel Bikorimana , Fabiana Napolitano , Maria Rosario Chica-Parrado , Cheung Li , Saurabh Mendiratta , Chuo Chen , Ariella B. Hanker , Carlos L. Arteaga

引用次数: 0

Keloids Revisited: Current Concepts in Treatment and Differential Diagnosis. 瘢痕疙瘩重述：当前治疗和鉴别诊断的概念。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-13 DOI: 10.1016/j.canlet.2025.217802

Yanhui Liu, Xiao Chen, Katharina S Fischer, Siqi Fu, Li Yuan, Xing Hu

{"title":"Keloids Revisited: Current Concepts in Treatment and Differential Diagnosis.","authors":"Yanhui Liu, Xiao Chen, Katharina S Fischer, Siqi Fu, Li Yuan, Xing Hu","doi":"10.1016/j.canlet.2025.217802","DOIUrl":"https://doi.org/10.1016/j.canlet.2025.217802","url":null,"abstract":"<p><p>Keloid is a special type of scar considered prototypic of skin fibrosis. Unlike hypertrophic scars, keloids exceed the margins of the original wound, and exist over time, without a quiescent or regressive phase. Although keloids do not metastasize, they exhibit tumor-like characteristics, and share many similarities. Large epidemiological study demonstrates that patients with keloids have a 1.49-fold higher risk for cancers. Keloids can lead to severe functional impairments and diminish quality of life which increases hidden costs for patients and medical systems. The main goals of treatments are to improve scar appearance, symptoms and patient's quality of life (QoL). However, the microenvironment, pathogenesis, formation and development of the keloid are complex, the efficacy of multiple treatments were limited. Therefore, this up-to-date review aimed to target the current concepts in keloid treatment and differential diagnosis. The goal is to provide a reference for doctors and researchers to improve the accuracy of diagnosis and facilitate the selection of personalized treatment methods for patients with keloids.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"217802"},"PeriodicalIF":9.1,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076208","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}

引用次数: 0

Patient-derived organoid co-culture systems as next-generation models for bladder cancer stem cell research 患者源性类器官共培养系统作为膀胱癌干细胞研究的下一代模型。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-12 DOI: 10.1016/j.canlet.2025.217793

Ruici Yang , Shanzhao Wang , Zhichao Li , Cong Yin , Wei Huang , Weiren Huang

{"title":"Patient-derived organoid co-culture systems as next-generation models for bladder cancer stem cell research","authors":"Ruici Yang , Shanzhao Wang , Zhichao Li , Cong Yin , Wei Huang , Weiren Huang","doi":"10.1016/j.canlet.2025.217793","DOIUrl":"10.1016/j.canlet.2025.217793","url":null,"abstract":"<div><div>Three-dimensional patient-derived organoids (PDOs) have emerged as a powerful model for investigating the molecular and cellular mechanisms underlying bladder cancer, particularly in the context of cancer stem cells (CSCs) and drug screening. However, a significant limitation of conventional PDOs is the absence of tumor microenvironment (TME), which includes critical stromal, immune and microbial components that influence tumor behavior and treatment response. In this review, we provide a comprehensive overview of the recent advancements in PDO co-culture systems designed to integrate TME elements. Additionally, we emphasize the role of biomedical engineering technologies, such as 3D bioprinting and organoids-on-a-chip, in enhancing the physiological relevance of these models. Furthermore, we explore how bladder PDO co-culture systems are applied in research on bladder CSC characterization, evolution and treatment responses. Finally, we discuss future directions for improving PDO systems to achieve more accurate preclinical modeling and drug discovery.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"625 ","pages":"Article 217793"},"PeriodicalIF":9.1,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076210","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}

引用次数: 0

Efficacy and safety of inetetamab plus pertuzumab and nab-paclitaxel as neoadjuvant therapy for HER2+ breast cancer: A single-arm multicenter phase II clinical trial. 一项单臂多中心II期临床试验：inetetamab联合pertuzumab和nab-紫杉醇作为HER2+乳腺癌新辅助治疗的疗效和安全性

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-10 DOI: 10.1016/j.canlet.2025.217785

Wen-Jia Zuo, Lin-Xiao-Xi Ma, Zhi-Hong Wang, Xu-Chen Cao, Xin-Jian Jia, Wen-He Zhao, Ming-Liang Zhang, Hong-Wei Yang, Mao-Shan Chen, Jing Wang, Xiao-Yu Liu, Hao Zhang, Xiu-Chun Chen, Dong Song, Hao Wang, Xiao-Peng Ma, Ya-Bing Wang, Hao Yu, Zhong-Hua Wang, Zhi-Ming Shao

{"title":"Efficacy and safety of inetetamab plus pertuzumab and nab-paclitaxel as neoadjuvant therapy for HER2+ breast cancer: A single-arm multicenter phase II clinical trial.","authors":"Wen-Jia Zuo, Lin-Xiao-Xi Ma, Zhi-Hong Wang, Xu-Chen Cao, Xin-Jian Jia, Wen-He Zhao, Ming-Liang Zhang, Hong-Wei Yang, Mao-Shan Chen, Jing Wang, Xiao-Yu Liu, Hao Zhang, Xiu-Chun Chen, Dong Song, Hao Wang, Xiao-Peng Ma, Ya-Bing Wang, Hao Yu, Zhong-Hua Wang, Zhi-Ming Shao","doi":"10.1016/j.canlet.2025.217785","DOIUrl":"https://doi.org/10.1016/j.canlet.2025.217785","url":null,"abstract":"<p><p>The combination of inetetamab and vinorelbine has demonstrated survival benefits with an acceptable toxicity profile in HER2+ metastatic breast cancer (MBC) patients. This multicenter, single-arm, phase II trial further evaluates the efficacy of inetetamab combined with pertuzumab and nab-paclitaxel as neoadjuvant therapy. Treatment-naïve patients with HER2+ early-stage or locally advanced BC received four cycles of intravenous inetetamab (8 mg/kg loading dose, then 6 mg/kg for subsequent doses), intravenous pertuzumab (840 mg loading dose, then 420 mg for subsequent doses), and weekly nab-paclitaxel (125 mg/m<sup>2</sup>). The primary endpoint was the total pathological complete response (tpCR) rate, defined as ypT0/is and ypN0, assessed by independent central review. From March 2023 to February 2024, 62 patients were enrolled, with the majority (61/62) completing 4 cycles of neoadjuvant therapy. The tpCR rate was 56.5% (95% CI: 43.3%-69.0%). Further analysis showed that patients with estrogen receptor (ER) negative tumors derived greater benefit, with a tpCR rate of 90.9%. The objective response rate was 90.3% (95% CI: 80.1%-96.4%). The most common grade 3 or higher adverse events were neutropenia (32.3%), decreased white blood cell count (19.4%), infectious pneumonia (3.2%), anemia (3.2%), and diarrhea (3.2%). No death occurred during the neoadjuvant treatment. Neoadjuvant treatment with inetetamab, in combination with pertuzumab and nab-paclitaxel, demonstrates good efficacy and tolerability, especially in ER-negative patients.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"217785"},"PeriodicalIF":9.1,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975224","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}

引用次数: 0

Association of CMV status with response to neoadjuvant chemoimmunotherapy in early triple-negative breast cancer 巨细胞病毒状态与早期三阴性乳腺癌新辅助化疗免疫治疗反应的关系

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-10 DOI: 10.1016/j.canlet.2025.217789

Vincent Walter , André Koch , Dorothea Hillmann , Dominik Dannehl , Annette Staebler , Kerstin Pfister , Lorenz Risch , Tobias Engler , Sara Brucker , Wolfgang Janni , Andreas Hartkopf , Lukas Flatz

引用次数: 0

Activated Schwann cells promote tumor growth in colon cancer 活化的雪旺细胞促进结肠癌肿瘤生长

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-10 DOI: 10.1016/j.canlet.2025.217791

Kexin He , Hao Wang , Hao Wu , Weihan Li , Ruixue Huo , Luju Jiang , Minhao Yu , Junli Xue

{"title":"Activated Schwann cells promote tumor growth in colon cancer","authors":"Kexin He , Hao Wang , Hao Wu , Weihan Li , Ruixue Huo , Luju Jiang , Minhao Yu , Junli Xue","doi":"10.1016/j.canlet.2025.217791","DOIUrl":"10.1016/j.canlet.2025.217791","url":null,"abstract":"<div><div>Schwann cells, traditionally recognized as glial cells of the peripheral nervous system, have emerged as pivotal cellular constituents within the tumor microenvironment. Colon cancer exhibits significant nerve dependence; however, the roles of Schwann cells in colon cancer progression remain insufficiently understood. Here, we identified a significant increase in tumor-associated nonmyelinating Schwann cells within colon tumor samples compared to their normal tissue counterparts. Furthermore, the elevated abundance of these cells was associated with poorer clinical outcomes in colon cancer. Within colon tumor tissues, Schwann cells displayed elevated expression of c-Jun, a key gene involved in their activation and reprogramming. Knocking down c-Jun hampered Schwann cell activation. Single-cell RNA sequencing analysis uncovered that glial cells engage in the most robust cell-cell interactions with malignant cells and fibroblasts. Co-culture experiments demonstrated that tumor cells and cancer-associated fibroblasts specifically promoted c-Jun activation in Schwann cells, whereas co-culture with immune cells did not elicit a similar response. Under <em>In vivo</em> conditions, Schwann cells enhance tumor growth in a c-Jun-dependent manner. Moreover, c-Jun knockout in Schwann cells orchestrated a reprogramming of their secretome, exemplified by a notable reduction in IL-6, a key effector of their tumor-promoting activity. Collectively, our study elucidates the critical role of activated Schwann cells in colon cancer, which may offer a novel therapeutic strategy for treatment.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"626 ","pages":"Article 217791"},"PeriodicalIF":9.1,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143935279","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}

引用次数: 0

A PP2A-mtATR-tBid axis links DNA damage-induced CIP2A degradation to apoptotic dormancy and therapeutic resistance in PDAC. PP2A-mtATR-tBid轴将DNA损伤诱导的CIP2A降解与PDAC的凋亡休眠和治疗抗性联系起来。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-10 DOI: 10.1016/j.canlet.2025.217790

Yibo Luo, Himadri Biswas, Yetunde Makinwa, Shi-He Liu, Zizheng Dong, Jing-Yuan Liu, Jian-Ting Zhang, Yue Zou

{"title":"A PP2A-mtATR-tBid axis links DNA damage-induced CIP2A degradation to apoptotic dormancy and therapeutic resistance in PDAC.","authors":"Yibo Luo, Himadri Biswas, Yetunde Makinwa, Shi-He Liu, Zizheng Dong, Jing-Yuan Liu, Jian-Ting Zhang, Yue Zou","doi":"10.1016/j.canlet.2025.217790","DOIUrl":"https://doi.org/10.1016/j.canlet.2025.217790","url":null,"abstract":"<p><p>DNA damage-based drugs are widely used in cancer therapy, yet resistance remains a significant challenge. In this study, we uncovered a non-DNA repair mechanism contributing to resistance in cancer cells. We found that in gemcitabine-resistant pancreatic ductal adenocarcinoma (PDAC) cells, CIP2A degradation via ubiquitination enhanced PP2A phosphatase activity, leading to the dephosphorylation of ATR at Ser428 in the cytoplasm. This dephosphorylation promoted the formation of the prolyl cis-isomeric form of ATR at its Ser428-Pro429 motif, a mitochondria-targeted antiapoptotic protein (mtATR). Surprisingly, the resistant PDAC cells paradoxically accumulated both mtATR and proapoptotic tBid at mitochondria, forming the mtATR-tBid complex. This complex silenced tBid, inducing apoptotic dormancy. Antagonizing mtATR, either through the PP2A inhibitor LB-100 or a cytoplasmic ATR-specific antibody, reactivated the pre-accumulated mitochondrial tBid and induced apoptosis in resistant PDAC cells. In an orthotopic PDAC mouse model, LB-100 alone significantly suppressed resistant tumor growth by disrupting the mtATR-tBid complex. These findings reveal a novel mechanism of resistance to DNA damage-based cancer drugs and introduce a new action mechanism of LB-100, which works through mtATR-tBid complex-mediated apoptotic dormancy triggered by CIP2A degradation-mediated PP2A activation. Disrupting the mtATR-tBid complex may represent a promising strategy to restore or sensitize resistant cancer cells to apoptosis.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"217790"},"PeriodicalIF":9.1,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975143","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}

引用次数: 0

Corrigendum to “CircMFN2/miR-361-3p/ELK1 feedback loop promotes glutaminolysis and the progression of hepatocellular carcinoma” [Cancer Lett. 614 (2025) 217473] “CircMFN2/miR-361-3p/ELK1反馈回路促进谷氨酰胺溶解和肝细胞癌的进展”的勘误表[Cancer Lett] . 614 (2025) 217473]

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-10 DOI: 10.1016/j.canlet.2025.217755

Xiaopei Hao , Xiangjun Qian , Chenxi Xie , Zhengzheng Wang , Xiaoqian Wang , Yang Ji , Xiaokai Zhang , Qingjun Li , Baishun Wan , Hong Cui , Li Wang , Nanmu Yang , Liang Qiao , Haibo Yu , Feng Han , Hao Zhuang , Jinxue Zhou

引用次数: 0