Cancer letters最新文献

{"title":"Cyst fluid proteins stratify malignant risk of intraductal papillary mucinous neoplasm of the pancreas","authors":"Chunliang Liu ,&nbsp;Amber Mosley ,&nbsp;Ehsan Irajizad ,&nbsp;Michele Yip-Schneider ,&nbsp;Huangbing Wu ,&nbsp;Whitney R. Smith-Kinnaman ,&nbsp;Thoa Tran ,&nbsp;James P. Long ,&nbsp;Kim-Anh Do ,&nbsp;Johannes Fahrmann ,&nbsp;John M. DeWitt ,&nbsp;Samir Hanash ,&nbsp;C. Max Schmidt ,&nbsp;Jianjun Zhang","doi":"10.1016/j.canlet.2025.217753","DOIUrl":"10.1016/j.canlet.2025.217753","url":null,"abstract":"<div><div>Intraductal papillary mucinous neoplasm (IPMN) is the most common type of pancreatic cyst often incidentally detected in asymptomatic patients. The current consensus guidelines, largely based on imaging features, have high sensitivity but low specificity in differentiating benign from malignant IPMNs, leading to unnecessary surgeries. Discovering biomarkers is thus warranted to improve the preoperative risk stratification of IPMN. Pancreatic cyst fluid samples were obtained from patients with pathologically confirmed low-grade (n = 73) or high-grade/invasive (n = 18) IPMN. Global proteome quantitation was performed using liquid chromatography-tandem mass spectrometry. Differentially expressed proteins (DEPs) between the two groups were analyzed using Wilcoxon rank-sum test. 152 upregulated and 74 downregulated DEPs were discovered by comparing low-grade IPMN with high-grade/invasive IPMN (all p &lt; 0.05). The enriched upstream regulators of these DEPs included let-7, miR-122, IL15, and FLT1 (p = 6.76 × 10⁻⁵ - 5.97 × 10⁻³). Five discriminatory biomarkers with the largest LASSO coefficients and each with AUCs of &gt;0.75 (FAHD2A, TCEAL3, TWF1, MMUT, and NTPCR) were identified. The combined five-protein model achieved a bootstrap-corrected AUC of 0.94. A combined analysis of TCGA and GTEx databases showed TWF1 overexpression in pancreatic cancer (p = 2.22 × 10⁻¹⁶) that was associated with poor prognosis (p = 0.0063). The present study identified several cyst fluid proteins (particularly TWF1) that are predictive of malignant pancreatic cyst lesions. If validated in other patient populations, these biomarkers may enhance the accuracy of the preoperative detection of high-risk IPMN and thereby improve patient outcomes.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"624 ","pages":"Article 217753"},"PeriodicalIF":9.1,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143887077","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":"Hormonal and neuronal interactions shaping the brain metastatic microenvironment","authors":"Stephen Shovlin ,&nbsp;Leonie S. Young ,&nbsp;Damir Varešlija","doi":"10.1016/j.canlet.2025.217739","DOIUrl":"10.1016/j.canlet.2025.217739","url":null,"abstract":"<div><div>Metastatic progression drives the majority of cancer-related fatalities, and involvement of the central nervous system (CNS) poses especially formidable challenges to patients and clinicians. Brain metastases (BrM), commonly originate from lung, breast and melanoma cancers, and carry disproportionately poor outcomes. Although therapeutic advances have extended survival for many extracranial tumors, BrM incidence continues to climb—underscoring critical knowledge gaps in understanding the unique biology of tumor colonization in the CNS. While definitive evidence remains limited, a growing focus on cancer neuroscience—especially regarding hormone dependent cancer cells in the brain—has begun to reveal that factors normally regulated by sex steroids and neurosteroids may similarly influence the specialized metastatic microenvironment in the CNS. Steroid hormones can permeate the blood-brain barrier (BBB) or be synthesized <em>de novo</em> by astrocytes and other CNS-resident cells, potentially influencing processes such as inflammation, synaptic plasticity, and immune surveillance. However, how these hormonal pathways are co-opted by disseminated cancer cells remains unclear. Here, we review the complex hormonal landscape of the adult brain and examine how neuroendocrine–immune interactions, often regulated by sex hormones, may support metastatic growth. We discuss the interplay between systemic hormones, local steroidogenesis, and tumor adaptation to identify novel therapeutic opportunities.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"624 ","pages":"Article 217739"},"PeriodicalIF":9.1,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143891596","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":"Corrigendum to “MED27 promotes melanoma growth by targeting AKT/MAPK and NF/κB/iNOS signaling pathway” [Cancer Lett. 373(1) (2016) 77-87 PMID 26797421]","authors":"Ranran Tang ,&nbsp;Xiangdong Xu ,&nbsp;Wenjing Yang ,&nbsp;Wendan Yu ,&nbsp;Shuai Hou ,&nbsp;Yang Xuan ,&nbsp;Zhipeng Tang ,&nbsp;Shilei Zhao ,&nbsp;Yiming Chen ,&nbsp;Xiangsheng Xiao ,&nbsp;Wenlin Huang ,&nbsp;Wei Guo ,&nbsp;Man Li ,&nbsp;Wuguo Deng","doi":"10.1016/j.canlet.2025.217717","DOIUrl":"10.1016/j.canlet.2025.217717","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217717"},"PeriodicalIF":9.1,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859191","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":"Cancer stem cells and tumor-associated macrophages: Interactions and therapeutic opportunities","authors":"Haitao Yuan ,&nbsp;Yun Qiu ,&nbsp;Zijie Mei,&nbsp;Jiaqing Liu,&nbsp;Lingna Wang,&nbsp;Kaiqing Zhang,&nbsp;Huicong Liu,&nbsp;Fangfang Zhu","doi":"10.1016/j.canlet.2025.217737","DOIUrl":"10.1016/j.canlet.2025.217737","url":null,"abstract":"<div><div>Cancer stem cells (CSCs) depend on the tumor microenvironment (TME) to sustain their stem-like properties by recruiting monocytes and reprogramming them into tumor-associated macrophages (TAMs), which in turn promote tumor progression. This review explores CSC-TAM interactions, emphasizing how CSCs drive monocyte recruitment and TAM polarization. We discuss how TAMs enhance CSC stemness and niche maintenance through chemokines, cytokines, exosome-mediated miRNA transfer, direct interactions, and extracellular matrix (ECM) remodeling. Furthermore, we examine therapeutic strategies targeting TAMs, including inhibiting TAM differentiation, reprogramming TAM polarization, and leveraging immune checkpoint blockade and CAR-macrophage immunotherapy to improve cancer treatment outcomes.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"624 ","pages":"Article 217737"},"PeriodicalIF":9.1,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143891597","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":"Extracellular Vesicles: Hermes between cancers and lymph nodes","authors":"Lei-Ming Cao ,&nbsp;Yu-Zhong Qiu ,&nbsp;Zi-Zhan Li ,&nbsp;Guang-Rui Wang ,&nbsp;Yao Xiao ,&nbsp;Han-Yue Luo ,&nbsp;Bing Liu ,&nbsp;Qiuji Wu ,&nbsp;Lin-Lin Bu","doi":"10.1016/j.canlet.2025.217735","DOIUrl":"10.1016/j.canlet.2025.217735","url":null,"abstract":"<div><div>Cancer is one of the main causes of death and a major obstacle to increasing life expectancy in all countries of the world. Lymph node metastasis (LNM) of in cancer patients indicates poor prognosis and it is an important indication to determine the therapeutic regime. Therefore, more attention should be given to the molecular mechanics of tumor lymphangiogenesis and LNM. Extracellular vesicles (EVs) are nanoscale cargo-bearing membrane vesicles that can serve as key mediators for the intercellular communication. Like Hermes, the messenger of the Greek gods, EVs can be secreted by tumor cells to regulate the LNM process. Many evidence has proved the clinical correlation between EVs and LNM in various cancer types. EVs plays an active role in the process of metastasis by expressing its connotative molecules, including proteins, nucleic acids, and metabolites. However, the clear role of EVs in the process of cancer LNM has not been thoroughly studied yet. In this review, we will summarize the clinical and mechanical findings of EVs regulating role on cancer LNM, and discuss the advanced modification of the research proposal. We propose the “PUMP” principle of EVs in LNM, including Preparation, Unleash, Migration, and Planting.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217735"},"PeriodicalIF":9.1,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143864489","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":"Microbiome, metabolome, and ionome profiling of cyst fluids reveals heterogeneity in pancreatic cystic neoplasms","authors":"Sen Yang ,&nbsp;Ya Hu ,&nbsp;Ming Cui ,&nbsp;Qiang Xu ,&nbsp;Xianlin Han ,&nbsp;Xiaoyan Chang ,&nbsp;Qingyuan Zheng ,&nbsp;Jinheng Xiao ,&nbsp;Tianqi Chen ,&nbsp;Pengyu Li ,&nbsp;Menghua Dai ,&nbsp;Yupei Zhao","doi":"10.1016/j.canlet.2025.217730","DOIUrl":"10.1016/j.canlet.2025.217730","url":null,"abstract":"<div><div>Pancreatic cystic neoplasms (PCNs) carry variable malignant potential, requiring precise clinical management. However, the heterogeneity and progression of PCNs remain poorly understood. This study analyzed the microbiome, metabolome, and ionome profiles of cyst fluids from 188 patients, including 165 with PCNs and 23 with other cyst types, using PacBio full-length 16S/ITS sequencing, LC-MS/MS, and ICP-MS. Bioinformatic analyses were performed, and metabolic enzyme and endoplasmic reticulum (ER) stress-related gene expression were examined using the PAAD TCGA dataset. PCNs were classified into distinct histopathological subtypes, including mucinous cystic lesions (MCLs) and serous cystic lesions (SCLs). MCLs demonstrated lower microbial diversity compared to SCLs, indicating microbial instability. <em>Streptococcus</em> and <em>Staphylococcus</em> were identified as key taxa in intraductal papillary mucinous neoplasms (IPMNs) and mucinous cystic neoplasms (MCNs), respectively. MCLs exhibited metabolic shifts towards lipid metabolism, while IPMNs showed distinct metabolic profiles potentially reflecting inflammation-related metabolic reprogramming. Ionic diversity varied among subtypes, with MCLs showing reduced diversity and IPMNs presenting broader ionic profiles. Palmitic acid (PA), a metabolite linked to <em>Streptococcus</em>, may contribute to pro-inflammatory metabolic alterations in IPMN. Our preliminary experiments demonstrated that co-culturing <em>Streptococcus orails (S. orails)</em> with ASAN-PaCa cells promoted their proliferation, accompanied by an elevation of PA levels in the supernatant. This integrative microbiome–metabolome–ionome analysis highlights histopathological heterogeneity among PCNs. While mechanistic associations remain to be fully defined, mucinous lesions may be more susceptible to microbe-driven metabolic disruption, with <em>Streptococcus</em>-associated lipid alterations as a potential contributing factor.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217730"},"PeriodicalIF":9.1,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143864491","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":"Loss of SPHK1 fuels inflammation to drive KRAS-mutated lung adenocarcinoma","authors":"Andreea C. Luca ,&nbsp;Margarita Kurnaeva ,&nbsp;Daniel K. John ,&nbsp;Michael Machtinger ,&nbsp;Nadja H.J. Vollmer ,&nbsp;Bernadette Mödl ,&nbsp;J. Thomas Hannich ,&nbsp;Margret Eckhard ,&nbsp;Hon S. Lam ,&nbsp;Laszlo Musiejovsky ,&nbsp;Christoph Trenk ,&nbsp;Monika Homolya ,&nbsp;Clemens Fürnsinn ,&nbsp;Andy Sombke ,&nbsp;Gernot Schabbauer ,&nbsp;Robert Eferl ,&nbsp;Omar Sharif ,&nbsp;Emilio Casanova ,&nbsp;Herwig P. Moll","doi":"10.1016/j.canlet.2025.217733","DOIUrl":"10.1016/j.canlet.2025.217733","url":null,"abstract":"<div><div>Inflammation is a widely recognized key contributor to KRAS-driven lung adenocarcinoma (LUAD). Tumor-associated macrophages (TAM) are an integral part of the tumor microenvironment and create a supportive niche that sustains inflammation-driven tumorigenesis. In the present study, we unravel a dual role of sphingosine kinase 1 (SPHK1) in KRAS-driven LUAD. While SPHK1 promotes tumorigenesis in in vitro experimental models, it paradoxically suppresses tumorigenesis in in vivo models of KRAS-mutated LUAD. Mechanistically, tumor-intrinsic loss of SPHK1 leads to disrupted lipid homeostasis, increased inflammation and infiltration by TAM, ultimately driving tumor progression. Thus, our study suggests that clinically targeting the SPHK1/S1P axis could potentially result in increased tumor progression, possibly by rewiring the tumor microenvironment toward a more inflammatory and pro-tumorigenic state.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217733"},"PeriodicalIF":9.1,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143858983","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":"COL1A1-positive endothelial cells promote gastric cancer progression via the ANGPTL4-SDC4 axis driven by endothelial-to-mesenchymal transition","authors":"Quanzhong Liu ,&nbsp;Miao Yu ,&nbsp;Zihan Lin ,&nbsp;Lingxiang Wu ,&nbsp;Peng Xia ,&nbsp;Mengyan Zhu ,&nbsp;Bin Huang ,&nbsp;Wei Wu ,&nbsp;Ruohan Zhang ,&nbsp;Kening Li ,&nbsp;Lingjun Zhu ,&nbsp;Qianghu Wang","doi":"10.1016/j.canlet.2025.217731","DOIUrl":"10.1016/j.canlet.2025.217731","url":null,"abstract":"<div><div>Gastric cancer (GC) is an aggressive and heterogeneous disease with poor survival outcomes. The progression of GC involves complex, multi-step processes. Endothelial cells (ECs) play a crucial role in tumor angiogenesis, proliferation, invasion, and metastasis, particularly through the process of endothelial-to-mesenchymal transition (EndoMT). However, the specific role and mechanisms of EndoMT in gastric cancer remain unclear. Based on 6 GC single-cell RNA-sequencing (scRNA-seq) cohorts (samples = 97), we established an EndoMT-related gene signature, termed EdMTS. Leveraging this gene signature, ssGSEA was applied to calculate sample scores across multiple bulk RNA-seq datasets, which include information on immunotherapy, metastasis, GC progression, and survival. Moreover, we applied the Monocle2 method to calculate cell pseudotime and used CellChat to analyze interactions between malignant and EC cells. We verified the molecular mechanism by multiple immunofluorescence and cell function experiments. Findings In this study, we established a single-cell atlas of ECs in GC and identified a subpopulation of <em>COL1A1</em>⁺ ECs that play a critical role in tumor progression and metastasis. These <em>COL1A1</em>⁺ ECs were significantly associated with worse clinical outcomes in GC patients. Further analysis revealed that <em>COL1A1</em>⁺ ECs originated from lymphatic ECs and underwent EndoMT through the upregulation of CEBPB, driving tumor invasiveness. Moreover, <em>COL1A1</em>⁺ ECs interacted with malignant cells via ANGPTL4-SDC4 axis, enhancing invasion and migration. These findings provide a deeper understanding of the role of <em>COL1A1</em>⁺ ECs in GC progression and highlight potential therapeutic targets for disrupting the EndoMT process in these cells to provide a benefit for GC patients.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217731"},"PeriodicalIF":9.1,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855862","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":"HNF4A functions as a hepatocellular carcinoma oncogene or tumor suppressor depending upon the AMPK pathway activity status","authors":"Zhaoyu Qin ,&nbsp;Yan Li ,&nbsp;Xiexiang Shao ,&nbsp;Kai Li ,&nbsp;Yihe Bai ,&nbsp;Bing Wang ,&nbsp;Fahan Ma ,&nbsp;Wenhao Shi ,&nbsp;Lei Song ,&nbsp;Aojia Zhuang ,&nbsp;Fuchu He ,&nbsp;Chen Ding ,&nbsp;Wenjun Yang","doi":"10.1016/j.canlet.2025.217732","DOIUrl":"10.1016/j.canlet.2025.217732","url":null,"abstract":"<div><div>Cancer cells frequently undergo energy metabolic stress induced by the increased dynamics of nutrient supply. Hepatocyte nuclear factor 4A (HNF4A) is a master transcription factor (TF) in hepatocytes that regulates metabolism and differentiation. However, the mechanism underlying how HNF4A functions in cancer progression remains unclear due to conflicting results observed in numerous studies. To address the roles of HNF4A in hepatocellular carcinoma (HCC), we investigated the regulatory functions of HNF4A in HCC cells under different glucose supply conditions. We found that HNF4A exhibited tumor-suppressive effects on the proliferation and migration of HCC cells in glucose-sufficient conditions and tumor-promotive effects on HCC cells in glucose-insufficient conditions. Further investigation revealed that this diverse function of HNF4A was dependent upon the AMPK pathway activity. Similarly, the prognosis predicted by HNF4A was also correlated with whether the AMPKa expression levels were low or high in clinical HCC patients. Multiomics approaches consisting of proteomics and ChIP-seq revealed that key HNF4A target genes, including NEDD4 and RPS6KA2, are involved in the diverse function of HNF4A in HCC in response to the AMPK activity status. Specifically, HNF4A could bind to the promoter region of NEDD4 and RPS6KA2, and upregulating their expression. Our study has demonstrated the relationship between and synergism of AMPK and HNF4A in the progression of HCC under diverse nutrient conditions.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217732"},"PeriodicalIF":9.1,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143858982","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":"The m6A hypermethylation-induced PIR overexpression regulates H3K4me3 and promotes tumorigenesis of uveal melanoma","authors":"Hao Tian ,&nbsp;Ying Chen ,&nbsp;Xiaokang Dong ,&nbsp;Xianqun Fan ,&nbsp;Ruobing Jia","doi":"10.1016/j.canlet.2025.217729","DOIUrl":"10.1016/j.canlet.2025.217729","url":null,"abstract":"<div><div>Uveal melanoma (UM) is the most common primary ocular malignancy in adults, characterized by high mortality, strong metastatic potential, and limited treatment options, necessitating the identification of novel therapeutic targets. Here, we identified Pirin (PIR) as a key oncogenic factor in UM through comprehensive multi-omics analyses, revealing that PIR is significantly upregulated and correlates with poor prognosis. Functional assays indicated that inhibiting PIR markedly suppressed UM progression, highlighting its critical role in tumorigenesis behavior. Mechanistically, PIR expression is driven by aberrant N6-methyladenosine (m⁶A) modifications mediated by METTL3 and IGF2BP3. Meanwhile, the high expressed PIR acts as a transcriptional co-regulator by interacting with WDR5, resulting in the regulation of H3K4me3 modifications at the ANAPC10 promoter region and subsequent promotion of ANAPC10 expression. Overall, our study uncovered the METTL3/IGF2BP3 (m6A)-PIR-WDR5 (H3K4me3)-ANAPC10 axis, bridging RNA methylation and histone methylation in UM pathogenesis. By unmasking these intricate epigenetic interactions, we provided novel insights into <span>UM</span> biology and identified potential therapeutic targets for tumor treatment, offering the theoretical support for future drug development and clinical applications.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217729"},"PeriodicalIF":9.1,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143868222","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}