{"title":"上皮细胞到间质细胞的转变驱动癌症基因组的不稳定性。","authors":"Julienne L Carstens, Sara Lovisa","doi":"10.1186/s13046-025-03402-x","DOIUrl":null,"url":null,"abstract":"<p><p>Epithelial-to-Mesenchymal Transition (EMT) is a form of embryonic cell plasticity reactivated in adult cells during injury and cancer. A recent study by Perelli et al. demonstrates that EMT confers an evolutionary advantage to tumors by inducing chromosomal instability, structural genomic rearrangements and chromothripsis, thus favoring the emergence of high-fitness malignant clones.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"44 1","pages":"135"},"PeriodicalIF":11.4000,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12042499/pdf/","citationCount":"0","resultStr":"{\"title\":\"Epithelial-to-mesenchymal transition drives cancer genomic instability.\",\"authors\":\"Julienne L Carstens, Sara Lovisa\",\"doi\":\"10.1186/s13046-025-03402-x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Epithelial-to-Mesenchymal Transition (EMT) is a form of embryonic cell plasticity reactivated in adult cells during injury and cancer. A recent study by Perelli et al. demonstrates that EMT confers an evolutionary advantage to tumors by inducing chromosomal instability, structural genomic rearrangements and chromothripsis, thus favoring the emergence of high-fitness malignant clones.</p>\",\"PeriodicalId\":50199,\"journal\":{\"name\":\"Journal of Experimental & Clinical Cancer Research\",\"volume\":\"44 1\",\"pages\":\"135\"},\"PeriodicalIF\":11.4000,\"publicationDate\":\"2025-04-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12042499/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Experimental & Clinical Cancer Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s13046-025-03402-x\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Experimental & Clinical Cancer Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13046-025-03402-x","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}
Epithelial-to-mesenchymal transition drives cancer genomic instability.
Epithelial-to-Mesenchymal Transition (EMT) is a form of embryonic cell plasticity reactivated in adult cells during injury and cancer. A recent study by Perelli et al. demonstrates that EMT confers an evolutionary advantage to tumors by inducing chromosomal instability, structural genomic rearrangements and chromothripsis, thus favoring the emergence of high-fitness malignant clones.
期刊介绍:
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