Yen T M Nguyen, Manabu Fujisawa, Shumpei Ishikawa, Mamiko Sakata-Yanagimoto
{"title":"克隆造血与实体癌。","authors":"Yen T M Nguyen, Manabu Fujisawa, Shumpei Ishikawa, Mamiko Sakata-Yanagimoto","doi":"10.1111/cas.70097","DOIUrl":null,"url":null,"abstract":"<p><p>Clonal hematopoiesis refers to the expansion of hematopoietic stem cells harboring somatic mutations, a phenomenon increasingly recognized in aging populations. This review highlights the emerging relationship between clonal hematopoiesis and solid cancers, focusing on the prevalence and impact of clonal hematopoiesis-associated mutations such as DNMT3A, TET2, ASXL1, and TP53 in tumorigenesis. Key risk factors for the co-occurrence of clonal hematopoiesis and solid cancers, including germline genetic factors, aging, and environmental factors, are also discussed. We explore how clonal hematopoiesis mutations shape the tumor microenvironments in solid cancers by modulating immunoregulation, inflammation, and angiogenesis, thereby contributing to tumor progression. These findings underscore the dual role of clonal hematopoiesis as both a marker of cancer risk and a potential driver of solid cancer progression. The clinical implications of clonal hematopoiesis are also considered, including the prognostic value, impact on treatment response, and potential as a therapeutic target. Future directions are outlined to advance our understanding of clonal hematopoiesis and to exploit its clinical potential for cancer management.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":5.7000,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Clonal Hematopoiesis and Solid Cancers.\",\"authors\":\"Yen T M Nguyen, Manabu Fujisawa, Shumpei Ishikawa, Mamiko Sakata-Yanagimoto\",\"doi\":\"10.1111/cas.70097\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Clonal hematopoiesis refers to the expansion of hematopoietic stem cells harboring somatic mutations, a phenomenon increasingly recognized in aging populations. This review highlights the emerging relationship between clonal hematopoiesis and solid cancers, focusing on the prevalence and impact of clonal hematopoiesis-associated mutations such as DNMT3A, TET2, ASXL1, and TP53 in tumorigenesis. Key risk factors for the co-occurrence of clonal hematopoiesis and solid cancers, including germline genetic factors, aging, and environmental factors, are also discussed. We explore how clonal hematopoiesis mutations shape the tumor microenvironments in solid cancers by modulating immunoregulation, inflammation, and angiogenesis, thereby contributing to tumor progression. These findings underscore the dual role of clonal hematopoiesis as both a marker of cancer risk and a potential driver of solid cancer progression. The clinical implications of clonal hematopoiesis are also considered, including the prognostic value, impact on treatment response, and potential as a therapeutic target. Future directions are outlined to advance our understanding of clonal hematopoiesis and to exploit its clinical potential for cancer management.</p>\",\"PeriodicalId\":48943,\"journal\":{\"name\":\"Cancer Science\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":5.7000,\"publicationDate\":\"2025-05-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer Science\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1111/cas.70097\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Science","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/cas.70097","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Medicine","Score":null,"Total":0}
Clonal hematopoiesis refers to the expansion of hematopoietic stem cells harboring somatic mutations, a phenomenon increasingly recognized in aging populations. This review highlights the emerging relationship between clonal hematopoiesis and solid cancers, focusing on the prevalence and impact of clonal hematopoiesis-associated mutations such as DNMT3A, TET2, ASXL1, and TP53 in tumorigenesis. Key risk factors for the co-occurrence of clonal hematopoiesis and solid cancers, including germline genetic factors, aging, and environmental factors, are also discussed. We explore how clonal hematopoiesis mutations shape the tumor microenvironments in solid cancers by modulating immunoregulation, inflammation, and angiogenesis, thereby contributing to tumor progression. These findings underscore the dual role of clonal hematopoiesis as both a marker of cancer risk and a potential driver of solid cancer progression. The clinical implications of clonal hematopoiesis are also considered, including the prognostic value, impact on treatment response, and potential as a therapeutic target. Future directions are outlined to advance our understanding of clonal hematopoiesis and to exploit its clinical potential for cancer management.
期刊介绍:
Cancer Science (formerly Japanese Journal of Cancer Research) is a monthly publication of the Japanese Cancer Association. First published in 1907, the Journal continues to publish original articles, editorials, and letters to the editor, describing original research in the fields of basic, translational and clinical cancer research. The Journal also accepts reports and case reports.
Cancer Science aims to present highly significant and timely findings that have a significant clinical impact on oncologists or that may alter the disease concept of a tumor. The Journal will not publish case reports that describe a rare tumor or condition without new findings to be added to previous reports; combination of different tumors without new suggestive findings for oncological research; remarkable effect of already known treatments without suggestive data to explain the exceptional result. Review articles may also be published.