恶性肿瘤
造血
髓样
髓系白血病
克隆(Java方法)
疾病
表观遗传学
生物
癌症的体细胞进化
祖细胞
癌症研究
免疫学
医学
干细胞
病理
癌症
遗传学
基因
作者
Juan Bautista Menendez-Gonzalez,Neil P. Rodrigues
出处
期刊:Methods in molecular biology
日期:2022-01-01
卷期号:: 73-88
被引量:4
标识
DOI:10.1007/978-1-0716-1924-7_5
摘要
Outgrowth of a mutated hematopoietic stem/progenitor clone and its descendants, also known as clonal hematopoiesis, has long been considered as either a potential forerunner to hematologic malignancy or as a clinically silent phase in leukemia that antedates symptomatic disease. That definition of clonal hematopoiesis has now been expanded to encompass patients who harbor specific genetic/epigenetic mutations that lead to clonal hematopoiesis of indeterminate potential (CHIP) and, with it, a relatively heightened risk for both myeloid malignancy and atherosclerosis during aging. In this review, we provide contemporary insights into the cellular and molecular basis for CHIP and explore the relationship of CHIP to myeloid malignancy and atherosclerosis. We also discuss emerging strategies to explore CHIP biology and clinical targeting of CHIP related malignancy and cardiovascular disease.
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