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急性髓系白血病干细胞干性维持的分子机制

Molecular mechanisms for stemness maintenance of acute myeloid leukemia stem cells.

作者信息

Wang Jiazhen, Wang Peipei, Zhang Tiantian, Gao Zhuying, Wang Jing, Feng Mengdie, Yin Rong, Zhang Haojian

机构信息

The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, China.

Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Wuhan University, Wuhan, China.

出版信息

Blood Sci. 2019 Sep 17;1(1):77-83. doi: 10.1097/BS9.0000000000000020. eCollection 2019 Aug.

Abstract

Human acute myeloid leukemia (AML) is a fatal hematologic malignancy characterized with accumulation of myeloid blasts and differentiation arrest. The development of AML is associated with a serial of genetic and epigenetic alterations mainly occurred in hematopoietic stem and progenitor cells (HSPCs), which change HSPC state at the molecular and cellular levels and transform them into leukemia stem cells (LSCs). LSCs play critical roles in leukemia initiation, progression, and relapse, and need to be eradicated to achieve a cure in clinic. Key to successfully targeting LSCs is to fully understand the unique cellular and molecular mechanisms for maintaining their stemness. Here, we discuss LSCs in AML with a focus on identification of unique biological features of these stem cells to decipher the molecular mechanisms of LSC maintenance.

摘要

人类急性髓系白血病(AML)是一种致命的血液系统恶性肿瘤,其特征为髓系母细胞的积累和分化停滞。AML的发生与一系列主要发生在造血干细胞和祖细胞(HSPCs)中的基因和表观遗传改变有关,这些改变在分子和细胞水平上改变了HSPC的状态,并将它们转化为白血病干细胞(LSCs)。LSCs在白血病的起始、进展和复发中起关键作用,要实现临床治愈就需要根除它们。成功靶向LSCs的关键在于充分了解维持其干性的独特细胞和分子机制。在此,我们讨论AML中的LSCs,重点是识别这些干细胞的独特生物学特征,以破译LSC维持的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3f/8975089/8fa756e59761/bls-1-077-g001.jpg

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