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Notch信号通路在乳腺癌干细胞中的研究进展
引用本文:郭瑢,张瑾. Notch信号通路在乳腺癌干细胞中的研究进展[J]. 中国肿瘤临床, 2014, 41(14): 938-941. DOI: 10.3969/j.issn.1000-8179.20140812
作者姓名:郭瑢  张瑾
作者单位:天津医科大学肿瘤医院乳腺肿瘤三科,国家肿瘤临床医学研究中心,中国天津乳腺癌防治研究中心,天津市肿瘤防治重点实验室,乳腺癌防治教育部重点实验室(天津市 300060)
基金项目:天津市科技项目12ZCDZSY15700
摘    要:乳腺癌干细胞是一群具有自我更新及多向分化潜能的细胞,在乳腺癌的发生、发展以及转移、复发中起着极其重要的作用。正常情况下,乳腺干细胞的分化、更新能力受相关信号转导通路的严格调控,当这些信号通路发生异常干细胞将会异常分化,形成乳腺癌干细胞,并无限增殖形成肿瘤。随着人们对乳腺癌干细胞的深入研究,Notch信号通路与其他信号通路的相互作用对乳腺癌干细胞的调控逐渐被人们所重视。本文为进一步了解Notch信号通路在乳腺癌的发生、发展以及靶向治疗中的重要意义,结合乳腺癌干细胞信号通路的最新研究进展进行综述。 

关 键 词:Notch   信号通路   乳腺癌   乳腺癌干细胞   靶向治疗
收稿时间:2014-05-15

Research progress in notch signaling pathway in breast cancer stem cells
Affiliation:The Third Department of Breast Cancer, China Tianjin Breast Cancer Prevention, Treatment, and Research Center, Tianjin Medical University Cancer Institute and Hospital; National Clinical Research Center of Cancer, Key Laboratory of Breast Cancer Prevention and Therapy of Ministry of Education, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China
Abstract:Breast cancer stem cells (BCSC) are group of cells exhibiting self-renewal and multi-directional differentiation potentials. These cells have an important role in the occurrence, development, metastasis, and recurrence of breast cancer. In normal circumstances, the ability of mammary stem cells to differentiate and undergo self-renewal is governed by related signaling pathways. After this mechanism is destroyed, breast stem cells undergo abnormal differentiation, forming breast cancer stem cells that unlimitedly proliferate to develop into breast cancer. As research on BCSC increasingly deepens, regulation of BCSC by notch signaling and its crosstalk with several signaling pathways have drawn a great deal of attention in this field. This paper reports the signaling pathways of breast cancer stem cells and latest studies on this field to better understand the essential role of notch signaling pathway in the occurrence and development of breast cancer and corresponding clinical targeted therapy. 
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