Rasighaemi Parisa, Ward Alister C
School of Medicine and Centre for Molecular and Medical Research, Deakin University, Geelong, Victoria, 3216, Australia.
Crit Rev Oncol Hematol. 2017 Aug;116:106-115. doi: 10.1016/j.critrevonc.2017.05.011. Epub 2017 Jun 3.
ETV6 (TEL1) and ETV7 (TEL2) are closely-related members of the ETS family of transcriptional regulators. Both ETV6 and ETV7 have been demonstrated to play key roles in hematopoiesis, particularly with regard to maintenance of hematopoietic stem cells and control of lineage-specific differentiation, with evidence of functional interactions between both proteins. ETV6 has been strongly implicated in the molecular etiology of a number of hematopoietic diseases, including as a tumor suppressor, an oncogenic fusion partner, and an important regulator of thrombopoiesis, but recent evidence has also identified ETV7 as a potential oncogene in certain malignancies. This review provides an overview of ETV6 and ETV7 and their contribution to both normal and disrupted hematopoiesis. It also highlights the key clinical implications of the growing knowledge base regarding ETV6 abnormalities with respect to prognosis and treatment.
ETV6（TEL1）和ETV7（TEL2）是ETS转录调节因子家族中密切相关的成员。ETV6和ETV7均已被证明在造血过程中发挥关键作用，特别是在维持造血干细胞和控制谱系特异性分化方面，并且有证据表明这两种蛋白质之间存在功能相互作用。ETV6与多种造血疾病的分子病因密切相关，包括作为肿瘤抑制因子、致癌融合伴侣以及血小板生成的重要调节因子，但最近的证据也表明ETV7在某些恶性肿瘤中是一种潜在的癌基因。本综述概述了ETV6和ETV7及其对正常和异常造血的贡献。它还强调了关于ETV6异常在预后和治疗方面的知识不断增加所带来的关键临床意义。
