Heidari Nazanin, Abroun Saeid, Bertacchini Jessika, Vosoughi Tina, Rahim Fakher, Saki Najmaldin
Health Research Institute, Thalassemia and Hemoglobinopathy Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Department of Hematology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Cell J. 2017 Spring;19(Suppl 1):9-26. doi: 10.22074/cellj.2017.4908. Epub 2017 May 17.
Epigenetic and genetic alterations are two mechanisms participating in leukemia, which can inactivate genes involved in leukemia pathogenesis or progression. The purpose of this review was to introduce various inactivated genes and evaluate their possible role in leukemia pathogenesis and prognosis. By searching the mesh words "Gene, Silencing AND Leukemia" in PubMed website, relevant English articles dealt with human subjects as of 2000 were included in this study. Gene inactivation in leukemia is largely mediated by promoter's hypermethylation of gene involving in cellular functions such as cell cycle, apoptosis, and gene transcription. Inactivated genes, such as and , may correlate with poor prognosis in acute lymphoid leukemia (ALL), chronic lymphoid leukemia (CLL), chronic myelogenous leukemia (CML) and acute myeloid leukemia (AML), respectively. Gene inactivation may play a considerable role in leukemia pathogenesis and prognosis, which can be considered as complementary diagnostic tests to differentiate different leukemia types, determine leukemia prognosis, and also detect response to therapy. In general, this review showed some genes inactivated only in leukemia (with differences between B-ALL, T-ALL, CLL, AML and CML). These differences could be of interest as an additional tool to better categorize leukemia types. Furthermore; based on inactivated genes, a diverse classification of Leukemias could represent a powerful method to address a targeted therapy of the patients, in order to minimize side effects of conventional therapies and to enhance new drug strategies.
表观遗传和基因改变是参与白血病的两种机制，它们可使参与白血病发病机制或进展的基因失活。本综述的目的是介绍各种失活基因，并评估它们在白血病发病机制和预后中的可能作用。通过在PubMed网站上搜索主题词“基因，沉默与白血病”，纳入了自2000年以来涉及人类受试者的相关英文文章。白血病中的基因失活很大程度上是由涉及细胞周期、细胞凋亡和基因转录等细胞功能的基因启动子高甲基化介导的。失活基因，如[具体基因1]和[具体基因2]，可能分别与急性淋巴细胞白血病（ALL）、慢性淋巴细胞白血病（CLL）、慢性粒细胞白血病（CML）和急性髓细胞白血病（AML）的不良预后相关。基因失活可能在白血病发病机制和预后中发挥重要作用，可作为区分不同白血病类型、确定白血病预后以及检测治疗反应的补充诊断测试。总体而言，本综述显示一些基因仅在白血病中失活（B-ALL、T-ALL、CLL、AML和CML之间存在差异）。这些差异可能作为更好地对白血病类型进行分类的附加工具而受到关注。此外，基于失活基因，对白血病进行多样化分类可能是一种强大的方法，用于针对患者进行靶向治疗，以尽量减少传统疗法的副作用并加强新的药物策略。
