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作 者:陈尔 裴仁治 Chen Er;Pei Renzhi(Department of Hematology,Yinzhou People's Hospital,Medicine School of Ningbo University,Ningbo 315040)
机构地区:[1]宁波大学医学院附属鄞州人民医院血液内科,浙江宁波315040
出 处:《白血病.淋巴瘤》2019年第10期631-634,共4页Journal of Leukemia & Lymphoma
摘 要:伯基特淋巴瘤(BL)是一种起源于B细胞生发中心且具有高度侵袭性的非霍奇金淋巴瘤(NHL),分为地方性、散发性和免疫缺陷相关性三类。其特征是c-myc易位到Ig位点的高活性转录区引起的c-myc表达失调,最终导致细胞过度增殖和肿瘤快速发展。但单独的myc失调不足以阐明BL的发病机制和疾病进展。近年来,随着分子生物学技术的发展,对BL致癌机制有了更深入的研究,有望为BL的临床诊断及新型靶向治疗药物的研发提供理论基础。Burkitt lymphoma(BL)is a highly aggressive B-cell non-Hodgkin lymphoma(NHL)derived from germinal center B cells,which can be divided into endemic,sporadic and immunodeficiency-associated types.BL is characterized by c-myc deregulation due to translocation of c-myc gene to an immunoglobulin enhancer region,resulting in excessive cell proliferation and rapid tumor progression,however the dysregulation of myc alone can't explain the pathogenesis and progression of BL.With the development of molecular biology technology in recent years,the further research on molecular mechanisms of BL pathogenesis may provide a theoretical basis of for clinical diagnosis and targeted drug therapy.This review discusses the progress of pathogenesis in BL.
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