| 弥漫性大B细胞淋巴瘤发病分子遗传机制的研究进展 |
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| 引用本文： | 崔蕴博,方琳,刘静.弥漫性大B细胞淋巴瘤发病分子遗传机制的研究进展[J].生命科学研究,2012,16(4):357-361. |
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| 作者姓名： | 崔蕴博 方琳 刘静 |
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| 作者单位： | 中南大学生物科学与技术学院分子生物学研究中心,中国湖南长沙,410078 |
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| 基金项目： | 教育部新世纪优秀人才计划项目(NCET-11-0518);国家自然科学基金资助项目(30971517);中央高校基本科研业务费资助项目(2011JQ015);中南大学研究生创新课题项目(2011ssxt133) |
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| 摘 要： | 弥漫大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)是恶性淋巴瘤REAL(revised European-American lymphoma)分类和WHO(world health organization)分类中最常见的非霍奇金淋巴瘤(non-hodgkin lym-phoma,NHL)类型,DLBCL是一种异质性很强的病症,发病机制错综复杂,涉及染色体易位,其中bcl-6基因的3q27染色体易位较为常见,还涉及bcl-2基因t(14;18)(q32;q21)的易位,以及t(8;14)(q24;q32)与IgH基因融合所发生的病变;异常体细胞高频突变涉及pim-1、myc、RhoH/TTF和PAX5等原癌基因;p53基因失活与其他基因突变;p16基因的沉默表达;原癌基因rel、myc和bcl-2扩增等多个方面,从以上方面总结不同基因病变在DLBCL发病中的作用.
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| 关 键 词： | 易位 异常体细胞高频突变 基因缺失 基因突变 基因扩增 多态性 |
Progresses on Molecular Pathogenesis of Diffuse Large B-cell Lymphoma |
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| CUI Yun-bo
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FANG Lin
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LIU Jing.Progresses on Molecular Pathogenesis of Diffuse Large B-cell Lymphoma[J].Life Science Research,2012,16(4):357-361. |
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| Authors: | CUI Yun-bo FANG Lin LIU Jing |
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| Institution: | (Molecular Biology Research Center,School of Biological Science and Technology,Central South University,Changsha 410078,Hunan,China) |
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| Abstract: | Diffuse large B-cell lymphoma is the most commonplace type of non-hodgkin’s lymphoma in ma-lignant lymphoma according to the Revised European-American Lymphoma(REAL) and World Health Organi-zation(WHO) classification.Diffuse distribution is the pathological feature of malignant large-B lymphoma in-cluding many morphological variants and subtypes.Diffuse large B-cell lymphoma is a genetically and clinically heterogeneous disease.The molecular pathogenesis of DLBCL is very complex involving recurrent translocation of chromosomal 3q27 of bcl-6 and t(14;18)(q32;q21) of bcl-2,abnormal somatic aberration of Proto-oncogene pim-1,c-myc,RhoH/TTF,and PAX5,genetic deletion and point mutation of p53,the epige-netic silence of p16 and the over amplification of Proto-oncogene rel,myc,bcl-2.The function of each gene lesion in DLBCL are reviewed. |
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| Keywords: | chromosomal translocation abnormal somatic aberration gene deletion gene mutation gene amplification polymorphisms |
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