胞苷脱氨酶
染色体易位
生物
活化诱导(胞苷)脱氨酶
基因
遗传学
免疫球蛋白基因
癌变
B细胞
胞苷
淋巴瘤
断点
体细胞突变
染色体
癌症研究
分子生物学
抗体
免疫学
酶
生物化学
作者
Davide F. Robbiani,Michel C. Nussenzweig
出处
期刊:Annual Review of Pathology-mechanisms of Disease
[Annual Reviews]
日期:2013-01-24
卷期号:8 (1): 79-103
被引量:164
标识
DOI:10.1146/annurev-pathol-020712-164004
摘要
Studies of B cell lymphomas in the early 1980s led to the cloning of genes (c-MYC and IGH) at a chromosome translocation breakpoint. A rush followed to identify recurrently translocated genes in all types of cancer, which led to remarkable advances in our understanding of cancer genetics. B lymphocyte tumors commonly bear chromosome translocations to immunoglobulin genes, which points to a role for antibody gene diversification processes in tumorigenesis. The discovery of activation-induced cytidine deaminase (AID) and the use of murine models to study translocation have led to a new understanding of how these events contribute to the genesis of lymphomas. Here, we review these advances with a focus on AID and insights gained from the study of translocations in primary cells.
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