Unniraman Shyam, Schatz David G
Howard Hughes Medical Institute/Section of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.
DNA Repair (Amst). 2006 Sep 8;5(9-10):1259-64. doi: 10.1016/j.dnarep.2006.05.019. Epub 2006 Jun 19.
Chromosomal translocations involving Ig heavy chain switch regions and an oncogene, like Myc, represent early initiating events in the development of many B cell malignancies. These translocations are widely believed to result from aberrant class switch recombination (CSR). Recent reports have produced conflicting models for the role of activation-induced cytidine deaminase (AID) in this process. Here, we discuss possible roles of AID, CSR, and somatic hypermutation in generating chromosomal translocations and in tumor progression.
涉及免疫球蛋白重链转换区和癌基因(如Myc)的染色体易位,是许多B细胞恶性肿瘤发生发展过程中的早期起始事件。人们普遍认为这些易位是由异常的类别转换重组(CSR)导致的。最近的报告针对激活诱导的胞嘧啶脱氨酶(AID)在此过程中的作用提出了相互矛盾的模型。在这里,我们讨论了AID、CSR和体细胞高频突变在产生染色体易位及肿瘤进展中的可能作用。