作者: A. Kotani , N. Kakazu , T. Tsuruyama , I.-m. Okazaki , M. Muramatsu
关键词: Cytidine deaminase 、 Activation-induced (cytidine) deaminase 、 Biology 、 Somatic hypermutation 、 Immunoglobulin class switching 、 Progenitor cell 、 B cell 、 Lymphoma 、 Transgene 、 Cancer research
摘要: Activation-induced cytidine deaminase (AID), which is essential to both class switch recombination and somatic hypermutation of the Ig gene, expressed in many types human B cell lymphoma/leukemia. AID a potent mutator because it involved DNA breakage not only but also other genes, including proto-oncogenes. Recent studies suggest that required for chromosomal translocation involving cmyc loci. However, unclear whether plays roles tumorigenesis. We examined effect deficiency on generation surface Ig-positive lymphomas Emu-cmyc transgenic mice. Almost all developed AID-deficient mice were pre-B lymphomas, whereas control had predominantly indicating development from overexpressing tumor progenitors. Thus, may play multiple lymphomagenesis.