Activation-induced cytidine deaminase (AID) promotes B cell lymphomagenesis in Emu-cmyc transgenic mice

被引：60

作者：

Kotani, Ai

Kakazu, Naoki

Tsuruyama, Tatsuaki

Okazaki, Il-mi

Muramatsu, Masamichi

Kinoshita, Kazuo

Nagaoka, Hitoshi

Yabe, Daisuke

Honjo, Tasuku

机构：

[1] Kyoto Univ, Grad Sch Med, Dept Immunol & Genom Med, Sakyo Ku, Kyoto 6068501, Japan

[2] Kyoto Univ, Grad Sch Med, Dept Pathol & Biol Dis, Sakyo Ku, Kyoto 6068501, Japan

[3] Shimane Univ, Sch Med, Dept Environm & Prevent Med, Izumo, Shimane 6938501, Japan

[4] Shiga Med Inst, Shiga 5248524, Japan

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2007年 / 104卷 / 05期

关键词：

somatic hypermutation; Pim1; secondary hit; clonal expansion;

D O I：

10.1073/pnas.0610732104

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Activation-induced cytidine deaminase (AID), which is essential to both class switch recombination and somatic hypermutation of the Ig gene, is expressed in many types of human B cell lymphoma/ leukemia. AID is a potent mutator because it is involved in DNA breakage not only of Ig but also of other genes, including proto-oncogenes. Recent studies suggest that AID is required for chromosomal translocation involving cmyc and Ig loci. However, it is unclear whether AID plays other roles in tumorigenesis. We examined the effect of AID deficiency on the generation of surface Ig-positive B cell lymphomas in Emu-cmyc transgenic mice. Almost all lymphomas that developed in AID-deficient transgenic mice were pre-B cell lymphomas, whereas control transgenic mice had predominantly B cell lymphomas, indicating that AID is required for development of B but not pre-B cell lymphomas from cmyc overexpressing tumor progenitors. Thus, AID may play multiple roles in B cell lymphomagenesis.

引用

页码：1616 / 1620

页数：5

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