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Carcinogenesis Advance Access first published online on September 4, 2007
This version published online on October 4, 2007
Carcinogenesis, doi:10.1093/carcin/bgm201
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Oncogenic Events Triggered by AID, the Adverse Effect of Antibody Diversification

Pablo Pérez-Durán1, Virginia G. de Yebenes1 and Almudena R. Ramiro1,*

1 DNA Hypermutation and Cancer group, Spanish Nacional Research Cancer Center, Melchor Fernandez Almagro 3, 28029 Madrid, Spain

* To whom correspondence should be addressed. Tel: 34 91 224 6900, Fax: 34 91 732 8033, email: aramiro{at}cnio.es

The generation of an efficient immune response depends on highly refined mechanisms of antibody diversification. Two of these mechanisms, Somatic HyperMutation (SHM) and Class Switch Recombination (CSR), are initiated by Activation Induced cytidine Deaminase (AID) upon antigen stimulation of mature B cells. AID deaminates cytosines on the DNA of immunoglobulin (Ig) genes thereby generating a lesion that can be processed into a mutation (SHM) or a DNA double strand break followed by a recombination reaction (CSR). A number of mechanisms are likely responsible for regulating AID function, such as transcriptional regulation, subcellular localization, post-transcriptional modifications and target specificity, but the issue remains of how unwanted DNA damage is fully prevented. Most lymphocyte neoplasias are originated from mature B cells and harbour hallmark chromosome translocations of lymphomagenic potential, such as the c-myc/IgH translocations found in Burkitt lymphomas. It has been recently shown that such translocations are initiated by AID and that ATM, p53 and ARF provide surveillance mechanisms to prevent these aberrations. In addition, evidence is accumulating that AID expression can be induced in B cells independently of the germinal center environment, such as in response to some viral infections, and occasionally in non-B cells, at least in certain inflammation-associated neoplasic situations. The most recent findings on AID expression and function and their relevance to the generation of oncogenic lesions will be discussed.

Received August 1, 2007; revised August 27, 2007; accepted August 28, 2007.


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