Document Type

Article

Publication Date

1-1-2008

Comments

This article has been peer reviewed and is published in BMC Journal of Experimental and Clinical Cancer Research Volume 27, Issue 1, 2008, Article number 3. The published version is available at DOI: 10.1186/1756-9966-27-3. Copyright © BioMed Central Ltd.

Abstract

The acquired immunodeficiency syndrome (AIDS) is accompanied by a significant increase in the incidence of neoplasms. Several causative agents have been proposed for this phenomenon. These include immunodeficiency and oncogenic DNA viruses and the HIV-1 protein Tat. Cancer in general is closely linked to genomic instability and DNA repair mechanisms. The latter maintains genomic stability and serves as a cellular anti-cancer barrier. Defects in DNA repair pathway are associated with carcinogenesis. This review focuses on newly discovered connections of the HIV-1 protein Tat, as well as cellular co-factors of Tat, to double-strand break DNA repair. We propose that the Tat-induced DNA repair deficiencies may play a significant role in the development of AIDS-associated cancer.