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HIV-1 Tat and AIDS-associated cancer: targeting the cellular anti-cancer barrier?
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 link...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2008
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2438332/ https://www.ncbi.nlm.nih.gov/pubmed/18577246 http://dx.doi.org/10.1186/1756-9966-27-3 |
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author | Nunnari, Giuseppe Smith, Johanna A Daniel, René |
author_facet | Nunnari, Giuseppe Smith, Johanna A Daniel, René |
author_sort | Nunnari, Giuseppe |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-2438332 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-24383322008-06-25 HIV-1 Tat and AIDS-associated cancer: targeting the cellular anti-cancer barrier? Nunnari, Giuseppe Smith, Johanna A Daniel, René J Exp Clin Cancer Res Review 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. BioMed Central 2008-05-15 /pmc/articles/PMC2438332/ /pubmed/18577246 http://dx.doi.org/10.1186/1756-9966-27-3 Text en Copyright © 2008 Nunnari et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Nunnari, Giuseppe Smith, Johanna A Daniel, René HIV-1 Tat and AIDS-associated cancer: targeting the cellular anti-cancer barrier? |
title | HIV-1 Tat and AIDS-associated cancer: targeting the cellular anti-cancer barrier? |
title_full | HIV-1 Tat and AIDS-associated cancer: targeting the cellular anti-cancer barrier? |
title_fullStr | HIV-1 Tat and AIDS-associated cancer: targeting the cellular anti-cancer barrier? |
title_full_unstemmed | HIV-1 Tat and AIDS-associated cancer: targeting the cellular anti-cancer barrier? |
title_short | HIV-1 Tat and AIDS-associated cancer: targeting the cellular anti-cancer barrier? |
title_sort | hiv-1 tat and aids-associated cancer: targeting the cellular anti-cancer barrier? |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2438332/ https://www.ncbi.nlm.nih.gov/pubmed/18577246 http://dx.doi.org/10.1186/1756-9966-27-3 |
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