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Insertional activation of STAT3 and LCK by HIV-1 proviruses in T cell lymphomas
Retroviruses cause cancers in animals by integrating in or near oncogenes. Although HIV-1 infection increases the risk of cancer, most of the risk is associated with immunodeficiency and coinfection by oncogenic virus (Epstein-Barr virus, Kaposi sarcoma herpesvirus, and human papillomavirus). HIV-1...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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American Association for the Advancement of Science
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8514100/ https://www.ncbi.nlm.nih.gov/pubmed/34644108 http://dx.doi.org/10.1126/sciadv.abi8795 |
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author | Mellors, John W. Guo, Shuang Naqvi, Asma Brandt, Leah D. Su, Ling Sun, Zhonghe Joseph, Kevin W. Demirov, Dimiter Halvas, Elias K. Butcher, Donna Scott, Beth Hamilton, Aaron Heil, Marintha Karim, Baktiar Wu, Xiaolin Hughes, Stephen H. |
author_facet | Mellors, John W. Guo, Shuang Naqvi, Asma Brandt, Leah D. Su, Ling Sun, Zhonghe Joseph, Kevin W. Demirov, Dimiter Halvas, Elias K. Butcher, Donna Scott, Beth Hamilton, Aaron Heil, Marintha Karim, Baktiar Wu, Xiaolin Hughes, Stephen H. |
author_sort | Mellors, John W. |
collection | PubMed |
description | Retroviruses cause cancers in animals by integrating in or near oncogenes. Although HIV-1 infection increases the risk of cancer, most of the risk is associated with immunodeficiency and coinfection by oncogenic virus (Epstein-Barr virus, Kaposi sarcoma herpesvirus, and human papillomavirus). HIV-1 proviruses integrated in some oncogenes cause clonal expansion of infected T cells in vivo; however, the infected cells are not transformed, and it is generally believed that HIV-1 does not cause cancer directly. We show that HIV-1 proviruses integrated in the first introns of signal transducer and activator of transcription 3 (STAT3) and lymphocyte-specific protein tyrosine kinase (LCK) can play an important role in the development of T cell lymphomas. The development of these cancers appears to be a multistep process involving additional nonviral mutations, which could help explain why T cell lymphomas are rare in persons with HIV-1 infection. |
format | Online Article Text |
id | pubmed-8514100 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | American Association for the Advancement of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-85141002021-10-22 Insertional activation of STAT3 and LCK by HIV-1 proviruses in T cell lymphomas Mellors, John W. Guo, Shuang Naqvi, Asma Brandt, Leah D. Su, Ling Sun, Zhonghe Joseph, Kevin W. Demirov, Dimiter Halvas, Elias K. Butcher, Donna Scott, Beth Hamilton, Aaron Heil, Marintha Karim, Baktiar Wu, Xiaolin Hughes, Stephen H. Sci Adv Biomedicine and Life Sciences Retroviruses cause cancers in animals by integrating in or near oncogenes. Although HIV-1 infection increases the risk of cancer, most of the risk is associated with immunodeficiency and coinfection by oncogenic virus (Epstein-Barr virus, Kaposi sarcoma herpesvirus, and human papillomavirus). HIV-1 proviruses integrated in some oncogenes cause clonal expansion of infected T cells in vivo; however, the infected cells are not transformed, and it is generally believed that HIV-1 does not cause cancer directly. We show that HIV-1 proviruses integrated in the first introns of signal transducer and activator of transcription 3 (STAT3) and lymphocyte-specific protein tyrosine kinase (LCK) can play an important role in the development of T cell lymphomas. The development of these cancers appears to be a multistep process involving additional nonviral mutations, which could help explain why T cell lymphomas are rare in persons with HIV-1 infection. American Association for the Advancement of Science 2021-10-13 /pmc/articles/PMC8514100/ /pubmed/34644108 http://dx.doi.org/10.1126/sciadv.abi8795 Text en Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC). https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial license (https://creativecommons.org/licenses/by-nc/4.0/) , which permits use, distribution, and reproduction in any medium, so long as the resultant use is not for commercial advantage and provided the original work is properly cited. |
spellingShingle | Biomedicine and Life Sciences Mellors, John W. Guo, Shuang Naqvi, Asma Brandt, Leah D. Su, Ling Sun, Zhonghe Joseph, Kevin W. Demirov, Dimiter Halvas, Elias K. Butcher, Donna Scott, Beth Hamilton, Aaron Heil, Marintha Karim, Baktiar Wu, Xiaolin Hughes, Stephen H. Insertional activation of STAT3 and LCK by HIV-1 proviruses in T cell lymphomas |
title | Insertional activation of STAT3 and LCK by HIV-1 proviruses in T cell lymphomas |
title_full | Insertional activation of STAT3 and LCK by HIV-1 proviruses in T cell lymphomas |
title_fullStr | Insertional activation of STAT3 and LCK by HIV-1 proviruses in T cell lymphomas |
title_full_unstemmed | Insertional activation of STAT3 and LCK by HIV-1 proviruses in T cell lymphomas |
title_short | Insertional activation of STAT3 and LCK by HIV-1 proviruses in T cell lymphomas |
title_sort | insertional activation of stat3 and lck by hiv-1 proviruses in t cell lymphomas |
topic | Biomedicine and Life Sciences |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8514100/ https://www.ncbi.nlm.nih.gov/pubmed/34644108 http://dx.doi.org/10.1126/sciadv.abi8795 |
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