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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...

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Autores principales: 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.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Association for the Advancement of Science 2021
Materias:
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.
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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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