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SAMHD1 is a barrier to antimetabolite-based cancer therapies
The outcome of acute myelogenous leukemia (AML) therapy depends on the propensity of leukemic blasts to accumulate ara-CTP, the active triphosphate of cytarabine (ara-C). We identified sterile α motif and HD domain-containing protein 1 (SAMHD1) as an ara-CTPase that protects cancer cells from cytara...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5383367/ https://www.ncbi.nlm.nih.gov/pubmed/28401188 http://dx.doi.org/10.1080/23723556.2017.1287554 |
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author | Rudd, Sean G. Schaller, Torsten Herold, Nikolas |
author_facet | Rudd, Sean G. Schaller, Torsten Herold, Nikolas |
author_sort | Rudd, Sean G. |
collection | PubMed |
description | The outcome of acute myelogenous leukemia (AML) therapy depends on the propensity of leukemic blasts to accumulate ara-CTP, the active triphosphate of cytarabine (ara-C). We identified sterile α motif and HD domain-containing protein 1 (SAMHD1) as an ara-CTPase that protects cancer cells from cytarabine-induced toxicity. Therefore, we propose targeting SAMHD1 as a strategy to potentiate cytarabine and possibly other antimetabolite-based therapies. |
format | Online Article Text |
id | pubmed-5383367 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-53833672018-02-03 SAMHD1 is a barrier to antimetabolite-based cancer therapies Rudd, Sean G. Schaller, Torsten Herold, Nikolas Mol Cell Oncol Author's View The outcome of acute myelogenous leukemia (AML) therapy depends on the propensity of leukemic blasts to accumulate ara-CTP, the active triphosphate of cytarabine (ara-C). We identified sterile α motif and HD domain-containing protein 1 (SAMHD1) as an ara-CTPase that protects cancer cells from cytarabine-induced toxicity. Therefore, we propose targeting SAMHD1 as a strategy to potentiate cytarabine and possibly other antimetabolite-based therapies. Taylor & Francis 2017-02-03 /pmc/articles/PMC5383367/ /pubmed/28401188 http://dx.doi.org/10.1080/23723556.2017.1287554 Text en © 2017 The Author(s). Published with license by Taylor & Francis Group, LLC http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way. |
spellingShingle | Author's View Rudd, Sean G. Schaller, Torsten Herold, Nikolas SAMHD1 is a barrier to antimetabolite-based cancer therapies |
title | SAMHD1 is a barrier to antimetabolite-based cancer therapies |
title_full | SAMHD1 is a barrier to antimetabolite-based cancer therapies |
title_fullStr | SAMHD1 is a barrier to antimetabolite-based cancer therapies |
title_full_unstemmed | SAMHD1 is a barrier to antimetabolite-based cancer therapies |
title_short | SAMHD1 is a barrier to antimetabolite-based cancer therapies |
title_sort | samhd1 is a barrier to antimetabolite-based cancer therapies |
topic | Author's View |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5383367/ https://www.ncbi.nlm.nih.gov/pubmed/28401188 http://dx.doi.org/10.1080/23723556.2017.1287554 |
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