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Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37
Unfortunately, the mutagenic activities of chemotherapy and radiotherapy can provoke development of therapy-induced malignancies in cancer survivors. Non-mutagenic anti-cancer therapies may be less likely to trigger subsequent malignant neoplasms. Here we present data regarding the DNA damaging and...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4773390/ https://www.ncbi.nlm.nih.gov/pubmed/26958630 http://dx.doi.org/10.1016/j.dib.2016.01.013 |
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author | Green, Maja M. Shekhar, Tanmay M. Hawkins, Christine J. |
author_facet | Green, Maja M. Shekhar, Tanmay M. Hawkins, Christine J. |
author_sort | Green, Maja M. |
collection | PubMed |
description | Unfortunately, the mutagenic activities of chemotherapy and radiotherapy can provoke development of therapy-induced malignancies in cancer survivors. Non-mutagenic anti-cancer therapies may be less likely to trigger subsequent malignant neoplasms. Here we present data regarding the DNA damaging and mutagenic potential of two drugs that antagonize proteins within the Bcl-2 family: ABT-263/Navitoclax and TW-37. Our data reveal that concentrations of these agents that stimulated Bax/Bak-dependent signaling provoked little DNA damage and failed to trigger mutations in surviving cells. The data supplied in this article is related to the research work entitled "Inhibition of Bcl-2 or IAP proteins does not provoke mutations in surviving cells" [1]. |
format | Online Article Text |
id | pubmed-4773390 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-47733902016-03-08 Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37 Green, Maja M. Shekhar, Tanmay M. Hawkins, Christine J. Data Brief Data Article Unfortunately, the mutagenic activities of chemotherapy and radiotherapy can provoke development of therapy-induced malignancies in cancer survivors. Non-mutagenic anti-cancer therapies may be less likely to trigger subsequent malignant neoplasms. Here we present data regarding the DNA damaging and mutagenic potential of two drugs that antagonize proteins within the Bcl-2 family: ABT-263/Navitoclax and TW-37. Our data reveal that concentrations of these agents that stimulated Bax/Bak-dependent signaling provoked little DNA damage and failed to trigger mutations in surviving cells. The data supplied in this article is related to the research work entitled "Inhibition of Bcl-2 or IAP proteins does not provoke mutations in surviving cells" [1]. Elsevier 2016-01-16 /pmc/articles/PMC4773390/ /pubmed/26958630 http://dx.doi.org/10.1016/j.dib.2016.01.013 Text en © 2016 Published by Elsevier Inc. http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Data Article Green, Maja M. Shekhar, Tanmay M. Hawkins, Christine J. Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37 |
title | Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37 |
title_full | Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37 |
title_fullStr | Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37 |
title_full_unstemmed | Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37 |
title_short | Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37 |
title_sort | data on the dna damaging and mutagenic potential of the bh3-mimetics abt-263/navitoclax and tw-37 |
topic | Data Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4773390/ https://www.ncbi.nlm.nih.gov/pubmed/26958630 http://dx.doi.org/10.1016/j.dib.2016.01.013 |
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