Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37
Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37
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DOI：
10.1016/j.dib.2016.01.013
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发表时间：
2016-03-01
期刊：
影响因子：
1.2
通讯作者：
Hawkins, Christine J.
中科院分区：
文献类型：
--
作者：
Green, Maja M.;Shekhar, Tanmay M.;Hawkins, Christine J.
不幸的是，化疗和放疗的致突变活性可在癌症幸存者中引起治疗诱导的恶性肿瘤的发展。非诱变性抗癌疗法可能不太可能引发随后的恶性肿瘤。在这里，我们提出的数据有关的DNA损伤和诱变潜力的两种药物，拮抗Bcl-2家族内的蛋白质：ABT-263/Navitoclax和TW-37。我们的数据显示，这些药物的浓度刺激Bax/Bak依赖性信号转导引起的DNA损伤很小，并且未能触发存活细胞的突变。本文提供的数据与题为“抑制Bcl-2或IAP蛋白不会引起存活细胞突变”的研究工作有关[1]。(C)2016作者爱思唯尔公司出版
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]. (C) 2016 The Authors. Published by Elsevier Inc.