Green Maja M, Shekhar Tanmay M, Hawkins Christine J
Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria 3086, Australia.
Data Brief. 2016 Jan 16;6:710-4. doi: 10.1016/j.dib.2016.01.013. eCollection 2016 Mar.
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].
不幸的是，化疗和放疗的诱变活性可促使癌症幸存者发生治疗诱导的恶性肿瘤。非诱变的抗癌疗法引发后续恶性肿瘤的可能性可能较小。在此，我们展示了关于两种拮抗Bcl-2家族蛋白的药物——ABT-263/维托克洛司和TW-37的DNA损伤和诱变潜力的数据。我们的数据显示，这些药物刺激Bax/Bak依赖性信号传导的浓度几乎不会引起DNA损伤，也不会在存活细胞中引发突变。本文提供的数据与题为“抑制Bcl-2或IAP蛋白不会在存活细胞中引发突变”的研究工作相关[1]。
