Abstract
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].
Highlights
Clonogenicity assays, hypoxanthine-guanine phosphoribosyltransferase (HPRT) mutagenesis assays, γH2AX flow cytometry quantitation Normalized data Murine embryonic fibroblasts from wild type or BaxÀ/À, BakÀ/À mice were treated with various concentrations of ABT-263 or TW-37, prior to the assays listed above
Cells were exposed to drugs for various periods of time, washed and either stained with anti-γH2AX for flow cytometry, seeded into normal media to quantitate clonogenicity, or seeded into media containing 6thioguanine to count 6-thioguanine-resistant clones
Data Embryonic fibroblasts derived from wildtype or Bax/Bak-deficient mice were treated with ABT-263 (Fig. 1) or TW-37 (Fig. 2), or incubated in normal medium
Summary
Clonogenicity assays, HPRT mutagenesis assays, γH2AX flow cytometry quantitation Normalized data Murine embryonic fibroblasts from wild type or BaxÀ/À, BakÀ/À mice were treated with various concentrations of ABT-263 or TW-37, prior to the assays listed above. Cells were exposed to drugs (or not) for various periods of time, washed and either stained with anti-γH2AX for flow cytometry, seeded into normal media to quantitate clonogenicity, or seeded into media containing 6thioguanine to count 6-thioguanine-resistant clones (presumably reflecting mutagenesis at the HPRT locus). Future research could define the pathways through which high concentrations of some BH3-. Embryonic fibroblasts derived from wildtype or Bax/Bak-deficient mice were treated with ABT-263 (Fig. 1) or TW-37 (Fig. 2), or incubated in normal medium. We measured the impact of these treatments on survival, DNA damage and mutagenicity at the HPRT locus
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