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      Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37

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      Author(s): , , *
      Publication date (Electronic):
      Journal: Data in Brief
      Publisher: Elsevier

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          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].

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          Expression of phosphorylated histone H2AX in cultured cell lines following exposure to X-rays.

          S Macphail, Yongmei Yu, Jenny E. Chu … (2003)
          Exposure to ionizing radiation results in phosphorylation of histone H2AX (gammaH2AX) at sites of DNA double-strand breaks. To determine the relationship between gammaH2AX formation and radiosensitivity, the rate of formation and loss of gammaH2AX were examined in several cultured cell lines following exposure to 253 kV X-rays. Flow and image cytometry were both performed using a mouse monoclonal antibody against gammaH2AX. Immunoblotting was used to confirm cell line-dependent differences in antibody staining. Cell lines examined included V79 and CHO-K1 hamster cells, the human tumour cell lines SiHa, WiDr, DU145, WIL-2NS, HT144, HCC1937 and U87, and the normal cell strain HFL1. Radiosensitivity was measured using a standard clonogenic assay. Using flow cytometry, gammaH2AX formation was detected 1 h after doses as low as 20 cGy. Peak levels of gammaH2AX were observed within 15-30 min after irradiation and both the rate of radiation-induced gammaH2AX formation and loss were cell type dependent. Maximum levels of gammaH2AX formation were lower for HT144 cells mutant for the ataxia telangiectasia gene. Half-times of loss after irradiation ranged from 1.6 to 7.2 h and were associated with a decrease in the total number of foci per cell. The half-time of loss of gammaH2AX was correlated with clonogenic survival for 10 cell lines (r2=0.66). GammaH2AX can be detected with excellent sensitivity using both flow and image analysis. The rate of gammaH2AX loss may be an important factor in the response of cells to ionizing radiation, with more rapid loss and less retention associated with more radioresistant cell lines.
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            TRAIL treatment provokes mutations in surviving cells

            M Lovric, C J Hawkins (2010)
            Chemotherapy and radiotherapy commonly damage DNA and trigger p53-dependent apoptosis through intrinsic apoptotic pathways. Two unfortunate consequences of this mechanism are resistance due to blockade of p53 or intrinsic apoptosis pathways, and mutagenesis of non-malignant surviving cells which can impair cellular function or provoke second malignancies. Death ligand-based drugs, such as tumor necrosis factor-related apoptosis inducing ligand (TRAIL), stimulate extrinsic apoptotic signaling, and may overcome resistance to treatments that induce intrinsic apoptosis. As death receptor ligation does not damage DNA as a primary mechanism of pro-apoptotic action, we hypothesized that surviving cells would remain genetically unscathed, suggesting that death ligand-based therapies may avoid some of the adverse effects associated with traditional cancer treatments. Surprisingly, however, treatment with sub-lethal concentrations of TRAIL or FasL was mutagenic. Mutations arose in viable cells that contained active caspases, and overexpression of the caspase-8 inhibitor crmA or silencing of caspase-8 abolished TRAIL-mediated mutagenesis. Downregulation of the apoptotic nuclease caspase-activated DNAse (CAD)/DNA fragmentation factor 40 (DFF40) prevented the DNA damage associated with TRAIL treatment. Although death ligands do not need to damage DNA in order to induce apoptosis, surviving cells nevertheless incur DNA damage after treatment with these agents.
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              Mammalian cell HPRT gene mutation assay: test methods.

              George E. Johnson (2012)
              Using the combination of bacterial gene mutation assay and chromosomal aberrations test in mammalian cells may not detect a small proportion of mammalian specific mutagenic agents. Therefore, at the current time a third assay should be used, except for compounds for which there is little or no exposure (DOH (2000) Department of Health Guidance for the testing of chemicals for Mutagenicity. Committee on Mutagenicity of Chemicals in Food, Consumer Products and the Environment). The hypoxanthine phosphorybosyl transferase (HPRT) gene is on the X chromosome of mammalian cells, and it is used as a model gene to investigate gene mutations in mammalian cell lines. The assay can detect a wide range of chemicals capable of causing DNA damage that leads to gene mutation. The test follows a very similar methodology to the thymidine kinase (TK) mouse lymphoma assay (MLA), and both are included in the guidelines for mammalian gene mutation tests (OECD (1997) Organisation for Economic Co-operation and Development. Ninth addendum to the OECD Guidelines for the Testing of Chemicals. In Vitro Mammalian Cell Gene Mutation Test: 476). The HPRT methodology is such that mutations which destroy the functionality of the HPRT gene and or/protein are detected by positive selection using a toxic analogue, and HPRT ( - ) mutants are seen as viable colonies. Unlike bacterial reverse mutation assays, mammalian gene mutation assays respond to a broad spectrum of mutagens, since any mutation resulting in the ablation of gene expression/function produces a HPRT ( - ) mutant. Human cells are readily used, and mechanistic studies using the HPRT test methodology with modifications, such as knock-out cell lines for DNA repair, can provide details of the mode of action (MOA) of the test compound (24).This chapter provides the methodology for carrying out the assay in different cell lines in the presence and absence of metabolism with technical information and general advice on how to carry out the test.
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                Author and article information

                Contributors
                Christine J. Hawkins
                Journal
                Journal ID (nlm-ta): Data Brief
                Journal ID (iso-abbrev): Data Brief
                Title: Data in Brief
                Publisher: Elsevier
                ISSN (Electronic): 2352-3409
                Publication date PMC-release: 16 January 2016
                Publication date Collection: March 2016
                Publication date (Electronic): 16 January 2016
                Volume: 6
                Pages: 710-714
                Affiliations
                [0005]Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria 3086, Australia
                Author notes
                [* ]Corresponding author. Tel.: + 61 3 9479 2339; fax: + 61 3 9479 1266. c.hawkins@ 123456latrobe.edu.au
                Article
                Publisher ID: S2352-3409(16)00019-6
                DOI: 10.1016/j.dib.2016.01.013
                PMC ID: 4773390
                PubMed ID: 26958630
                SO-VID: 6c9a7a48-ed36-4ffd-b453-7e0b17c7fad3
                Copyright © © 2016 Published by Elsevier Inc.
                License:

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 22 September 2015
                Date revision received : 5 January 2016
                Date accepted : 8 January 2016
                Categories
                Subject: Data Article

                Data availability:

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