Inhibition of DNA synthesis is a potent mechanism by which cytostatic drugs induce homologous recombination in mammalian cells (Q40845470)

24 September 2017

Inhibition of DNA synthesis is a potent mechanism by which cytostatic drugs induce homologous recombination in mammalian cells (English)

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24 September 2017

4

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24 September 2017

Arnaudeau C

1

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24 September 2017

Tenorio Miranda E

series ordinal

2

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24 September 2017

Jenssen D

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3

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24 September 2017

language of work or name

English

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publication date

1 November 2000

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24 September 2017

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24 September 2017

461

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24 September 2017

3

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24 September 2017

221-228

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Mitotic recombination produces the majority of recessive fibroblast variants in heterozygous mice.

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Antioncogenes and human cancer

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The role of mitotic recombination in carcinogenesis

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Increase of spontaneous intrachromosomal homologous recombination in mammalian cells expressing a mutant p53 protein

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p53 is linked directly to homologous recombination processes via RAD51/RecA protein interaction

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A partial hprt gene duplication generated by non-homologous recombination in V79 Chinese hamster cells is eliminated by homologous recombination

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Effects of carcinogenic agents upon different mechanisms for intragenic recombination in mammalian cells

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Relationship between pharmacokinetic parameters in patients and cytotoxicity in vitro of standard and investigational anticancer drugs

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Mutagenic and carcinogenic properties of platinum-based anticancer drugs

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International Commission for Protection Against Environmental Mutagens and Carcinogens. The subtlety of alkylating agents in reactions with biological macromolecules

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Evaluation of synergism of drugs cis-mdiamminedichloroplatinum (II) and arabinosylcytosine on the level of chemical interaction with DNA and on the growth of mouse leukemia

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International Commission for Protection Against Environmental Mutagens and Carcinogens. Mutagenicity and carcinogenicity of topoisomerase-interactive agents

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Tubulin as a target for anticancer drugs: agents which interact with the mitotic spindle.

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Mechanistic and methodological aspects of chemically-induced somatic mutation and recombination in Drosophila melanogaster.

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Studies on intrachromosomal recombination in SP5/V79 Chinese hamster cells upon exposure to different agents related to carcinogenesis.

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Induction, by thymidylate stress, of genetic recombination as evidenced by deletion of a transferred genetic marker in mouse FM3A cells

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Inversion due to intrachromosomal recombination produced by carcinogens in a transgenic mouse model

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Characterization of mutants involving partial exon duplications in the hprt gene of Chinese hamster V79 cells

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The RAD51 protein supports homologous recombination by an exchange mechanism in mammalian cells

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Chromosome breaks and genomic instability

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Sister chromatid fusion initiates amplification of the dihydrofolate reductase gene in Chinese hamster cells

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Site specificity of N-methyl-N-nitrosourea-induced transition mutations in the hprt gene.

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Toxicity and mutagenicity of 6 anti-cancer drugs in Chinese hamster V79 cells co-cultured with rat hepatocytes.

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Synergistic enhancement of the frequency of chromatid aberrations in cultured human lymphocytes by combinations of inhibitors of DNA repair

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DNA synthesis inhibition as an indirect mechanism of chromosome aberrations: comparison of DNA-reactive and non-DNA-reactive clastogens

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Nonrandom distribution of methotrexate-induced aberrations on human chromosomes. Detection of further folic acid sensitive fragile sites

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Effects of inhibitors of DNA synthesis on spontaneous and ultraviolet light-induced sister-chromatid exchanges in Chinese hamster cells

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Arsenic[III] and heavy metal ions induce intrachromosomal homologous recombination in the hprt gene of V79 Chinese hamster cells

1 reference

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Cis-platinum(II) diamine dichloride causes mutation, transformation, and sister-chromatid exchanges in cultured mammalian cells

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Molecular analysis of mutation at the hprt locus of Chinese hamster V79 cells induced by ethyl methanesulphonate and mitomycin C

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DOI

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24 September 2017

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