9-β-D-Arabinofuranosyladenine Increases the Frequency of X-ray Induced Chromosome Abnormalities in Mammalian Cells

Pe, Bryant

doi:10.1080/09553008314550521

Cited by 7 publications

(1 citation statement)

References 15 publications

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“…52], and cell lines specifically hypersensitive to ionising radiation have been reported to be deficient in the repair of D N A double strand breaks [53. 54], This has led to a growing opinion that the double-strand break may be the critical lesion in determining differences in response to DNA-damaging agents between cell lines [55] as well as studies of the rela tionship between double-strand breaks and chromosomal aberrations and cell survival [56,57], More recently, tech niques to measure the fidelity of double-strand break repair have been established using plasmid transfection techniques [58. 55],…”

Section: Dna Repairmentioning

confidence: 99%

Genomic Instability and Metastatic Progression

Usmani

1993

Pathobiology

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Recently, there has been a growing body of opinion that tumour cells progress from a less malignant to a more malignant (metastatic) phenotype, due to an inherent instability within the genome. It has also been suggested that genomic instability and the rate of generation of metastatic variants both increase as the tumour cells achieve a higher state of malignancy. In this review, several different aspects of genomic instability have been discussed with particular reference to the low (Fl) and high (BL6, ML8) metastatic variants of a B16 murine melanoma. The induced mutation frequency, gene amplification, and sister chromatid recombination correlated with the order of metastatic potential. Survival data for x-irradiation and bleomycin were similar between the three cell lines. When these agents were used to induce strand breakage, no difference was detectable in either the rate or extent of DNA single or double strand break repair. The fidelity of double strand break religation was measured using the PMH16 plasmid, and the frequency of homologous recombination was measured using the DR plasmid. Surprisingly, both of these parameters showed a correlation with metastasis which was opposite to the expected result, with regard to the concept of genomic instability. A basis for this might be the functional heterogeneity within the cell lines in respect of the properties measured. Therefore, some aspects of instability may have to be measured at a more critical level if they are to be of value in estimating the inherent instability of the genome.

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Section: Dna Repairmentioning

confidence: 99%

Genomic Instability and Metastatic Progression

Usmani

1993

Pathobiology

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Differences in inhibition by beta-arabinofuranosyladenine (araA) of radiation induced DNA damage repair in exponentially growing and plateau-phase CHO-cells

Iliakis

Seaner

1988

Radiat Environ Biophys

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The effect of beta-arabinofuranosyladenine (araA) on the repair of radiation induced DNA damage, as measured by the DNA unwinding technique, was studied in exponentially growing and plateau-phase CHO-cells after exposure to x-rays. Induction of DNA damage by radiation was found to be similar in exponentially growing and plateau-phase cells. In the absence of araA, repair of radiation induced DNA damage proceeded with similar kinetics in exponentially growing and plateau-phase cells. AraA at concentrations between 0-1500 microM inhibited DNA repair both in exponentially growing and in plateau-phase cells. However, the degree of inhibition was significantly higher (by a factor of 3) in plateau-phase cells. A similar degree of repair inhibition by araA was observed in plateau phase cells treated in their conditioned medium, as well as in plateau phase cells that were transfered in fresh growth medium just before treatment initiation. These results indicate the importance of biochemical parameters associated with alterations in the growth state of the cells for the inhibitory effect of araA and may help in the elucidation of the molecular mechanism(s) underlying repair inhibition by inhibitors of DNA replication.

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Effects of trypsin on X-ray-induced cell killing, chromosome abnormalities and kinetics of DNA repair in mammalian cells

Sprunt

Bryant

1990

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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9-β-D-Arabinofuranosyladenine Increases the Frequency of X-ray Induced Chromosome Abnormalities in Mammalian Cells

Cited by 7 publications

References 15 publications

Genomic Instability and Metastatic Progression

Genomic Instability and Metastatic Progression

Differences in inhibition by beta-arabinofuranosyladenine (araA) of radiation induced DNA damage repair in exponentially growing and plateau-phase CHO-cells

Effects of trypsin on X-ray-induced cell killing, chromosome abnormalities and kinetics of DNA repair in mammalian cells

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