Genetic recombination in human melanoma and astrocytoma cell lines involves oncogenes and growth factor genes

Lakshmi, M. S.; Sherbet, Gajanan V.

doi:10.1007/bf00155594

Cited by 8 publications

(1 citation statement)

References 25 publications

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“…The mechanism by which SCEs are produced in mammalian cells is yet to be fully determined, and its bio logical significance is unknown. However, SCEs can be induced by DNA-damaging properties of physical and chemical agents [74], Recent literature has revealed that spontaneous and induced SCEs frequently occur close to fragile sites on chromosomes indicating that fragility and SCE are variable cytogenetic manifestations of the same D N A structural alteration [75][76][77], SCEs might therefore represent variable expressions in inherent genomic insta bility within normal and transformed cell lines. For exam ple, elevated SCE levels have been found in mouse B16 melanoma cells and in cells from patients with Bloom's syndrome [78][79][80].…”

Section: Sce and Gene Amplificationmentioning

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: Sce and Gene Amplificationmentioning

confidence: 99%

Genomic Instability and Metastatic Progression

Usmani

1993

Pathobiology

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Recombination and its roles in DNA repair, cellular immortalization and cancer

Shammas

Reis

1999

AGE

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Genetic recombination is the creation of new gene combinations in a cell or gamete, which differ from those of progenitor cells or parental gametes. In eukaryotes, recombination may occur at mitosis or meiosis. Mitotic recombination plays an indispensable role in DNA repair, which presumably directed its early evolution; the multiplicity of recombination genes and pathways may be best understood in this context, although they have acquired important additional functions in generating diversity, both somatically (increasing the immune repertoire) and in germ line (facilitating evolution). Chromosomal homologous recombination and HsRad51 recombinase expression are increased in both immortal and preimmortal transformed cells, and may favor the occurrence of multiple oncogenic mutations. Tumorigenesis in vivo is frequently associated with karyotypic instability, locus-specific gene rearrangements, and loss of heterozygosity at tumor suppressor loci - all of which can be recombinationally mediated. Genetic defects which increase the rate of somatic mutation (several of which feature elevated recombination) are associated with early incidence and high risk for a variety of cancers. Moreover, carcinogenic agents appear to quite consistently stimulate homologous recombination. If cells with high recombination arise, either spontaneously or in response to "recombinogens," and predispose to the development of cancer, what selective advantage could favor these cells prior to the occurrence of growth-promoting mutations? We propose that the augmentation of telomere-telomere recombination may provide just such an advantage, to hyper-recombinant cells within a population of telomerase-negative cells nearing their replicative (Hayflick) limit, by extending telomeres in some progeny cells and thus allowing their continued proliferation.

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Oncogenes: cause or consequence in the development of glial tumors

Akbasak

Sunar-Akbasak

1992

Journal of the Neurological Sciences

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Genetic recombination in human melanoma and astrocytoma cell lines involves oncogenes and growth factor genes

Cited by 8 publications

References 25 publications

Genomic Instability and Metastatic Progression

Genomic Instability and Metastatic Progression

Recombination and its roles in DNA repair, cellular immortalization and cancer

Oncogenes: cause or consequence in the development of glial tumors

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