Homologous recombination in variants of the B16 murine melanoma with reference to their metastatic potential.

摘要: Genomic instability has been accepted as providing a phenotypic variety of malignant cells within developing tumour. Defects in genetic recombination can often lead to differences; therefore, it is possible that metastatic variant cell lines exhibit their particular phenotype result an altered ability catalyse homologous recombination. We have investigated efficiency B16 melanoma variants, using plasmid, pDR, substrate. The plasmid contains two truncated, nontandem but overlapping segments the neomycin resistance gene (neo 1 and neo 2), separated by functional gpt unit. Only successful will generate functionally intact gene. Extrachromosomal here was transient measure recombine fragments intra- or intermolecular manner. frequencies were higher high metastasis variants (BL6, ML8) compared with low F1 cells. On other hand, frequency chromosomal (after integration) for (F1) line highly BL6 ML8. Since assay measures only events, we interpreted observed incidence indicative more stable genome. Similarly, inherent genome would render these less efficient at producing maintaining this found be true Southern analysis. results presented show may adduced evidence implicating genomic generation populations during spread. Such interpretation also compatible Nowell hypothesis tumour progression. © 1996 Wiley-Liss, Inc.