Identification of a gene(s) involved in carcinogenic progression of ataxia telangiectasia cells (Meeting abstract).

Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.

Identification of a gene(s) involved in carcinogenic progression of ataxia telangiectasia cells (Meeting abstract).

Proc Annu Meet Am Assoc Cancer Res; 36:A857 1995. Unique Identifier : AIDSLINE ICDB/95608636
Jung M; Zhang Y; Dritschilo A; Georgetown University Medical Center, Washington, DC 20007

Abstract: Genetic mechanisms have been correlated to phenotypic changes observed in the steps involved in immortalization, promotion, and progression to tumorigenicity. Using ataxia telangiectasia (AT) fibroblasts as a model system, we have employed vector-mediated gene transfer and expression cloning to identify candidate cDNAs of genes that cause phenotypic conversion of cells from flat, contact inhibited growth to foci formation and anchorage independent growth. Such morphologic growth changes are consistent with carcinogenic progression. Plasmid rescue and polymerase chain reaction amplification has permitted the rescue of four candidate cDNAs (two unknowns and two known) that are present in these transformed cells. Partial sequence analysis shows that one unknown gene contains a sequence homologous to the envelope sequences of the human retrovirus (HIV-1). This characteristic suggests that the isolated sequence may be part of an oncogene. Further studies of this gene are in progress.

Keywords: Ataxia Telangiectasia/GENETICS/*PATHOLOGY Carcinogens/*TOXICITY Cell Division Cell Transformation, Neoplastic Cells, Cultured Cloning, Molecular DNA, Complementary HIV-1/GENETICS Plasmids ABSTRACT
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M9580999

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