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Activated Ki-ras proto-oncogene in spontaneously transformed and chemical tumor-derived cell lines related to the mouse lung alveologenic carcinoma by Don A. Leigh; Vicki Ferguson; Jacqueline M. Bentel; Juliet O. Miller; Garry J. Smith is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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## Abstract An in vitro cell model of mouse lung alveologenic carcinoma consisting of preneoplastic nonmalignant cells, spontaneously transformed cells, and urethane‐induced malignant cells was analyzed for phenotypic and genotypic changes associated with the transition to neoplasia. The polymerase chain reaction (PCR) was used to amplify the cDNA derived from the c‐Ki‐__ras__ mRNA corresponding to exons 1 and 2 of the proto‐oncogene. This approach allowed analysis of the gene transcription product rather than potentially unexpressed DNA. Direct sequencing of the PCR product identified a common single point mutation, alone or together with wild‐type mRNA for c‐Ki‐__ras__, in all of the malignant clones. An A → G transition in the second base position of codon 61 was common to spontaneously malignant and chemical tumor‐derived cell lines and to lines selected for lung metastatic behavior. The absence of the mutation in the nonmalignant cells suggests that the Ki‐__ras__ mutation may be a factor in onset or maintenance of the malignant phenotype and, at least in vitro, may be a late event in the transformation process.

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Author

Don A. Leigh; Vicki Ferguson; Jacqueline M. Bentel; Juliet O. Miller; Garry J. Smith

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0899-1987)

Published

1990

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)