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A novel combination of K‐ras and myc amplification accompanied by point mutational activation of K‐ras in a human lung cancer.
Author(s) -
Taya Y.,
Hosogai K.,
Hirohashi S.,
Shimosato Y.,
Tsuchiya R.,
Tsuchida N.,
Fushimi M.,
Sekiya T.,
Nishimura S.
Publication year - 1984
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1984.tb02236.x
Subject(s) - biology , point mutation , lung cancer , cancer research , gene duplication , genetics , microbiology and biotechnology , mutation , gene , medicine
Amplifications of two oncogenes, c‐K‐ras‐2 and c‐myc, were found in a human lung giant cell carcinoma (LGCC) Lu‐65, which is maintained in nude mice. The extent of c‐K‐ras‐2 and myc amplifications were estimated to be 10‐ and 8‐fold, respectively, by means of the Southern hybridization procedure. In addition, NIH3T3 cells were transformed by transfection of Lu‐65 DNA and the transforming gene was identified as c‐K‐ras‐2. c‐K‐ras‐2 genes were cloned from a gene library of Lu‐65 and a single point mutation causing a substitution of cysteine for glycine in codon 12 was found by DNA sequencing. It was concluded that the amplification of the c‐myc and c‐K‐ras‐2 genes are accompanied by point mutational activation of c‐K‐ras‐2 in the human LGCC Lu‐65. This is the first report of multiple gene amplification accompanied by a point mutation of oncogenes in human cancer cells, providing further support for the idea that co‐operation of at least two activated cellular oncogenes is required for carcinogenesis.