Low incidence of point mutation of c-Ki-ras and N-ras oncogenes in human hepatocellular carcinoma.
We examined the incidence of point mutation in codons 12, 13 and 61 of c-Ki-ras and N-ras genes in human hepatocellular carcinoma (HCC) using the polymerase chain reaction and oligonucleotide hybridization techniques. Among 34 tissues specimens surgically resected from 30 patients and 5 cell lines of human HCC, only two had ras point mutations; in one case, codon 12 of c-Ki-ras was altered from GGT, coding glycine, to GTT, coding valine; in the other case, codon 61 of N-ras was altered from CAA, coding glutamine, to AAA, coding lysine. Thus, point-mutational activation of ras oncogenes is an uncommon event in human HCC.
Tsuda
H
H
Pathology Division, National Cancer Center Research Institute, Tokyo.
Hirohashi
S
S
Shimosato
Y
Y
Ino
Y
Y
Yoshida
T
T
Terada
M
M
D006528:Carcinoma, Hepatocellular / Q000235:genetics*; D003062:Codon; D004247:DNA / Q000235:genetics; D006801:Humans; D008113:Liver Neoplasms / Q000235:genetics*; D008565:Membrane Proteins; D009154:Mutation; D009693:Nucleic Acid Hybridization; D015345:Oligonucleotide Probes; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016283:Proto-Oncogene Proteins p21(ras); D011519:Proto-Oncogenes; D014407:Tumor Cells, Cultured
D003062:Codon; D008565:Membrane Proteins; D015345:Oligonucleotide Probes; D011518:Proto-Oncogene Proteins; D004247:DNA; C501009:HRAS protein, human; D016283:Proto-Oncogene Proteins p21(ras)