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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 hepatocellnlar carcinoma (HCC) using the polymerase chain reaction and oligonucleotide hybridization techniques. Among 34 tissue specimens surgically resected from 30 patients and 5 cell lines of...

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Detalles Bibliográficos
Autores principales: Tsuda, Hitoshi, Hirohashi, Setsuo, Shimosato, Yukio, Ino, Yoshinori, Yoshida, Teruhiko, Terada, Masaaki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 1989
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5917712/
https://www.ncbi.nlm.nih.gov/pubmed/2542205
http://dx.doi.org/10.1111/j.1349-7006.1989.tb02290.x
Descripción
Sumario:We examined the incidence of point mutation in codons 12, 13 and 61 of c‐Ki‐ras and N‐ras genes in human hepatocellnlar carcinoma (HCC) using the polymerase chain reaction and oligonucleotide hybridization techniques. Among 34 tissue 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.