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Mutations of Ki‐ ras oncogene codon 12 in betel quid chewing‐related human oral squamous cell carcinoma in Taiwan
Author(s) -
Kuo M. Y. P.,
Jeng J. H.,
Chiang C. P.,
Hahn L. J.
Publication year - 1994
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1994.tb00259.x
Subject(s) - carcinogenesis , oncogene , betel , polymerase chain reaction , biology , cancer , mutation , epidermoid carcinoma , cancer research , point mutation , microbiology and biotechnology , cell cycle , genetics , gene , structural engineering , nut , engineering
In Taiwan, there are two million people who have a betel quid chewing habit, and approximately 80% of all oral cancer deaths are associated with this habit. To investigate the incidence and types of Ki‐ ras codon 12 mutations in oral cancer associated with betel quid chewing, we used a sensitive mutation‐specific two‐stage polymerase chain reaction (PCR) technique to examine human oral squamous cell carcinomas from formalin‐fixed, paraffin‐embedded tissues. DNA sequence analysis of PCR products revealed that 6 of 33 (18%) tumour specimens contained Ki‐ ras codon 12 mutations. Hour of the tumours contained more than one mutation. Three different base changes were detected, resulting from a substitution of wild type glycine (GGT) to either serine (AGT), aspartic acid (GAT) or cysteine (TAT). These results indicate that Ki‐ ras oncogene activation may play a role in the oncogenesis of betel quid chewing‐related human oral squamous cell carcinomas.