1994/02/01 by Mark Yen‐Ping Kuo, Jiiang‐Huei Jeng, Chun‐Pin Chiang +1 · 1 citation
Dentistry · Medicine · #Oral Health Pathology and Treatment #Head and Neck Cancer Studies #Cancer-related Molecular Pathways
paper · doi:10.1111/j.1600-0714.1994.tb00259.x
openalex publication_date 1994/02/01 · openalex created_date 2016/06/24 · openalex updated_date 2026/07/28
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. Four 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.