Br J Cancer  1991 Apr;63(4):573-8 

High frequency mutation in codons 12 and 61 of H-ras oncogene in chewing
tobacco-related human oral carcinoma in India.

Saranath D, Chang SE, Bhoite LT, Panchal RG, Kerr IB, Mehta AR, Johnson NW, Deo
MG.

Cell and Developmental Pathology Division, Cancer Research Institute, Bombay,
India.

57 primary tumour samples from Indian oral cancer patients with a 5-15 year
tobacco chewing habit, were examined for mutational activation in codons 12, 13
and 61 of the H-ras, K-ras and N-ras oncogenes. The highly sensitive assay based
on specific oligonucleotide hybridisation following in vitro amplification of
unique sequences by polymerase chain reaction was employed. Mutations were
detected in twenty (35%) of the samples and were restricted to H-ras, codons 12,
13 and 61. Two cases had concurrent mutations in codons 12 and 61. The majority
of the mutations were at H-ras 61.2 (Glutamine to Arginine) and H-ras 12.2
(Glycine to Valine). Three of the less frequent mutations are apparently novel.
Interestingly, eight of the samples with H-ras mutations also showed loss of
wild-type H-ras, as judged by absence of signals for wild-type codons 12 or 61
on dot blots. The specific H-ras mutations in these oral malignancies associated
with tobacco chewing, may represent an important example of an environmental
carcinogen-induced step, in a pathway leading to malignant transformation.

PMID: 2021541 [PubMed - indexed for MEDLINE]