Open AccessOncogene Amplification in Squamous Cell Carcinoma of the Oral Cavity
Author(s) -
Saranath Dhananjaya,
Panchal Rekha G.,
Nair Rama,
Mehta Ashok R.,
Sanghavi Vikram,
Sumegi Janos,
Klein George,
Deo Madhav G.
Publication year - 1989
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1989.tb02332.x
Subject(s) - oncogene , carcinogenesis , biology , gene duplication , microbiology and biotechnology , cancer research , in situ hybridization , epidermoid carcinoma , southern blot , cell , dna , carcinoma , cancer , gene , cell cycle , gene expression , genetics
We have determined the prevalence of amplification of c‐ myc , N‐ myc , L‐ myc , H‐ ras , Ki‐ ras , and N‐ ras oncogenes in 23 cases of squamous cell carcinoma of the oral cavity, using Southern hybridization analysis of DNA extracted from the primary tumor tissues. Nick‐translated oncogene probes and oncogene inserts labeled to high specific activities were used. We observed a 5‐ to 10‐fold amplification of one or more of c‐ myc , N‐ myc , Ki‐ ras and N‐ ras oncogenes in 56% of the tumor tissue samples, with these oncogenes not being amplified in the peripheral blood cells of the same patients, L‐ myc and H‐ ras were not amplified in any of our samples. The oncogene amplifications seemed to be associated with advanced stages of squamous cell carcinomas, with the ras and myc family oncogenes being amplified in stages 3 and 4. Hybridization with N‐ myc detected an additional 2.3 kb Eco RI fragment, along with the normal 2.1 kb fragment. Our data also demonstrated amplification of multiple oncogenes in the same tumor tissue sample. About 60% of the samples with amplified oncogenes showed simultaneous amplification of 2 or more oncogenes. The results showing different oncogene amplifications in similar tumors, as well as multiple oncogene amplifications in the same tumor, suggest that these oncogenes may be alternatively or simultaneously activated in oral carcinogenesis.