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p53 gene mutations in oral carcinomas from India
Author(s) -
Munirajan Arasambattu K.,
TutsumiIshii Yuko,
Mohanprasad Bagavathi K. C.,
Hirano Yasumasa,
Munakata Nobuo,
Shanmugam Govindaswamy,
Tsuchida Nobuo
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19960503)66:3<297::aid-ijc4>3.0.co;2-u
Subject(s) - transversion , exon , gene , mutation , biology , epidermoid carcinoma , guanine , cancer research , tumor suppressor gene , genetics , microbiology and biotechnology , single strand conformation polymorphism , carcinoma , carcinogenesis , nucleotide
In this study, we analyzed 53 oral squamous‐cell carcinomas among Indians for the presence of alterations in the tumor‐suppressor gene p53 by PCR‐SSCP and sequencing methods. Our results showed that 21% (II/53) of oral carcinomas analyzed carried mutations within the exons 5–8 of the p53 gene. We have identified II single‐base pair substitutions consisting of 10 mis‐sense mutations and one at the splice acceptor site, and one deletion mutation involving 4 consecutive bases. The majority of the base substitutions were transitions (5 TA to CG and 5 GC to AT), while only one transversion (TA to GC) was observed. Probable hot‐spots for the mutation induction were identified at codons 149 and 274, which have not been observed before in head‐and‐neck cancers. The mutational spectrum might have originated from base alkylations at guanine and thymine residues, caused by some alkylating agents. The present results are thus consistent with the involvement of tobacco‐related nitrosoamines in the etiology of oral squamous‐cell carcinoma. © 1996 Wiley‐Liss, Inc.