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TP 53 mutation and human papilloma virus status of oral squamous cell carcinomas in young adult patients
Author(s) -
Braakhuis BJM,
Rietbergen MM,
Buijze M,
Snijders PJF,
Bloemena E,
Brakenhoff RH,
Leemans CR
Publication year - 2014
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.12178
Subject(s) - missense mutation , frameshift mutation , carcinogenesis , immunohistochemistry , mutation , papilloma , cancer research , basal cell , human papilloma virus , medicine , carcinoma , biology , oncology , pathology , cancer , gene , genetics , cervical cancer
Objective Little is known about the molecular carcinogenesis of oral squamous cell carcinoma ( OSCC ) in young adult patients. The aim of this study was to investigate the detailed TP 53 mutation and human papilloma virus ( HPV ) status of OSCC in patients, younger than 45 years. Methods TP 53 mutations were determined with direct sequencing on paraffin‐embedded carcinoma tissue from 31 young patients and compared with two older age OSCC reference groups: one from the same institute ( N = 87) and an independent one ( N = 675). Biologically active tumour HPV was detected by p16‐immunohistochemistry followed by a HPV ‐ DNA GP 5 + /6 + ‐ PCR . Results HPV 16 was present in one OSCC (3%). TP 53 mutations were found in 14 (45%) OSCC : five were missense and nine resulted in a truncated protein. Six of these latter were insertions or deletions of one or more nucleotides leading to frameshift, one was at a splice site and two resulted in a stop codon. The percentage of truncating mutations (64% of all mutations) was higher than that observed in the institute's reference group (44%, P = 0.23) and in the independent reference group (24%, P = 0.002). Conclusions This study shows that TP 53 mutations are common in OSCC of young adult patients; infection with biologically active HPV is rare.