TP53 mutation and human papilloma virus status of oral squamous cell carcinomas in young adult patients

Authors

  • BJM Braakhuis,

    Corresponding author
    1. Department of Otolaryngology/Head-Neck Surgery, VU University Medical Center, Amsterdam, The Netherlands
    • Correspondence: Boudewijn J. M. Braakhuis, PhD, Section Tumor Biology, Department Otolaryngology/Head-Neck Surgery, VU University Medical Center, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands. Tel: +31 20 44 40905, Fax: +31 20 44 43688, E-mail: bjm.braakhuis@vumc.nl

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  • MM Rietbergen,

    1. Department of Otolaryngology/Head-Neck Surgery, VU University Medical Center, Amsterdam, The Netherlands
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  • M Buijze,

    1. Department of Otolaryngology/Head-Neck Surgery, VU University Medical Center, Amsterdam, The Netherlands
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  • PJF Snijders,

    1. Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands
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  • E Bloemena,

    1. Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands
    2. Department of Oral and Maxillofacial Surgery/Oral Pathology, Academic Centre for Dentistry Amsterdam (ACTA), Amsterdam, The Netherlands
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  • RH Brakenhoff,

    1. Department of Otolaryngology/Head-Neck Surgery, VU University Medical Center, Amsterdam, The Netherlands
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  • CR Leemans

    1. Department of Otolaryngology/Head-Neck Surgery, VU University Medical Center, Amsterdam, The Netherlands
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Abstract

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 TP53 mutation and human papilloma virus (HPV) status of OSCC in patients, younger than 45 years.

Methods

TP53 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 GP5 + /6 + -PCR.

Results

HPV16 was present in one OSCC (3%). TP53 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 TP53 mutations are common in OSCC of young adult patients; infection with biologically active HPV is rare.

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