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Chapter-048 Etiology of Head and Neck Cancers

BOOK TITLE: Head & Neck Surgery (2 Volumes)

Author
1. Hobbs Christopher GL
ISBN
9788184486797
DOI
10.5005/jp/books/10351_48
Edition
1/e
Publishing Year
2009
Pages
16
Author Affiliations
1. Laryngeal Research Group, University of Bristol, Langford House, Langford, Bristol, UK; Nobel ENT, Head & Neck and Thyroid Surgery Centre, Singapore, Royal College of Surgeons, Laryngeal Research Group, University of Bristol, Bristol, UK
Chapter keywords
neck cancer, head cancer, genetic alterations, clonal expansion, malignant phenotype, metabolizing enzymes, glutathione S-transferases, UADT cancer, B lymphocytes, epithelial cells, carcinogens, double-stranded DNA virus

Abstract

This chapter discusses etiology of head and neck cancers, where accumulation of genetic alterations enables the clonal expansion of transformed cells, which may or may not lead to a malignant phenotype. Attention has focused on inherited differences in DNA repair systems and metabolizing enzymes which would clearly influence a subject’s susceptibility to potential environmental carcinogens. One group of enzymes involved in the detoxification of tobacco-related carcinogens are the glutathione S-transferases (GSTs) and indeed their activity has been found to be suppressed in HNSCC patients. Smokeless tobacco is essentially any tobacco that is not ignited for its use and includes chewing tobacco and snuff. Genetic polymorphisms in the enzymes metabolizing alcohol are associated with increased risk of developing UADT cancer. Epstein–Barr virus (EBV) is a member of the herpesviridae family, and is a double-stranded DNA virus which infects B lymphocytes and occasionally, squamous epithelial cells of the oropharynx.

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