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BMC Genetics  2002 

Chromosomal aberrations in patients with head and neck squamous cell carcinoma do not vary based on severity of tobacco/alcohol exposure

DOI: 10.1186/1471-2156-3-22

Keywords: head and neck neoplasms, squamous cell carcinoma, tobacco, alcohol, comparative genomic hybridization

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Abstract:

Although the median number of abnormalities (9), gains (6) and losses (2) per case and the overall pattern of abnormalities did not vary significantly by the extent of tobacco/alcohol exposure, individual abnormalities segregating these patients were identified. Gain of 1p (p = 0.03) and 3q amplification (p = 0.05) was significantly more common in patients with a history of tobacco/alcohol exposure.This data suggests that the overall accumulated chromosomal aberrations in head and neck squamous cell carcinoma are not significantly influenced by the severity of tobacco/alcohol exposure with limited exceptions.A causal association between squamous cell carcinoma arising in the head and neck region (HNSCC) and exposure to tobacco and alcohol is well established [1-3]. However, 10–15% HNSCC occur in patients without any antecedent history of tobacco or alcohol exposure [4,5]. Several studies have suggested that these patients have a divergent clinical course compared to patients with tobacco associated HNSCC, which may be a reflection of differences in the genetic composition [4-6]. Empiric evidence suggesting that non-smokers may respond differently to carcinogenic insults is offered in a report by Schantz et al., showing the highest levels of chromosomal sensitivity in lymphocytes after exposure to the clastogen bleomycin in HNSCC patients who were non-smokers [7]. Relatively few studies have directly investigated the impact of tobacco/alcohol exposure on the genetic composition of HNSCC. Amplification and expression of cyclin D1, p53 mutation and deletions of 3p, 5q, and 9p21 are suggested to be influenced by the degree of tobacco exposure [4,6,8]. The largest effort on this topic has been reported by Koch and colleagues, who found significantly higher rates of p53 mutation and loss of heterozygosity at 3p, 4q, and 11q as part of allelotyping analysis of 10 individual loci [4]. No studies have utilized true genome-wide evaluative measures to analyze the impact of car

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