Document Detail


Duration but not intensity of alcohol and tobacco exposure predicts p16INK4A homozygous deletion in head and neck squamous cell carcinoma.
MedLine Citation:
PMID:  16618779     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In tobacco-associated solid tumors, evidence suggests that the pattern of carcinogen exposure is related to the nature of somatic gene inactivation within crucial pathways, including the retinoblastoma (Rb) pathway. One somatic event in this pathway, homozygous deletion of the p16INK4A gene, is commonly observed in head and neck squamous cell carcinoma (HNSCC). Alcohol and tobacco are both well-established risk factors for HNSCC but there has been little characterization of the relationship of exposure to these carcinogens and inactivation of the p16INK4A gene. Hypothesizing that p16INK4A homozygous deletion is associated with tobacco and alcohol exposure, we investigated 330 consecutive HNSCC tumors. The odds ratio (OR) for p16INK4A homozygous deletion among alcohol consumers in the upper tertile (>43 years used) was 5.2 [95% confidence interval (95% CI), 2.1-12.8] as compared with those with < or = 43 years of alcohol consumption. Intensity of alcohol exposure, measured as average alcoholic drinks per week, was not associated with gene deletion. When we examined the distribution of duration of tobacco use, the OR for p16(INK4A) homozygous deletion was 1.3 (95% CI, 0.5-3.0) and 1.9 (95% CI, 0.9-4.0) for 29 to 39 years and >39 years of tobacco smoking, respectively, as compared with those that smoked < or = 28 years. As in the case of alcohol use, intensity of tobacco exposure (measured as packs per day) was not associated with gene deletion. Hence, the duration of alcohol use and duration of smoking, but not intensity of either, significantly predicted p16(INK4A) homozygous deletion in HNSCC.
Authors:
Kim S Kraunz; Michael D McClean; Heather H Nelson; Edward Peters; Henry Calderon; Karl T Kelsey
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Cancer research     Volume:  66     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  2006 Apr 
Date Detail:
Created Date:  2006-04-18     Completed Date:  2006-06-07     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4512-5     Citation Subset:  IM    
Affiliation:
Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
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MeSH Terms
Descriptor/Qualifier:
Alcohol Drinking / adverse effects*,  genetics
Case-Control Studies
Cyclin-Dependent Kinase Inhibitor p16 / genetics*
Female
Gene Deletion
Head and Neck Neoplasms / epidemiology,  etiology*,  genetics*
Humans
Male
Middle Aged
Smoking / adverse effects*,  genetics
Grant Support
ID/Acronym/Agency:
P30 ES00002/ES/NIEHS NIH HHS; R01 CA078609/CA/NCI NIH HHS; R01 CA100679/CA/NCI NIH HHS; T32ES07155/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Cyclin-Dependent Kinase Inhibitor p16

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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