Alcohol and head and neck cancer risk in a prospective study

Freedman, Neal D.; Schatzkin, Arthur; Leitzmann, Michael F.; Hollenbeck, Albert R.; Abnet, Christian C.

doi:10.1038/sj.bjc.6603713

Cited by 86 publications

(68 citation statements)

References 26 publications

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“…13 Cancer sites were identified by anatomic site and histologic code of the International Classification of Disease for Oncology (ICD-O, third edition) 14 as previously described. 15 The total head and neck cancer category included those diagnosed with a cancer of the oral cavity, oro-hypopharynx, larynx and those with squamous cell carcinomas of other anatomical head and neck sites, including those overlapping these regions.…”

Section: Identification Of Cancer Casesmentioning

confidence: 99%

Fruit and vegetable intake and head and neck cancer risk in a large United States prospective cohort study

Freedman

Park

Subar

et al. 2007

Intl Journal of Cancer

201

146

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Squamous head and neck cancers include cancers of the oral cavity, pharynx and larynx are the sixth leading cause of cancer mortality worldwide, resulting in more than 350,000 deaths annually. Intake of fruit and vegetables may protect against head and neck cancer incidence, although few prospective studies have examined this association. We investigated this relation in 490,802 United States participants of the NIH-AARP Diet and Health cohort using Cox proportional hazard models adjusted for potential confounders. During 2,193,751 person years of follow-up from 1995/ 1996-2000, 787 participants were diagnosed with head and neck cancer. We found an inverse association between total fruit and vegetable intake and head and neck cancer risk (per serving/day/ 1,000 calories, Hazard Ratio, 95% Confidence interval: 0.94, 0.89-0.99). In models mutually adjusted for fruit and vegetable intake, the association was stronger for vegetables (fifth vs. first quintile: 0.65, 0.50-0.85) than for fruits (fifth vs. first quintile: 0.87, 0.68-1.11). When further subclassified into botanical groups, those in the highest tertile of leguminosae (dried beans, string beans and peas, 0.80, 0.67-0.96), rosaceae (apples, peach, nectarines, plums, pears and strawberries, 0.60, 0.49-0.73), solanaceae (peppers and tomatoes, 0.82, 0.69-0.98) and umbelliferae (carrots, 0.73, 0.60-0.89) had decreased risk of head and neck cancer, but no significant associations were seen for 9 other botanical groups. Results from this large prospective observational study are consistent with previous case-control studies and support the hypothesis that total fruit and vegetable intake is associated with reduced risk of head and neck cancer. ' 2007 Wiley-Liss, Inc.

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Section: Identification Of Cancer Casesmentioning

confidence: 99%

Fruit and vegetable intake and head and neck cancer risk in a large United States prospective cohort study

Freedman

Park

Subar

et al. 2007

Intl Journal of Cancer

201

146

View full text Add to dashboard Cite

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“…Squamous cell cancers of the head and neck (HNC) are heterogeneous and oral and oropharyngeal cancers have differing aetiology. Alcohol and tobacco use are the major risk factors for oral and oropharyngeal cancers,2, 3 explaining approximately 65–70% of the population attributable risk 4. Infection with human papillomavirus (HPV) has emerged as an important risk factor, particularly in oropharyngeal cancers 5.…”

Section: Introductionmentioning

confidence: 99%

Assessing the causal association between 25‐hydroxyvitamin D and the risk of oral and oropharyngeal cancer using Mendelian randomization

Dudding

Johansson

Thomas

et al. 2018

Intl Journal of Cancer

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Circulating 25‐hydroxyvitamin D (25OHD) is an appealing potential intervention for cancer risk and has been associated with oral and oropharyngeal cancer risk but evidence is inconsistent. The availability of genetic variants, uncorrelated with known confounders, but predictive of 25OHD and genetic data in a large oral and oropharyngeal cancer collaboration aids causal inference when assessing this association. A total of 5,133 oral and oropharyngeal cancer cases and 5,984 controls with genetic data were included in the study. Participants were based in Europe, North America and South America and were part of the Genetic Associations and Mechanisms in Oncology (GAME‐ON) Network. Five genetic variants reliably associated with circulating 25OHD were used to create a relative genetic measure of 25OHD. In the absence of measured 25OHD, two‐sample Mendelian randomization using individual level outcome data were used to estimate causal odds ratios (OR) for cancer case status per standard deviation increase in log25OHD. Analyses were replicated in an independent population‐based cohort (UK Biobank). In the GAME‐ON study, there was little evidence of a causal association between circulating 25OHD and oral cancer (OR = 0.86 [0.68;1.09], p = 0.22), oropharyngeal cancer (OR = 1.28 [0.72;2.26], p = 0.40) or when sites were combined (OR = 1.01 [0.74;1.40], p = 0.93). Replication in UK Biobank and pooled estimates produced similar results. Our study suggests that a clinically relevant protective effect of 25OHD on oral and oropharyngeal cancer risk is unlikely and supplementation of the general population with 25OHD is unlikely to be beneficial in preventing these cancers.

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“…Alcohol abuse and dependence are frequently seen in individuals diagnosed with Head and Neck Squamous Cell Carcinoma [3]. Moreover, prospective epidemiological data show that alcohol use has a significant dose-response relationship with increased hazard ratios for developing cancer starting at three drinks per day [4]. Consumption of alcohol appears to have a direct effect on gastrointestinal tissue promoting the development of malignancy.…”

Section: Aimmentioning

confidence: 99%

Cross-Generational Effects of Alcohol Dependence in Humans on HRAS and TP53 Methylation in Offspring

et al. 2017

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Aim:We hypothesized that cross-generational effects of alcohol exposure could alter DNA methylation and expression of the HRAS oncogene and TP53 tumor suppressor gene that drive cancer development. Methods: DNA methylation of the HRAS and TP53 genes was tested in samples from young participants (Mean age of 13.4 years). Results: Controlling for both personal use and maternal use of substances during pregnancy, familial alcohol dependence was associated with hypomethylation of CpG sites in the HRAS promoter region and hypermethylation of the TP53 gene. Conclusion: The results suggest that ancestral exposure to alcohol can have enduring effects that impact epigenetic processes such as DNA methylation that controls expression of genes that drive cancer development such as HRAS and TP53. Alcohol use is responsible for about 4% of all deaths worldwide [1]. A portion of this increased incidence of all-cause mortality is due to head and neck cancers, particularly of the pharynx, larynx, oral cavity and esophagus as well as the liver [2]. Alcohol abuse and dependence are frequently seen in individuals diagnosed with Head and Neck Squamous Cell Carcinoma [3]. Moreover, prospective epidemiological data show that alcohol use has a significant dose-response relationship with increased hazard ratios for developing cancer starting at three drinks per day [4]. Consumption of alcohol appears to have a direct effect on gastrointestinal tissue promoting the development of malignancy. The incidence of the head and neck cancers is in direct proportion to the dilution of alcohol in the gut so that mouth cancers are most common followed by esophageal cancers with the least incidence occurring in stomach and intestinal cancers [5].Integrated approaches to understanding cancer risk appear to require analysis of genetic and epigenetic factors along with gene expression profiles to address the complexity of cancer etiology [6]. In addition to the direct effect of alcohol on tissues exposed to alcohol, the potential exists for alcohol to change the methylation of oncogenes and tumor suppressor genes involved in tumor development. Defining the factors that contribute to this increased risk for these cancers is critical to the ultimate goal of reducing cancer development.A diverse set of environmental conditions affect DNA methylation [7][8][9] with the potential for altering gene expression [10]. Alcohol use and smoking can produce altered methylation in humans [11,12]. Cross generational effects have been reported with famine experienced by parents affecting medical conditions and longevity in offspring [13,14]. Although not previously reported in humans, animal studies have shown that ethanol administration can influence DNA methylation through the germline in offspring exposed either through fetal exposure [15] or as a result of paternal exposure [16,17]; changes with the potential to alter every somatic cell in the body across generations. Determining if alcohol consumption in the preconception period in parents influences genes involv...

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Alcohol and head and neck cancer risk in a prospective study

Cited by 86 publications

References 26 publications

Fruit and vegetable intake and head and neck cancer risk in a large United States prospective cohort study

Fruit and vegetable intake and head and neck cancer risk in a large United States prospective cohort study

Assessing the causal association between 25‐hydroxyvitamin D and the risk of oral and oropharyngeal cancer using Mendelian randomization

Cross-Generational Effects of Alcohol Dependence in Humans on HRAS and TP53 Methylation in Offspring

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