Interaction between Tobacco and Alcohol Use and the Risk of Head and Neck Cancer: Pooled Analysis in the International Head and Neck Cancer Epidemiology Consortium

Hashibe, Mia; Brennan, Paul; Chuang, Shu Chun; Boccia, Stefania; Castellsagué, Xavier; Chen, Chu; Curado, María Paula; Maso, Luigino Dal; Daudt, Alexander W.; Fabiánovà, Eleonóra; Fernández, Leticia; Wünsch-Filho, Victor; Franceschi, Silvia; Hayes, Richard B.; Herrero, Rolando; Kelsey, Karl T.; Koifman, Sérgio; Vecchia, Carlo La; Lazarus, Philip; Levi, Fabio; Lence, Juan J; Mateș, Dana; Matos, Elena; Menezes, Ana; McClean, Michael D.; Muscat, Joshua E.; Eluf-Neto, José; Olshan, Andrew F.; Purdue, Mark P.; Rudnai, Péter; Schwartz, Stephen M.; Smith, Elaine; Sturgis, Erich M.; Szeszenia-Dabrowska, Neonilia; Talamini, Renato; Wei, Qingyi; Winn, Deborah M.; Shangina, Oxana; Pilarska, Agnieszka; Zhang, Zuo‐Feng; Ferro, Gilles; Berthiller, Julien; Boffetta, Paolo

doi:10.1158/1055-9965.epi-08-0347

Cited by 934 publications

(842 citation statements)

References 19 publications

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“…There is a known synergistic effect of alcohol and tobacco consumption on the risk of cancer of the oral cavity, pharynx and esophagus [22][23][24]. For example, the risk of oral cavity and pharynx cancers is about 5-10 times higher for heavy smokers than for nonsmokers, and about 5 times higher for heavy drinkers than for nondrinkers.…”

Section: Discussionmentioning

confidence: 99%

A local mechanism by which alcohol consumption causes cancer

López‐Lázaro

2016

Oral Oncology

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Epidemiological data indicate that 5.8% of cancer deaths world-wide are attributable to alcohol consumption. The risk of cancer is higher in tissues in closest contact on ingestion of alcohol, such as the oral cavity, pharynx and esophagus. The risk of these cancers is increased even in people who have only one alcoholic drink per day. However, since ethanol is not mutagenic and the carcinogenic metabolite of ethanol (acetaldehyde) is mostly produced in the liver, it is not clear why alcohol use preferentially exerts a local carcinogenic effect. It is well known that ethanol causes cell death at the concentrations present in alcoholic beverages; however, this effect has been overlooked probably because dead cells cannot give rise to cancer. Here I discuss that the cytotoxic effect of ethanol on the cells lining the oral cavity, pharynx and esophagus activates the division of the stem cells located in deeper layers of the mucosa to replace the dead cells. Every time stem cells divide, they become exposed to unavoidable errors associated with cell division (e.g., mutations arising during DNA replication and chromosomal alterations occurring during mitosis) and also become highly vulnerable to the genotoxic activity of endogenous and exogenous DNA-damaging agents (e.g., reactive oxygen species, acetaldehyde and tobacco carcinogens). Alcohol consumption probably increases the risk of developing cancer of the oral cavity, pharynx and esophagus by promoting the accumulation of cell divisions in the stem cells that maintain these tissues in homeostasis. Because the cytotoxic activity of ethanol is concentration-dependent, the risk of these cancers will not only increase with increasing amounts of ethanol, but also with increasing concentrations; an ounce of whisky is probably more carcinogenic when taken undiluted than when taken mixed with non-alcoholic beverages. The local cytotoxic effect of ethanol can also explain the known synergistic effect of alcohol and tobacco use on the risk of these cancers. Understanding the mechanisms of carcinogenicity of alcohol is important to reinforce the epidemiological evidence and to raise public awareness of the strong link between alcohol consumption and cancer.

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Section: Discussionmentioning

confidence: 99%

A local mechanism by which alcohol consumption causes cancer

López‐Lázaro

2016

Oral Oncology

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“…HNSCC is a heterogeneous disease and is the sixth most common form of cancer worldwide (2). Subtype analysis of significant miRNAs and genes associated with HNSCC will be of great significance for individualized clinical treatment and prevention of HNSCC.…”

Section: Discussionmentioning

confidence: 99%

“…Head and neck squamous cell carcinoma (HNSCC), one type of epithelial head and neck cancer, is a heterogeneous disease and the sixth most common form of cancer worldwide (2). The 5-year survival rate of HNSCC patients with stage III or IV is extremely poor (3) and various complications will be faced by HNSCC survivors during their life time (4).…”

Section: Introductionmentioning

confidence: 99%

Subpath analysis of each subtype of head and neck cancer based on the regulatory relationship between miRNAs and biological pathways

Zhang²,

Xia

et al. 2015

Oncology Reports

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Abstract. The aim of the present study was to explore the potential mechanisms involved in each subtype of head and neck squamous cell carcinoma (HNSCC) via subpath analysis and to investigate their relevance in the prevention of HNSCC. Gene expression profiles of GSE6631 and GSE39366 containing 44 and 168 HNSCC samples, respectively, were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) from samples in GSE6631 and GSE393666 were screened using the Detection of Imbalanced Differential Signal (DIDS) method respectively. DEGs in GSE39366 were matched with the DEGs in GSE6631 and were used to classify the subtypes of HNSCC based on hierarchical clustering analysis. Furthermore, DEGs were separated into different subtypes and then the pathway information was analyzed. The regulated miRNAs for the DEGs in each subtype were analyzed to select the significant subpaths. Totally, 1,095 DEGs from GSE6631 and 2,528 DEGs from GSE39366 were screened. Samples in GSE39366 were separated into four subtypes. Specific genes in each subtype and DEGs in the common gene set involved in a variety of pathways were identified. In addition, the significant miRNAtarget-pathway subpath of each subtype of HNSCC and the common gene set of HNSCC were also enriched. Our data suggest that human papillomavirus (HPV) is positively correlated with HNSCC in subtype 2. Several miRNAs (miRLet-7A, miR-1, miR-206, miR-153, miR-519A and miR-506) and their target genes (CYP46A1, BPNT1, MCM7 and COL5A1) are crucial for HNSCC prevention via different pathways and may provide further knowledge of the mechanisms involved in the progression of HNSCC.

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“…Alcohol: effects of smoking and alcohol on the risk of upper aero-digestive tract cancer are synergetic and cumulative rather than additive (Hashibe et al, 2009;de Menzes et al, 2013 DOI:http://dx.doi.org/10.7314/APJCP.2014.15.15…”

Section: Behavioural Risk Factorsmentioning

confidence: 99%