Head And Neck Cancer Risk Research Articles

Head and neck cancer and non-steroidal anti-inflammatory drugs: Systematic review and meta-analysis.

The objective was to assess the effects of non-steroidal anti-inflammatory drugs (NSAIDs) on head and neck cancer (HNC) outcomes. A systematic review was conducted following the PRISMA guidelines. The MEDLINE and the Cochrane Central Register databases were searched. Risk of bias was assessed by the Cochrane Collaboration's tool and by the Newcastle-Ottawa Scale. Meta-analyses were performed with the RevMan software. Seventeen articles met the inclusion criteria. Quality scores for observational studies ranged between 5 and 8 stars and the RCT was assessed as high risk of bias. NSAIDs use was associated with a 13% risk reduction of HNC (OR: 0.87 95% CI 0.77-0.99). NSAIDs use was associated with a 30% reduced cancer-specific mortality and with a 40% decreased risk on disease-recurrence. NSAIDs may have a modest protective effect on HNC risk and a positive impact on cancer-specific survival and disease-recurrence. The findings do not support a protective role of aspirin on HNC outcomes.

Association Between the Aldehyde Dehydrogenase-2 rs671 G>A Polymorphism and Head and Neck Cancer Susceptibility: A Meta-Analysis in East Asians.

Aldehyde dehydrogenase-2 (ALDH2) plays an important role in the alcohol detoxification and acetaldehyde metabolism. Published studies have demonstrated some inconsistent associations between ALDH2 rs671 G>A polymorphism and head and neck cancer (HNC) risk. A meta-analysis was performed to provide pooled data on the association between the ALDH2 rs671 G>A polymorphism and HNC risk. Electronic databases were searched to identify relevant studies. Odds ratios and 95% confidence intervals (CIs) were used to examine the pooled effect size of each genetic model. In addition, heterogeneity test, accumulative analysis, sensitivity analysis, and publication bias were conducted to test the statistical power. Thirteen publications (14 independent case-control studies) involving 10,939 subjects were selected. The stratified analysis indicated that both light/moderated drinking (e.g., GA vs. GG: OR=1.47, 95% CI=1.16 to 1.86, p<0.01, I2 =81.1%) and heavy drinking would increase HNC risk with rs671 G>A mutation (e.g., GA vs. GG: OR=2.30, 95% CI=1.11 to 4.77, p=0.03, I2 =81.9%). In summary, this meta-analysis suggested that the ALDH2 rs671 G>A polymorphism may play an important synergistic effect in the pathogenesis of HNC development in East Asians.

Effects of in IL-1B/IL-1RN variants on the susceptibility to head and neck cancer in a chinese Han population

BackgroundThe study aimed to evaluate the relationship of IL-1B/IL-1RN polymorphisms to the predisposition of head and neck cancer (HNC) in a Chinese Han population.MethodsNine single-nucleotide polymorphisms (SNPs) in IL-1B/IL-1RN were genotyped based on Agena MassARRAY platform. Logistic regression models were used to analyze the genetic association between these SNPs and HNC risk by calculating odds ratios (ORs) and 95% confidence intervals (CI). Haplotype analysis were performed using Haploview program and logistic regression model.ResultsThe genetic association between rs1143643 in IL-1B and the higher risk of HNC was found (OR = 1.23, 95% CI 1.04–1.46) in the overall. IL-1RN rs17042888 was related to a reduced risk of HNC in the subjects aged > 46 years (OR = 0.70, 95% CI: 0.50–0.98) and in females (OR = 0.71, 95% CI 0.52–0.98), while rs1143643 increased the predisposition of HNC among females (OR = 1.76, 95% CI 1.13–2.74). Furthermore, rs1143643 had an increased susceptibility to thyroid carcinoma (OR = 1.61, 95% CI 1.10–2.34). Moreover, compared with stage I–II, the frequency of IL-1RN rs452204-AG genotype was lower in patients with stage III–IV.ConclusionsIL-1B (rs1143643) and IL-1RN (rs17042888 and rs452204) polymorphisms might be related to the individual susceptibility of HNC in the Chinese Han population. These results might help to improve the understanding of IL-1B and IL-1RN genes in the occurrence of HNC.

Type 2 diabetes mellitus and risk of head and neck cancer subtypes: a systematic review and meta-analysis of observational studies.

The association between type 2 diabetes mellitus (T2DM) and risk of head and neck cancer (HNC) remains unclear. This study aims to perform a system review and meta-analysis to explore this relationship. PubMed, Web of Science, and Embase databases were searched for studies published up to July 31, 2020, regarding the association between T2DM and HNC risk. A random-effects model was utilized to calculate summary relative risks (RRs) with corresponding 95% confidence intervals (CIs). Fourteen case-control studies and thirteen cohort studies were included in our analysis. We observed a weak association between T2DM and risk of HNC overall, but there was no statistical significance (RR, 1.04; 95% CI, 0.88-1.23; I2 = 83.2%). Interestingly, there was a strong association in East Asia (RR, 1.46; 95% CI, 1.21-1.77; I2 = 36.6%). For HNC subtypes, T2DM conferred a significantly elevated risk in oral cancer (RR, 1.22; 95% CI, 1.01-1.47; I2 = 89.0%). However, in subgroup analyses of smoking, alcohol use, and body mass index (BMI)/obesity adjustments, the association between T2DM and oral cancer risk became insignificant. In addition, T2DM was not associated with a statistically elevated risk of pharyngeal cancer (RR, 1.18; 95% CI, 0.94-1.49; I2 = 72.9%) and laryngeal cancer (RR, 1.03; 95% CI, 0.88-1.22; I2 = 71.2%). This meta-analysis indicates that T2DM is associated with an increased risk of HNC in East Asia. As for site-specific cancer types, the risk of oral cancer was significantly increased in T2DM patients, which appear to be mediated or confounded by smoking, alcohol use, or BMI/obesity.

The Association Between the XRCC1 Arg399Gln Polymorphism and the Risk of Head and Neck Cancer: An Updated Meta-Analysis Including 14586 Subjects.

Background:Accumulated evidence shows that DNA repair gene X-ray repair cross complementing group 1 (XRCC1) may determine individual susceptibility to head and neck cancer (HNC) as a major DNA repair gene. However, the results from previous studies have been conflictive and inconsistent. In order to more accurately estimate and integrate the association between XRCC1 Arg399Gln polymorphism and HNC risk, we conducted a meta-analysis including 14586 subjects.Methods:In this meta-analysis, literatures were collected up until September 15, 2020 through multifarious retrieval strategies by searching through electronic databases of PubMed, Cochrane Library, EMBASE, Medline, Web of Science and CNKI. The association between the XRCC1 Arg399Gln polymorphism and HNC was analyzed through calculating summary odds ratios (OR) and 95% confidence intervals (CI).Results:Thirty-one studies consisting of 6025 cases and 8561 controls were identified and analyzed. No significant association between XRCC1 Arg399Gln polymorphisms and HNC risk was found under the allelic (OR = 0.94, 95% CI: 0.82-1.07, P = 0.35), homozygous (OR = 0.99, 95% CI: 0.81-1.21, P = 0.91), heterozygous (OR = 1.01, 95% CI: 0.90-1.13, P = 0.91), dominant (OR = 1.05, 95% CI: 0.85-1.29, P = 0.67) or recessive (OR = 0.93, 95% CI: 0.80-1.08, P = 0.35) genetic models in the overall comparison. In addition, subgroup analyses according to tumor site also displayed no significant association between XRCC1 Arg399Gln polymorphisms and HNC risk. However, subgroup analyses based on ethnicity indicated that HNC risk was significantly related to Arg399Gln genetic heterozygous model (OR = 1.21, 95%CI: 1.04-1.42, P = 0.02) and dominant model (OR = 1.27, 95%CI: 1.02-1.60, P = 0.04) in Caucasians populations.Conclusion:The results from this meta-analysis suggest that the XRCC1 Arg399Gln variants (Arg/Gln and Arg/Arg+Arg/Gln) may contribute to high HNC risk among Caucasians. Further well-designed studies and larger sample sizes are needed to validate our findings.

Smoking and Drinking Adjusted Association between Head and Neck Cancers and Oral Health Status Related to Periodontitis: a Meta-Analysis.

BackgroundNot so many reports about the association between head and neck cancer (HNC) and oral health status related to periodontitis (OHS-P) has been published in different countries with different methods. So, there is a need for an extensive meta-analysis with the total articles published until 2020. Hence, this study aimed to estimate the association between HNC and OHS-P through a meta-analysis.MethodsBased on Preferred Reporting Items for Systematic Reviews and Meta Analyses guidelines, 22 studies were selected through PubMed and Cochrane Library databases. Meta-analysis using them was performed to evaluate the association. The risk of bias assessment using the Newcastle-Ottawa Scale (NOS) was applied to evaluate the quality of non-randomized studies. Publication bias was evaluated by funnel plot and Egger's regression test.ResultsSince heterogeneity was significant (I2 = 88%, P < 0.001), we adopted the random effect model for 22 studies. Those with bad OHS-P, compared to those with good OHS-P, were more likely to have the risk of HNC by 2.4 times (odds ratio [OR], 2.42; 95% confidence interval [CI], 1.88–3.13) for random effect model. The association included publication bias (Egger's regression, P value < 0.001). The association among five studies (I2 = 39%, P = 0.16) using alveolar bone loss (ABL) or clinical attachment level (CAL) for assessing periodontitis increased to OR of 3.85 (CI, 3.04–4.88) in the fixed effect model without publication bias (Egger's regression, P = 0.66). Moreover, the association was higher in 10 fair or good NOS studies (OR, 3.08) and in 7 Asian studies (OR, 2.68), which were from the fixed model without publication bias.ConclusionOur meta-analysis showed that bad OHS-P was associated with the risk of HNC. The association was stronger in studies using ABL or CAL for assessing periodontitis.

Electronic Cigarettes and Head and Neck Cancer Risk-Current State of Art.

Simple SummaryThe risk of developing cancer is always higher for tobacco smokers than for non-smokers. Electronic cigarettes (e-cigarettes) have become increasingly popular in the last decade and are considered less harmful than traditional tobacco products, due to the lower content of toxic and carcinogenic compounds. However, this is still a controversial issue. This paper contains a review of previous reports on the composition of e-cigarettes and their impact on the pathogenesis and risk of head and neck cancer (HNC). The authors reviewed articles on both toxic and carcinogenic compounds contained in e-cigarettes and their molecular and health effects on the upper respiratory tract in comparison to traditional tobacco cigarettes. In conclusion, the studies discussed in the review strongly suggest that more long-term studies are needed to better address the safety of e-cigarettes.E-cigarettes have become increasingly popular in the last decade and are considered less harmful than traditional tobacco products due to the lower content of toxic and carcinogenic compounds. However, this is still a controversial issue. This paper contains a review of previous reports on the composition of e-cigarettes and their impact on the pathogenesis and risk of head and neck cancer (HNC). The objective of the review was to compare the molecular and health effects of e-cigarette use in relation to the effects of traditional cigarette smoking in the upper respiratory tract, and to assess the safety and effect of e-cigarettes on HNC risk. A review for English language articles published until 31 August 2020 was made, using a PubMed (including MEDLINE), CINAHL Plus, Embase, Cochrane Library and Web of Science data. The authors reviewed articles on both toxic and carcinogenic compounds contained in e-cigarettes and their molecular and health effects on the upper respiratory tract in comparison to tobacco cigarettes. The risk of developing head and neck squamous cell carcinoma (HNSCC) remains lower in users of e-cigarettes compared with tobacco smokers. However, more long-term studies are needed to better address the safety of e-cigarettes.

Prognostic Role of Serum Amino Acids in Head and Neck Cancer.

Introduction Serum amino acid (AA) profiles represent a valuable tool in the metabolic assessment of cancer patients; still, information on the AA pattern in head and neck cancer (HNC) patients is insufficient. The aim of the study was to assess whether serum AA levels were associated with the stage of neoplastic disease and prognosis in primary HNC patients. Methods Two hundred and two primary HNC patients were included in the study. Thirty-one AAs and derivatives were measured in serum through an ultraperformance liquid chromatography-mass spectrometry (UPLC-MS). The association between AA concentrations and the stage (advanced versus early) of HNC was estimated using a multivariable logistic regression model. A multivariable Cox regression model was used to evaluate the prognostic significance of each AA. Results At the multivariable logistic regression analysis, increased levels of alpha-aminobutyric acid, aminoadipic acid, histidine, proline, and tryptophan were associated with a reduced risk of advanced stage HNC, while high levels of beta-alanine, beta-aminobutyric acid, ethanolamine, glycine, isoleucine, 4-hydroxyproline, and phenylalanine were associated with an increased risk of advanced stage HNC. Furthermore, at multivariate analysis, increased levels of alpha-aminobutyric acid were associated with increased overall survival (OS), while high levels of arginine, ethanolamine, glycine, histidine, isoleucine, 4-hydroxyproline, leucine, lysine, 3-methylhistidine, phenylalanine, and serine were associated with decreased OS. Conclusions Our study suggests that AA levels are associated with the stage of disease and prognosis in patients with HNC. More study is necessary to evaluate if serum AA levels may be considered a hallmark of HNC and prove to be clinically useful markers of disease status and prognosis in HNC patients.

Development and validation of a multivariable risk prediction model for head and neck cancer using the UK Biobank.

Head and neck cancer (HNC) is the eighth most common cancer in the UK, with over 12,000 new cases every year. The incidence of HNC is predicted to increase by 33% by2035. Risk modelling produces personalised risk estimates for specific diseases, which can be used to inform education, screening programmes and recruitment to clinical trials. The present study describes the development and validation of the first risk prediction model for absolute risk of HNC, using a nested case‑control study within the UK Biobank dataset. The UK Biobank recruited 502,647 individuals aged 40‑69years from around the UK. In total, 859cases of HNC were identified, with 253 incident cases (individuals who developed HNC in the 7years following recruitment to the UK Biobank study). Logistic regression was used to develop the model, then the model performance was validated using a cohort from the North West of England. Overall, increasing age, male sex, positive history of smoking and alcohol consumption and higher levels of material deprivation were significantly associated with a higher risk of HNC. Consuming at least five portions of fruit and vegetables per day, exercising at least once per week and higher BMI offered a protective effect against HNC. The C‑statistic was 0.69 [95% confidence interval (CI), 0.66‑0.71] and the model displayed good calibration. Upon external validation, the C‑statistic was 0.64 (95% CI, 0.60‑0.68) with reasonable calibration. The model developed and validated in the present study allows calculation of a personalised risk estimate for HNC. This could be used to guide clinicians when counselling individuals on risk behaviour, and there is potential for such models to inform recruitment to screening trials.

Alcohol drinking and head and neck cancer risk: the joint effect of intensity and duration

BackgroundAlcohol is a well-established risk factor for head and neck cancer (HNC). This study aims to explore the effect of alcohol intensity and duration, as joint continuous exposures, on HNC risk.MethodsData from 26 case-control studies in the INHANCE Consortium were used, including never and current drinkers who drunk ≤10 drinks/day for ≤54 years (24234 controls, 4085 oral cavity, 3359 oropharyngeal, 983 hypopharyngeal and 3340 laryngeal cancers). The dose-response relationship between the risk and the joint exposure to drinking intensity and duration was investigated through bivariate regression spline models, adjusting for potential confounders, including tobacco smoking.ResultsFor all subsites, cancer risk steeply increased with increasing drinks/day, with no appreciable threshold effect at lower intensities. For each intensity level, the risk of oral cavity, hypopharyngeal and laryngeal cancers did not vary according to years of drinking, suggesting no effect of duration. For oropharyngeal cancer, the risk increased with durations up to 28 years, flattening thereafter. The risk peaked at the higher levels of intensity and duration for all subsites (odds ratio = 7.95 for oral cavity, 12.86 for oropharynx, 24.96 for hypopharynx and 6.60 for larynx).ConclusionsPresent results further encourage the reduction of alcohol intensity to mitigate HNC risk.

Low-dose aspirin use and risk of head and neck cancer-A Danish nationwide case-control study.

Results concerning a potential preventive effect of aspirin on head and neck cancer (HNC) are conflicting. We examined the association between low-dose aspirin use and HNC risk overall and by degree of human papillomavirus association in a nested case-control study using nationwide registries. Cases (n = 12 389) were all Danish residents diagnosed with primary HNC (2000-2015). Age- and sex-matched population controls (n = 185 835) were selected by risk-set-sampling. Using conditional logistic regression, we estimated multivariable-adjusted odds ratios and 95% confidence intervals for HNC associated with low-dose aspirin use (≥2 prescriptions). No association was observed between low-dose aspirin ever-use and overall HNC (odds ratio: 1.03, 95% confidence interval: 0.97-1.10). Estimates remained neutral according to patterns of use. Low-dose aspirin use appeared to slightly decrease HNC risk among the eldest (71-84 y), independently of human papillomavirus association, while slightly increase HNC risk among younger age groups (30-60, 61-70 y), driven by an increased risk of oral cancer. However, no consistent patterns in risk estimates were found according to duration and consistency of low-dose aspirin use in the age-stratified analyses.

Impact of IL1R1 polymorphisms on the risk of head and neck cancer in Chinese Han population.

The incidence of head and neck cancer (HNC) is increasing but its pathogenic factors are complex. Changes in both internal (genetic) and external (environmental) causes HNC to some extent. The purpose of our study was to investigate the influence of IL1R1 polymorphisms on HNC risk in Chinese Han population. Genotypes of 535 HNC patients and 538 healthy controls were analyzed by Agena MassARRAY. Odds ratio (ORs) and 95% confidence interval (CIs) were calculated by logistic regression analysis to evaluate the relationship between single nucleotide polymorphisms (SNPs) and HNC susceptibility. It was found that the rs956730 of IL1R1 reduced the risk of HNC in multiple models (allele: OR=0.76, 95% CI: 0.62-0.93, p=0.008; codominant: OR=0.43, 95% CI: 0.25-0.75, p=0.003; recessive: OR=0.45, 95% CI: 0.26-0.77, p=0.004; additive: OR=0.77, 95% CI: 0.63-0.94, p=0.01). IL1R1 rs956730 had a protective effect on HNC at age≤46. However, the rs3917225 increased a 1.31-fold HNC risk in the codominant model (OR=1.31, 95% CI: 1.00-1.70, p=0.03). Our study showed that the rs956730 of IL1R1 gene in Chinese Han population was associated with a reduced risk of HNC, while the rs3917225 of IL1R1 might increase the risk of HNC.

Familial cancer risk in family members and spouses of patients with early-onset head and neck cancer.

Reported patterns of familial aggregation of head and neck cancer (HNC) vary greatly, with many studies hampered by the limited number of subjects. Altogether 923 early-onset (≤40 years old) HNC probands, their first-degree relatives, spouses, and siblings' offspring were ascertained. Cumulative risk and standardized incidence ratios (SIRs) were estimated. Of all early-onset HNC families, only 21 (2.3%) had familial HNC cancers at any age and less than five familial early onset HNC cancers among first-degree relatives. The cumulative risk of HNC for siblings by age 60 (0.52%) was at population level (0.33%). No increased familial risk of early-onset HNC could be discerned in family members (SIR 2.68, 95% CI 0.32-9.68 for first-degree relatives). Our study indicates that the cumulative and relative familial risk of early-onset HNC is modest in the Finnish population and, at most, only a minor proportion of early-onset HNCs are due solely to inherited genetic mutations.

Identification of nsSNPs of transcription factor E2F1 predisposing individuals to lung cancer and head and neck cancer

E2Fs transcription factors family is involved in the G1/S transition and DNA replication and their deregulated expression have been reported in various human cancers. Studies have shown that the genetic variants of E2F1 family members play an important role in head and neck carcinogenesis. In this study, we predicted six highly deleterious nsSNPs (C227F, R252H, V295D, C298Y, R56W, and Y59C) of E2F1 gene through in silico analyses. The latter was based on protein structure, function, and amino acid conservation. Molecular dynamics studies showed a deviation of the structures of the mutant proteins from the global protein parameters. Further, a case-control study that included total 535 samples (305 cancer patients and 230 controls) was conducted to find the association of the predicted SNPs with the susceptibility to lung cancer (LC) and head and neck cancer (HNC). The genotyping was done applying in-house artificial-RFLP method. Statistical analysis showed that the mutant alleles/genotypes of rs3213172 (R252H) were found to increase ∼ 2–5 fold risk of LC and HNC in all the genetic models. These results suggest that the rs3213172C/T polymorphism of the E2F1 gene could be used as an effective biomarker for genetic susceptibility to LC and HNC in our population.

Epidemiology of head and neck cancers: an update.

This review attempts to give an update of epidemiological knowledge on head and neck cancers (HNC). Worldwide, from 1990 to 2017, incidence rates for larynx and nasopharyngeal cancers decreased, whereas they increased for oro/hypopharyngeal cancers and lip/oral cavity cancers. They are still markedly higher among men than women. South Asia has the highest HNC incidence rate, followed by Europe, North America, and Australasia.Tobacco and alcohol remain the major risk factors. Rate of cancers attributable to human papillomavirus (HPV) among HNCs is highly depending on world region and tobacco use prevalence. It increases in high-income countries. In the US population, the number of HPV-attributable oropharyngeal cancers now exceeds the number of cervix cancers. HPV vaccination for boys is recommended in an increasing number of countries. Many occupations are associated with an increased HNC risk. Fruits and vegetables intake have a protective effect against HNC. To decrease HNC incidence, measures to reduce tobacco use and alcohol consumption remain essential. Improvement of HPV vaccination coverage is also a major objective. Reduction of carcinogens at occupation, protection of workers from carcinogen exposures, education for better diet, and easy and affordable access to fruits and vegetables can contribute to incidence decrease.

Tobacco smoking, chewing habits, alcohol drinking and the risk of head and neck cancer in Nepal.

Although tobacco smoking, pan chewing and alcohol drinking are important risk factors for head and neck cancer (HNC), the HNC risks conferred by products available in Nepal for these habits are unknown. We assessed the associations of tobacco smoking, chewing habits, and alcohol drinking with HNC risk in Nepal. A case-control study was conducted in Nepal with 549 incident HNC cases and 601 controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using unconditional logistic regression adjusting for potential confounders. We observed increased HNC risk for tobacco smoking (OR: 1.54; 95% CI: 1.14, 2.06), chewing habits (OR: 2.39; 95% CI: 1.77, 3.23), and alcohol drinking (OR: 1.57; 95% CI: 1.14, 2.18). The population attributable fraction (PAF) was 24.3% for tobacco smoking, 39.9% for chewing habits and 23.0% for alcohol drinking. Tobacco smoking, chewing habits, and alcohol drinking might be responsible for 85.3% of HNC cases. Individuals who smoked tobacco, chewed products and drank alcohol had a 13-fold increase in HNC risk (OR: 12.83; 95% CI: 6.91, 23.81) compared to individuals who did not have any of these habits. Both high frequency and long duration of these habits were strong risk factors for HNC among the Nepalese with clear dose-response trends. Preventive strategies against starting these habits and support for quitting these habits are necessary to decrease the incidence of HNC in Nepal.

Genetic Polymorphisms in the RAD51 Gene with a Risk of Head and Neck Cancer and Esophageal Cancer: A Meta-Analysis.

Background The role of RAD51 gene polymorphisms with the development of head and neck cancer (HNC) and esophageal cancer (EC) remains controversial. This meta-analysis was conducted to evaluate the correlation between the RAD51 polymorphisms and these two cancers quantitatively. Methods Databases of PubMed, Web of Science, and Embase were used to search relevant papers prior to August 17, 2019. STATA 11.0 was performed to observe the correlation. Results Ten relevant papers were enrolled in our analysis. Overall, a significant correlation was observed between the rs1801320 polymorphism and the increased risk of these two cancers (OR = 1.32, 95%CI = 1.03‐1.71 for C vs. G; OR = 1.50, 95%CI = 1.03‐2.19 for CG vs. GG; and OR = 1.44, 95%CI = 1.05‐1.99 for CC+CG vs. GG). In subgroup analyses, an increased risk was found for EC (OR = 2.07, 95%CI = 1.01‐4.25 for C vs. G; OR = 2.08, 95%CI = 1.17‐3.71 for CC vs. GG; and OR = 1.78, 95%CI = 1.00‐3.15 for CC vs. CG+GG), but not for HNC. Moreover, our analysis revealed that no statistical evidence of correlation was discovered between the polymorphism of rs1801321 and the increased risk of HNC. However, stratified analysis based on ethnicity suggested that rs1801321 polymorphism was related to the decreased risk of HNC among Caucasians (OR = 0.82, 95%CI = 0.72‐0.95 for T vs. G). Conclusions rs1801320 polymorphism was strongly associated with the risk of these two associated cancers, especially with esophageal cancer. Moreover, our results revealed that rs1801321 polymorphism was correlated to the decreased risk of HNC among Caucasians.

Relationship of single nucleotide polymorphisms and haplotype interaction of mitochondrial unfolded protein response pathway genes with head and neck cancer.

Aim: In this study, we evaluated the effect of selected polymorphisms of mitochondrial unfolded protein response (UPRmt) pathway in 500 head and neck cancer (HNC) patients and 500 healthy controls from Pakistan. Materials & methods: The experiments were conducted using tetra-ARMS PCR followed by DNA sequencing. Results: Multivariate analysis showed that AA genotype of rs3782116 showed fivefold, GG genotype of rs6598072 approximately twofold and CC genotype of rs4946936 and TT genotype of rs12212067 showed twofold increased risk of HNC. Furthermore, haplotype analysis showed that certain haplotypes of UPRmt pathway single nucleotide polymorphisms have significant association with increased HNC risk. Conclusion: These results show that genetic aberrations in UPRmt pathway genes have association with increased HNC risk and can be an indicator of advance clinical outcome especially invasion and metastasis.

Latency of tobacco smoking for head and neck cancer among HPV-positive and HPV-negative individuals.

Human papillomavirus (HPV) infection and tobacco smoking are well-known risk factors for head and neck cancers (HNC). Although an effect modification between oral HPV infection and tobacco smoking may exist, evidence is lacking on how they interact temporally. We investigated the latency and life course effects of tobacco smoking on risk of HNC among HPV-positive (HPV+ve ) and negative (HPV-ve ) individuals. We used data from 631 ever-smoker participants of a hospital-based case-control study conducted in four major hospitals in Montréal, Canada. Cases (n = 320), incident, histologically confirmed, primary squamous cell carcinomas, were frequency-matched to controls (n = 311) by age and sex. Sociodemographic and behavioral factors (e.g., tobacco and alcohol use and sexual history) were collected using a structured interview applying a life grid technique. Oral exfoliated cells were used for HPV DNA detection and genotyping. Latency effects were estimated flexibly using a Bayesian relevant exposure model and further extended with a life course approach. Retrospective smoking trajectories for HPV+ve cases and controls had similar shapes. Exposure to tobacco smoking even 40 years before diagnosis was associated with an increased HNC risk among both HPV+ve and HPV-ve participants. The effect of smoking before the start of sexual activity compared to afterwards was higher among HPV+ve individuals. This pattern of association was less profound among HPV-ve participants. Temporal interactions may exists between oral HPV infection and life course smoking trajectories in relation to HNC risk.

Polymorphisms of CHRNA3 and CHRNA5: Head and neck cancer and cigarette consumption intensity in a Brazilian population.

BackgroundCigarette consumption has been identified as the main non‐etiological factor in head and neck cancer (HNC) development. One of the main compounds in cigarettes is nicotine, which binds directly to nicotine acetylcholine receptors (nAchRs) in the body, which are encoded by different genes of the CHRNA family. Polymorphisms in some of these genes have been studied in relation to the risk of HNC and cigarette consumption intensity. The aim of this study was to evaluate whether there were associations between the CHRNA3 (rs578776) and CHRNA5 (rs16969968) polymorphisms and HNC risk and between the polymorphisms and the intensity of cigarette consumption.MethodsA total of 1,067 individuals from Heliopolis Hospital in São Paulo were investigated, including 619 patients with HNC and 448 patients without diagnosed tumors. All participants answered a questionnaire about sociodemographic information and cigarette consumption data. The polymorphisms were determined by TaqMan genotyping by real‐time PCR.ResultsThe polymorphisms studied, rs578776 (CHRNA3) and rs16969968 (CHRNA5), did not have an association with HNC risk, but the rs16969968 homozygous genotype was associated with increased cigarette consumption intensity (OR 1.93, 95% CI 1.05–3.58).ConclusionThe polymorphism CHRNA5 can be considered an indirect risk factor for neoplasms in these Brazilian samples when cigarette consumption increased.