Age at start of using tobacco on the risk of head and neck cancer: Pooled analysis in the International Head and Neck Cancer Epidemiology Consortium (INHANCE)

BackgroundTobacco use is a well-established risk factor for head and neck cancer (HNC). However, less is known about the potential impact of exposure to tobacco at an early age on HNC risk.MethodsWe analyzed individual-level data on ever tobacco smokers from 27 case-control studies (17,146 HNC cases and 17,449 controls) in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using random-effects logistic regression models.ResultsWithout adjusting for tobacco packyears, we observed that younger age at starting tobacco use was associated with an increased HNC risk for ever smokers (OR_{<10 years vs. ≥30 years}: 1.64, 95% CI: 1.35, 1.97). However, the observed association between age at starting tobacco use and HNC risk became null after adjusting for tobacco packyears (OR_{<10 years vs. ≥30 years}: 0.97, 95% CI: 0.80, 1.19). In the stratified analyses on HNC subsites by tobacco packyears or years since quitting, no difference in the association between age at start and HNC risk was observed.ConclusionsResults from this pooled analysis suggest that increased HNC risks observed with earlier age at starting tobacco smoking are largely due to longer duration and higher cumulative tobacco exposures.     

Short- and long-term survival outcomes among never smokers who developed lung cancer

BackgroundLung cancer is the leading cause of cancer death in the US. While an extensive literature exists detailing lung cancer risk factors and mortality among patients with a history of tobacco use, the data are more limited among individuals who have never smoked. The purpose of this investigation is to compare survival rates between the two groups and evaluate potential risk factors among never smokers.MethodsThis retrospective study included 3380 smokers and 334 never smokers who were diagnosed with lung cancer at Stony Brook University Hospital between 2003 and 2016. 1-, 3-, 5- and 10-year survival outcomes, stratified by smoking status, were compared and Kaplan-Meier curves for overall survival are provided. Cox Proportional Hazard models were used to evaluate factors influencing survival among never smokers.ResultsNever smokers with lung cancer were more likely to be female, be diagnosed with adenocarcinoma histology, and had fewer comorbidities than lung cancer patients who smoked. Although 60% of patients were diagnosed at a later stage of disease development, regardless of smoking status, overall short- and long-term survival was significantly higher among never smokers compared to those with a history of tobacco use. In addition to age and stage at diagnosis, a history of diabetes was found to be a significant prognostic factor for decreased survival among never smokers (HR=3.15, 95% CI (1.74, 5.71)).ConclusionsData from the present investigation suggest that, regardless of smoking status, approximately three of every five lung cancer patients are diagnosed at a later stage, and that both short- and long-term survival outcomes are significantly better among never smokers compared to those with a history of tobacco use. Additional studies are required to validate these findings and better explain the mechanistic drivers for the improved outcomes among never smokers.     

Smoking cessation and subsequent risk of cancer: A pooled analysis of eight population-based cohort studies in Japan

BackgroundAlthough East Asia is one of the largest tobacco-epidemic regions in the world, only a few prospective studies from Asia have investigated the impact of smoking and cessation of smoking on cancer. We aimed to assess the effect of cessation of smoking on the risk of cancer using eight population-based cohort studies in Japan.MethodsWe analyzed pooled data from eight population-based prospective cohort studies in Japan with more than 320,000 participants to assess the effect of smoking cessation on the risk of total cancers and smoking-related cancers.ResultsAfter adjustment for potential confounders, cancer risks in men with >21 years of smoking cessation before baseline were found to decrease to the same level as never smokers for total cancer (never smokers: reference; former smokers with ≥21 years since smoking cessation: HR, 1.01; 95%CI: 0.91, 1.11). Even men who are heavy smokers (more than 20 pack-years) reported a reduced risk of total cancer (never smokers: reference; former smokers with ≥21 years since smoking cessation: HR, 1.06; 95%CI: 0.92, 1.23). In women, the risk of total cancer did not differ from that of never smokers after 11 years of smoking cessation before baseline (never smokers: reference; former smokers with ≥11 years since smoking cessation: HR, 0.96; 95%CI: 0.74, 1.23).ConclusionsOur study suggests that longer duration of smoking cessation may attenuate the risk of cancer in both men and women, and that even heavy smokers (more than 20 pack-years) were found to benefit from quitting smoking.     

Risk factors associated with head and neck cancer in former smokers: A Brazilian multicentric study

BackgroundReduced tobacco consumption in the population has not been associated with reduced incidence rates of head and neck cancer in several countries.ObjectiveTo explore the associations between HNC and sociodemographic characteristics and lifestyle of former smokers from three Brazilian cancer centers.MethodsA multicenter case-control study was conducted with 229 former smokers diagnosed with squamous cell carcinoma of the oral cavity, oropharynx, larynx, and 318 controls (former smokers without head and neck cancer). Bivariate and multiple logistic regression analyses were conducted to estimate odds ratios (ORs) with a 95% confidence interval (CI).Results11–20 years after smoking cessation showed significant impact on HNC reduction (OR 0.22, 95% CI, 0.12–0.39), which reached 82% (95% CI, 0.09–0.35) among 20 + former smokers when compared to individuals who had stopped smoking for up to 5 years. A history of high-intensity smoking (>40 pack-years) increased HNC risk by 2.09 times (95% CI 1.13–3.89) when compared to subjects who smoked up to 20 pack-years. Past alcohol consumption (OR 1.99, 95% CI, 1.06–3.82) was also associated with head and neck cancer risk in former smokers when compared to no alcohol consumption. There was a decreased head and neck cancer risk in former smokers who had high school level of education (OR 0.38, 95% CI, 0.16–0.91) compared to illiterate former smokers; and former smokers with moderate intake of vegetables (OR 0.49, 95% CI, 0.28–0.85) and fruits (OR 0.43, 95% CI, 0.25–0.73) compared to those with low intake.ConclusionHead and neck cancer risk in former smokers decreases after 11 years after smoking cessation, former smokers with past alcohol consumption showed an increased risk of HNC. High school level of education and moderate intake of vegetables and fruits reduced HNC risk among former smokers.     

Heterogeneity in head and neck cancer incidence among black populations from Africa,the Caribbean and the USA: Analysis of cancer registry data by the AC3

BackgroundAfrica and the Caribbean are projected to have greater increases in Head and neck cancer (HNC) burden in comparison to North America and Europe. The knowledge needed to reinforce prevention in these populations is limited. We compared for the first time, incidence rates of HNC in black populations from African, the Caribbean and USA.MethodsAnnual age-standardized incidence rates (IR) and 95% confidence intervals (95%CI) per 100,000 were calculated for 2013–2015 using population-based cancer registry data for 14,911 HNC cases from the Caribbean (Barbados, Guadeloupe, Trinidad & Tobago, N = 443), Africa (Kenya, Nigeria, N = 772) and the United States (SEER, Florida, N = 13,696). We compared rates by sub-sites and sex among countries using data from registries with high quality and completeness.ResultsIn 2013–2015, compared to other countries, HNC incidence was highest among SEER states (IR: 18.2, 95%CI = 17.6–18.8) among men, and highest in Kenya (IR: 7.5, 95%CI = 6.3–8.7) among women. Nasopharyngeal cancer IR was higher in Kenya for men (IR: 3.1, 95%CI = 2.5–3.7) and women (IR: 1.5, 95%CI = 1.0–1.9). Female oral cavity cancer was also notably higher in Kenya (IR = 3.9, 95%CI = 3.0–4.9). Blacks from SEER states had higher incidence of laryngeal cancer (IR: 5.5, 95%CI = 5.2–5.8) compared to other countries and even Florida blacks (IR: 4.4, 95%CI = 3.9–5.0).ConclusionWe found heterogeneity in IRs for HNC among these diverse black populations; notably, Kenya which had distinctively higher incidence of nasopharyngeal and female oral cavity cancer. Targeted etiological investigations are warranted considering the low consumption of tobacco and alcohol among Kenyan women. Overall, our findings suggest that behavioral and environmental factors are more important determinants of HNC than race.     

Waterpipe Tobacco Smoking and Gastric Cancer Risk among Vietnamese Men

BackgroundThe association of waterpipe tobacco (WPT) smoking with gastric cancer (GC) risk was suggested.MethodsA hospital-based case-control study was conducted to examine the association of WPT with GC risk among Vietnamese men, in Hanoi city, during the period of 2003–2011. Newly-diagnosed GC cases (n = 454) and control patients (n = 628) were matched by age (+/- 5 years) and the year of hospitalization. Information on smoking and alcohol drinking habits and diet including salty food intake and fruits/vegetables consumption were obtained by the interview. Maximum likelihood estimates of odds ratios (ORs) and corresponding 95% confidence intervals (Cis) were obtained using conditional logistic regression models.ResultsThe group with the highest consumption of citrus fruits showed a significantly low GC risk (OR = 0.6, 95%CI = 0.4–0.8, P for trend = 0.002). However, there was no association of raw vegetable consumption with GC risk. Referring to never smokers, GC risk was significantly higher in current WPT smokers (OR = 1.8, 95%CI = 1.3–2.4), and it was more evident in exclusively WPT smokers (OR = 2.7, 95%CI = 1.2–6.5). GC risk tended to be higher with daily frequency and longer duration of WPT smoking but these trends were not statistically significant (P for trend: 0.144 and 0.154, respectively). GC risk of those who started smoking WPT before the age of 25 was also significantly high (OR = 3.7, 95%CI = 1.2–11.3). Neither cigarette smoking nor alcohol drinking was related to GC risk.ConclusionThe present findings revealed that WPT smoking was positively associated with GC risk in Vietnamese men.     

Diet and the risk of head-and-neck cancer among never-smokers and smokers in a Chinese population

BackgroundFew studies have been conducted in China to investigate the association between diet and the risk of head-and-neck cancer (HNC). The aim of this study was to determine the relationship between diet and HNC risk in the Chinese population and to examine whether smoking status has any effect on the risk.MethodsOur multicenter case–control study included 921 HNC cases and 806 controls. We obtained information on the frequency of both animal- and plant-based food consumption. Unconditional logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals (95%CIs).ResultsThe risk of HNC increased with more frequent consumption of processed meat and fermented foods but decreased with frequent consumption of fruits and vegetables. There was a significant increasing P for trend of 0.006 among smokers who consumed meat and an increased OR among smokers who consumed processed meat (OR 2.95, 95%CI 1.12–7.75). Protective odds ratios for vegetable consumption were observed among smokers only. We also observed protective odds ratios for higher egg consumption among never-smokers (P for trend = 0.0.003).ConclusionsReduced HNC risks were observed for high fruit and vegetable intake, a finding consistent with the results of previous studies. Processed meat intake was associated with an increased risk. The role of dietary factors in HNC in the East Asian population is similar to that in European populations.     

Occupational exposure to petroleum-based and oxygenated solvents and oral and oropharyngeal cancer risk in men: A population-based case-control study in France

ObjectiveTo examine the association between occupational exposure to petroleum-based and oxygenated solvents and the risk of oral and oropharyngeal cancer.MethodsThe ICARE study is a large population-based case-control study conducted in France between 2001 and 2007. This present analysis was restricted to men and included 350 and 543 cases of squamous cell-carcinoma of the oral cavity and oropharynx, respectively, and 2780 controls. Lifetime tobacco, alcohol consumption and complete occupational history were assessed through detailed questionnaires. Job-exposure matrices allowed us to assess occupational exposure to five petroleum-based solvents (white spirits; diesel/fuel oils/kerosene; gasoline; benzene; special petroleum products) and five oxygenated solvents (diethyl ether; tetrahydrofuran; ketones and esters; alcohols; ethylene glycol). Odds-ratios (ORs), adjusted for age, smoking, alcohol consumption and socioeconomic status, and 95% confidence intervals (CI) were estimated using unconditional logistic models.ResultsAssociations between oral cancer risk and exposure to white spirits and diesel/fuel oils/kerosene were suggested, but there was no exposure-response trend. Concerning exposure to oxygenated solvents, participants with the highest levels of cumulative exposure to diethyl ether had a significant excess risk of oropharyngeal cancer (OR = 7.78, 95%CI 1.42 to 42.59; p for trend = 0.04). Ever exposure to tetrahydrofuran was associated with a borderline significant increased risk of oral cancer (OR = 1.87, 95%CI 0.97 to 3.61), but no exposure-response trend was observed. Additional adjustments for exposure to other solvents did not substantially change the results.ConclusionOur results do not provide evidence for a major role of petroleum-based and oxygenated solvents in the occurrence of oral and oropharyngeal cancers in men.     

Tea and coffee consumption and risk of oral cavity cancer: Results of a large population-based case-control study,the ICARE study

BackgroundResults on the relationship between coffee and tea drinking and the risk of oral cavity cancer are contrasted.The aim of this study was to evaluate the relation between coffee and tea drinking and the risk of oral cavity cancer in France, a high incidence area.Material and methodsWe conducted a population based case–control study with face-to-face interviews and standardized questionnaires (the ICARE study, Investigation of occupational and environmental causes of respiratory cancers). We used data from 689 cases of oral cavity squamous cell carcinoma and 3481 controls. Odds-ratios (ORs) and 95% confidence intervals (95% CI) associated with tea and coffee consumption (quantity, duration, cumulative consumption) were estimated by unconditional logistic regression with adjustment for age, gender, area of residence, education, body mass index, tobacco smoking and alcohol drinking.ResultsWe observed inverse associations between oral cavity cancer and tea or coffee consumption (odds ratio, 0.39; 95% CI 0.21–0.70, for the highest quartile of tea consumption, and 0.60, 95% CI 0.34–1.05, for the highest quartile of coffee consumption). Exclusive tea or coffee consumption was associated with a reduced risk of oral cavity cancer and their joint effect was multiplicative. No differences in risk between men and women or between consumers of tobacco and alcohol and non-consumers were observed. The odds ratios related to the subsites usually included in the oropharynx (soft palate and base of the tongue) did not differ significantly from that observed for the other subsites of the oral cavity.ConclusionsTea and coffee drinking may decrease the risk of oral cavity cancer through antioxidant components which play a role in the repair of cellular damages. These findings need further investigation in prospective studies and the underlying mechanisms in humans remain to be clarified.     

Associations between oral hygiene habits,diet, tobacco and alcohol and risk of oral cancer: A case–control study from India

ObjectiveThis study examines the association between the incidence of oral cancer in India and oral hygiene habits, diet, chewing and smoking tobacco, and drinking alcohol. We also assessed the effects of oral hygiene habits with oral cancer risk among chewers versus never chewers.MethodsA hospital-based case–control study was conducted in Pune, India, based on face-to-face interviews, anthropometry, and intra-oral examinations conducted for 187 oral cancer cases and 240 controls.ResultsPoor oral hygiene score was associated with a significant risk of oral cancer (adjusted OR = 6.98; 95%CI 3.72–13.05). When stratified by tobacco-chewing habit, the poor oral hygiene score was a significant risk factor only among ever tobacco chewers (adjusted OR = 14.74; 95%CI 6.49–33.46) compared with never chewers (adjusted OR = 0.71; 95%CI 0.14–3.63). Dental check-ups only at the time of pain by ever-chewers with poor oral hygiene was associated with an elevated risk (adjusted OR = 4.22; 95%CI 2.44–7.29), while consumption of green, yellow, and cruciferous vegetables and citrus fruits was protective. A linear dose–response association was observed between oral cancer and chewing tobacco in terms of age at initiation, duration, and frequency of chewing per day (P < 0.001). Smoking more than 10 bidis/cigarettes per day (adjusted OR = 2.74; 95%CI 1.28–5.89) and for a duration >25 years (adjusted OR = 2.31; 95%CI 1.14–4.71) elevated the risk of oral cancer.ConclusionGood oral hygiene habits – as characterized by healthy gums, brushing more than once daily, use of toothpaste, annual dental check-ups, and a minimal number of missing teeth – can reduce the risk of oral cancer significantly. In addition to refraining from chewing/smoking tobacco, a diet adequate in fruits and vegetables may protect against the disease.     

Deaths in Canada from lung cancer due to involuntary smoking.

Recently published evidence indicates that involuntary smoking causes an increased risk of lung cancer among nonsmokers. Information was compiled on the proportion of people who had never smoked among victims of lung cancer, the risk of lung cancer for nonsmokers married to smokers and the prevalence of such exposure. On the basis of these data we estimate that 50 to 60 of the deaths from lung cancer in Canada in 1985 among people who had never smoked were caused by spousal smoking; about 90% occurred in women. The total number of deaths from lung cancer attributable to exposure to tobacco smoke from spouses and other sources (mainly the workplace) was derived by applying estimated age- and sex-specific rates of death from lung cancer attributable to such exposure to the population of Canadians who have never smoked; about 330 deaths from lung cancer annually are attributable to such exposure.     

Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98

Objective To measure the relation between environmental tobacco smoke, as estimated by smoking in spouses, and long term mortality from tobacco related disease.Design Prospective cohort study covering 39 years.Setting Adult population of California, United States.Participants 118 094 adults enrolled in late 1959 in the American Cancer Society cancer prevention study (CPS I), who were followed until 1998. Particular focus is on the 35 561 never smokers who had a spouse in the study with known smoking habits.Main outcome measures Relative risks and 95% confidence intervals for deaths from coronary heart disease, lung cancer, and chronic obstructive pulmonary disease related to smoking in spouses and active cigarette smoking.Results For participants followed from 1960 until 1998 the age adjusted relative risk (95% confidence interval) for never smokers married to ever smokers compared with never smokers married to never smokers was 0.94 (0.85 to 1.05) for coronary heart disease, 0.75 (0.42 to 1.35) for lung cancer, and 1.27 (0.78 to 2.08) for chronic obstructive pulmonary disease among 9619 men, and 1.01 (0.94 to 1.08), 0.99 (0.72 to 1.37), and 1.13 (0.80 to 1.58), respectively, among 25 942 women. No significant associations were found for current or former exposure to environmental tobacco smoke before or after adjusting for seven confounders and before or after excluding participants with pre-existing disease. No significant associations were found during the shorter follow up periods of 1960-5, 1966-72, 1973-85, and 1973-98.Conclusions The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality, although they do not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed.     

Body mass index and the risk of head and neck cancer in the Chinese population

ObjectiveTo investigate potential associations between body mass index (BMI) and head and neck cancer (HNC) risk in an East Asian population.MethodsWe conducted a hospital-based multicenter case-control study in East Asia including 921 cases and 806 controls. We estimated the odds ratios (ORs) and 95% confidence intervals (95% CI) for HNC risks by using logistic regression, adjusting on potential confounders.ResultsCompared to normal BMI at interview (18.5–<25 kg/m²), being underweight (BMI < 18.5 kg/m²) was associated with a higher HNC risk (OR = 2.71, 95% CI 1.40–5.26). Additionally, obesity (BMI > 30 kg/m²) was associated with a lower HNC risk (OR = 0.30, 95% CI 0.16–0.57). Being underweight at age 20 was also associated with an increased risk of HNC. However, being underweight at 5 years or 2 years before interview was not associated with a higher risk of HNC.ConclusionWe observed an inverse association between BMI and HNC risk, which is consistent with previous studies in other geographic regions. Being underweight at age 20 was also associated with a higher risk of HNC, suggesting that reverse causality was not the main source of the association.     

Genotoxicity of environmental tobacco smoke: a review

Environmental tobacco smoke (ETS), or second-hand smoke, is a widespread contaminant of indoor air in environments where smoking is not prohibited. It is a significant source of exposure to a large number of substances known to be hazardous to human health. Numerous expert panels have concluded that there is sufficient evidence to classify involuntary smoking (or passive smoking) as carcinogenic to humans. According to the recent evaluation by the International Agency for Research on Cancer, involuntary smoking causes lung cancer in never-smokers with an excess risk in the order of 20% for women and 30% for men. The present paper reviews studies on genotoxicity and related endpoints carried out on ETS since the mid-1980s. The evidence from in vitro studies demonstrates induction of DNA strand breaks, formation of DNA adducts, mutagenicity in bacterial assays and cytogenetic effects. In vivo experiments in rodents have shown that exposure to tobacco smoke, whole-body exposure to mainstream smoke (MS), sidestream smoke (SS), or their mixture, causes DNA single strand breaks, aromatic adducts and oxidative damage to DNA, chromosome aberrations and micronuclei. Genotoxicity of transplacental exposure to ETS has also been reported. Review of human biomarker studies conducted among non-smokers with involuntary exposure to tobacco smoke indicates presence of DNA adducts, urinary metabolites of carcinogens, urinary mutagenicity, SCEs and hypoxanthine-guanine phosphoribosyltransferase (HPRT) gene mutations (in newborns exposed through involuntary smoking of the mother). Studies on human lung cancer from smokers and never-smokers involuntarily exposed to tobacco smoke suggest occurrence of similar kinds of genetic alterations in both groups. In conclusion, these overwhelming data are compatible with the current knowledge on the mechanisms of carcinogenesis of tobacco-related cancers, occurring not only in smokers but with a high biological plausibility also in involuntary smokers.     

Esophageal cancer in relation to alcohol drinking and tobacco use among men in Kerala,India – Karunagappally cohort

BackgroundIn the Karunagappally cohort, esophageal cancer is the third most common cancer with an age-adjusted incidence rate of 6.2 per 100,000 person-years among men. The present study analyzed the risk of esophageal cancer in relation to alcohol drinking and tobacco use.MethodsThe study included 65,528 men aged 30–84 years in the Karunagappally cohort, India.ResultsPoisson regression analysis showed that alcohol drinking significantly increased (P = 0.027) the risk of esophageal cancer and the relative risk (RR) for current drinkers was 1.6, (95 % confidence interval (CI) = 1.1–2.3). The risk increased significantly in heavy alcohol drinkers (250 g of ethanol or above per day) (RR = 2.1, 95 % CI = 1.2–3.5) (P for trend = 0.014) and among current arrack consumers (RR = 1.8, 95 % CI = 0.99–3.29) (P for trend = 0.025). Current bidi and cigarette smokers showed an increase in the trend of cancer risk. A significantly higher risk was seen in those who had started smoking bidi before the age of 18 years, RR = 1.9 (95 % CI = 1.1–3.3) (P for trend = 0.044). Furthermore, increased RR for heavy bidi and cigarette smokers were 1.6 (95 % CI = 1.1–2.5) and 2.4 (95 % CI = 1.3–4.5), respectively.ConclusionTo the best of our knowledge, this is the first cohort study in India to report an increased esophageal cancer risk with respect to alcohol drinking.     

Analysis of erythrocyte glycophorin-A variants by flow cytometry in lung disease patients detects the effect of tobacco smoke.

The glycophoryn A (GPA) assay evaluates somatic in vivo mutations. It is considered a cumulative biodosimeter for genotoxic exposures and is under evaluation in cancer risk assessment. GPA, a polymorphic membrane protein of the erythrocytes, determines the MN blood groups. The NO and NN variant frequencies (VF) may be detected in MN subjects (about 50% of the population) by flow cytometry using two differently labelled antibodies. We explored if GPA NO and NN VF might be relevant to the assessment of individual lung cancer risk and susceptibility, in a small population with a high prevalence of heavy tobacco smokers: 8 lung cancer patients and 16 subjects with non-malignant lung diseases associated with increased risk of lung cancer. There was a wide interindividual variability and complete overlap between non-neoplastic and neoplastic patients. A significant positive correlation was seen with smoking duration in NO VF (p = 0.04, age-adjusted). Current smokers (n = 12) displayed higher NO values than never (n = 1) or ex-smokers (n = 11), 36.3 +/- 18.2 and 21.0 +/- 13.2, respectively (p < 0.01). No association was shown with occupational exposure. The present exploratory study suggests that assessment of individual lung cancer risk and susceptibility by the GPA assay does not seem to be feasible. The assay appears to provide a biomarker of longterm exposure to tobacco smoke.     

Gastrin-releasing peptide receptor expression in non-cancerous bronchial epithelia is associated with lung cancer: a case-control study

Background

Normal bronchial tissue expression of GRPR, which encodes the gastrin-releasing peptide receptor, has been previously reported by us to be associated with lung cancer risk in 78 subjects, especially in females. We sought to define the contribution of GRPR expression in bronchial epithelia to lung cancer risk in a larger case-control study where adjustments could be made for tobacco exposure and sex.

Methods

We evaluated GRPR mRNA levels in histologically normal bronchial epithelial cells from 224 lung cancer patients and 107 surgical cancer-free controls. Associations with lung cancer were tested using logistic regression models.

Results

Bronchial GRPR expression was significantly associated with lung cancer (OR = 4.76; 95% CI = 2.32-9.77) in a multivariable logistic regression (MLR) model adjusted for age, sex, smoking status and pulmonary function. MLR analysis stratified by smoking status indicated that ORs were higher in never and former smokers (OR = 7.74; 95% CI = 2.96-20.25) compared to active smokers (OR = 1.69; 95% CI = 0.46-6.33). GRPR expression did not differ by subject sex, and lung cancer risk associated with GRPR expression was not modified by sex.

Conclusions

GRPR expression in non-cancerous bronchial epithelium was significantly associated with the presence of lung cancer in never and former smokers. The association in never and former smokers was found in males and females. Association with lung cancer did not differ by sex in any smoking group.     

No dramatic age-related loss of hair cells and spiral ganglion neurons in Bcl-2 over-expression mice or Bax null mice

The extent to which the effect of risk factors on cognitive ageing is dependent on APOE ε4 remains unclear. The objective of this study is to examine whether APOE ε4 allele modifies the association between health behaviors and cognition in late midlife. Data are drawn from 5447 participants of the Whitehall II study, health behaviors were assessed in 1997-1999 (mean age = 55.6, Standard Deviation (SD) = 6.0) and APOE genotype and cognitive function in 2002-2004 (mean age = 60.9, SD = 5.9). Among APOE ε4 non-carriers, current smokers had lower scores on memory (difference in T-score = -2.49, 95%CI: -3.37, -1.60), reasoning (-2.88, 95%CI: -3.74, -2.01), phonemic (-2.66, 95%CI: -3.56, -1.76) and semantic (-2.38, 95%CI: -3.28, -1.47) fluency compared to never smokers. In APOE ε4 carriers, difference between current and never smokers was seen only for reasoning (-1.92, 95%CI: -3.31, -0.51). Interaction terms supported differential effects of smoking as a function of APOE ε4 status for memory (p = 0.01), and phonemic (p = 0.008) and semantic fluency (p = 0.02). Cognitive scores were lower among non-drinkers compared to moderate drinkers, among the sedentary participants and those who ate fruits and vegetable less than 2 times per day irrespective of APOE ε4 status. This study suggests that the APOE ε4 allele modifies the association of smoking but not that of other health behaviors - alcohol consumption, physical activity, fruit and vegetable consumption - with cognitive function in late midlife.     

Differences in risk factors for head and neck cancer among men and women in Nepal: A case-control study

BackgroundHead and neck cancer (HNC) is a major cause of cancer morbidity and mortality in Nepal. The study aims to investigate differences in risk factors for head and neck cancer by sex in Nepal.MethodsA hospital-based case-control study was conducted at the B.P. Koirala Memorial Cancer Hospital in Nepal from 2016 to 2018. A semi-structured questionnaire consisting of socio-demographic characteristics, dietary habits, reproductive factors, household air pollution, tobacco use (smoking and chewing), alcohol consumption, and second-hand smoking was used to collect the data. Odds ratios (OR) and 95 % confidence intervals (CI) were estimated using unconditional logistic regression adjusting for potential confounders.ResultsA total of 549 HNC cases (438 men and 111 women) and 601 age-matched healthy controls (479 men and 122 women) were recruited in this study. An increased risk of HNC for low education level and family income were observed among men (adjusted odds ratio (AOR) for 3rd grade and less= 1.58, 95 % CI= 1.14–2.18; AOR for family monthly income < 5000 Rupees = 1.64, 95 % CI 1.20–2.24). The AORs among women were higher than the men for known risk factors (AOR for smoking 1.34 (95 % CI 0.96–1.86) for men, 2.94 (95 % CI 1.31–6.69) for women; AOR for tobacco chewing 1.76 (95 % CI 1.27–2.46) for men, 10.22 (95 % CI 4.53–23.03) for women).ConclusionOur results point to an effect modification by sex for HNC risk factors with high AORs observed among women.     

Infection with Human Papilloma Virus (HPV) and risk of subsites within the oral cancer

BackgroundThe aim of this study was to investigate the relationship between high-risk genotypes of Human Papilloma Virus (HPV) and cancer of different subsites of the oral cavity.Material and methodsA pooled analysis of five studies included on the International Head and Neck Cancer Epidemiology (INHANCE) Consortium was conducted. HPV 16 and HPV 18 were considered. Adjusted odds ratios (ORs) and corresponding 95 % confidence intervals (CIs) for HPV and each oral cavity subsites were simultaneously estimated using multinomial logistic regression models.ResultsThe analysis included 1157 cases and 3272 controls. This study showed a slightly higher prevalence of HPV infection among oral cancer cases than controls. In particular, an increased risk of other and not otherwise specified (NOS) sites within the oral cavity, oral tongue, palate and floor of mouth cancer was observed for overall HPV16 positivity (OR = 1.66, 95 % CI: 1.01−2.72; OR = 1.97, 95 % CI: 1.36−2.85; OR = 2.48, 95 % CI: 1.50−4.11; OR = 2.71, 95 % CI: 1.06−6.95, respectively). In particular, HPV16E7 was related to cancer of floor of mouth, oral cavity NOS and palate (OR = 2.71, 95 % CI: 1.06−6.95; OR = 3.32, 95 % CI:1.53−7.19; OR = 3.34, 95 % CI:1.38−8.06). Results were inconsistent for HPV18 due to low prevalence of infection.ConclusionOur study suggests that HPV16 infection may increase the risk of developing floor of mouth, gum, tongue, and palate cancers.Clinical relevanceSubjects with HPV infection have a higher risk of cancer from all sites of the oral cavity.