Smoking and other risk factors for pancreatic cancer: A cohort study in men in Lithuania

Background: Cancer of the pancreas is a relatively rare, but highly fatal cancer worldwide. Cigarette smoking has been recognized as an important risk factor, but the relation to other potential determinants is still inconsistent. We investigated the association between different lifestyle, biological and anthropometric factors and the risk of pancreatic cancer in a prospective population-based cohort study from Kaunas, Lithuania. Methods: Our study included 7132 urban men initially free from any diagnosed cancer, followed for up to 30 years. 77 incident cases of pancreatic cancer were identified. Cox proportional hazards regression models were used to estimate hazard ratios (HR) and corresponding 95% confidence intervals (95% CI). Results: Compared to never smokers, current smokers had a significantly increased risk of pancreatic cancer, HR was 1.79 (95% CI 1.03–3.09) after adjustment for age, body mass index, education and alcohol consumption. Among smokers, a significant association with higher smoking intensity was shown (≥20 cigarettes/day: HR = 2.60; 95% CI 1.42–4.76, P_trend = 0.046). We also observed a significantly increased risk for ≥30 pack-years of smoking (HR = 2.24; 95% CI 1.12–4.49, P_trend = 0.16) and for age at starting smoking <18 years (HR = 2.29; 95% CI 1.11–4.70, P_trend = 0.43) as compared to never smokers. Alcohol consumption, body mass index and total cholesterol level were not significantly associated with pancreatic cancer. Conclusions: Smoking significantly increases pancreatic cancer incidence and its high prevalence in Lithuania may partly explain high incidence of the disease. No convincing evidence was found that alcohol consumption, body mass index or serum cholesterol level were associated with pancreatic cancer risk, although the assessment was limited by the lack of statistical power.     

Smoking (active and passive), N-acetyltransferase 2, and risk of breast cancer

Background: The relationship between smoking and breast cancer remains controversial. The study aim was to assess the relationship of passive and active smoking to breast cancer risk by N-acetyltransferase 2 (NAT2) phenotype, using a comprehensive assessment of both passive and active smoking. Methods: We undertook a population-based case–control study in Northeastern Ontario, Canada of 347 women diagnosed (2002–2004) with breast cancer and 775 population-based controls. The mailed study package included a questionnaire requesting information about established breast cancer risk factors, passive and active smoking, and a buccal swab for genetic analyses. Results: Among never-active smokers, a long duration of passive smoking was associated with an increased risk of breast cancer (odds ratio (OR) 1.86 (95% confidence interval (95% CI) 1.01–3.44) (test for trend (p = 0.07)); that risk was more elevated for NAT2 slow acetylators (OR 2.76, 95% CI 1.16–6.59) (and highest in extremely slow acetylators), but not elevated for NAT2 fast acetylators (OR 1.17, 95% CI 0.42–3.23). Among active smokers more than 20 pack-years of smoking was associated with an OR of 1.34 (95% CI 0.92-1.96); more elevated among NAT2 fast acetylators OR 1.93 (95% CI 1.01–3.69) but not elevated among NAT2 slow acetylators. Women who were NAT2 fast acetylators in the highest quartile for duration of active smoking had an OR of 2.74 (95% CI 1.42–5.27), with a significant test of trend (p = 0.005). Conclusions: These findings suggest that passive and active smoking may be related to breast cancer, and the effect may be differentially modified by NAT2 phenotype. Further research into the genetic modification of a breast cancer–smoking relationship may help to reconcile earlier discrepant findings.     

Pre-diagnostic smoking behaviour and poorer prognosis in a German breast cancer patient cohort – Differential effects by tumour subtype,NAT2 status,BMI and alcohol intake

BackgroundInconsistent associations of smoking and breast cancer-specific mortality might be explained by subgroups of patients with different susceptibility to harmful effects of smoking.MethodsWe used a prospective cohort of 3340 postmenopausal breast cancer patients aged 50–74 and diagnosed with invasive tumours 2001–2005 in Germany, with a median follow-up time of 6 years. The effect of pre-diagnostic smoking behaviour on mortality outcomes and risk of recurrence was investigated using delayed entry Cox regression analysis. Differential effects according to N-acetyltransferase (NAT2) status, BMI, alcohol consumption, and tumour subtypes were assessed.ResultsOverall, smoking at time of breast cancer diagnosis versus never/former smoking was non-significantly associated with increased breast cancer-specific mortality and risk of recurrence (HR 1.23, 95% CI 0.93–1.64, and HR 1.29, 95% CI 0.95–1.75, respectively). Associations were consistently stronger in NAT2 slow than in fast acetylators for all mortality outcomes. Breast cancer-specific mortality was significantly increased in smokers with NAT2 slow acetylating status (HR 1.77, 95% CI 1.13–2.79) but not in those with fast acetylating status (HR 1.09, 95% CI 0.60–1.98; P_{heterogeneity} = 0.19). Smoking was associated with significantly poorer outcomes for triple negative and luminal A-like tumours (e.g. all-cause mortality: HR 1.93, 95% CI 1.02–3.65, and HR 2.08, 95% CI 1.40–3.10, respectively). Risk of recurrence was significantly increased for women with HER2 positive tumours (HR 3.64, 95% CI 1.22–10.8). There was significant heterogeneity by BMI for non-breast cancer-specific mortality (<25 kg/m²: HR 2.52, 95% CI 1.52–4.15 vs. ≥25 kg/m²: HR 0.94, 95% CI 0.38–2.36; P_{heterogeneity} = 0.04).ConclusionThe harmful effects of smoking may be particularly relevant for certain subgroups of breast cancer patients. This may include patients with NAT2 slow acetylation status or with tumour subtypes other than luminal B, such as luminal A tumours who usually have a rather good prognosis. Emphasis on smoking cessation programmes for all cancer patients should be strengthened.     

Pre-diagnostic cigarette smoking and risk of second primary cancer: The Melbourne Collaborative Cohort Study

Enhanced survival following a diagnosis of cancer has led to a steep rise in the number of individuals diagnosed with a second primary cancer. We examined the association between pre-cancer cigarette smoking and risk of second cancer in 9785 participants diagnosed with first invasive cancer after enrolment in the Melbourne Collaborative Cohort Study. Follow-up was from date of first invasive cancer until diagnosis of second primary invasive cancer, death, or 31 July 2019, whichever came first. Data on cigarette smoking was collected at enrolment (1990–94) along with information on other lifestyle factors including body size, alcohol intake and diet. We estimated hazard ratios (HR) and 95 % confidence intervals (CI) for incident second cancer with several smoking measures, adjusted for potential confounders. After a mean follow-up of 7.3 years, 1658 second cancers were identified. All measures of smoking were associated with increased risk of second cancer. We observed a 44 % higher risk of second cancer for smokers of ≥ 20 cigarettes/day (HR=1.44, 95 % CI: 1.18–1.76), compared with never smokers. We also observed dose-dependent associations with number of cigarettes smoked (HR=1.05 per 10 cigarettes/day, 95 % CI: 1.01–1.09) and duration of smoking (HR=1.07 per 10 years, 95 % CI: 1.03–1.10). The risk of second cancer increased by 4 % per 10 pack-years of smoking (HR=1.04, 95 % CI: 1.02–1.06; p < 0.001). There was suggestive evidence of stronger associations with number of cigarettes smoked and pack-years of smoking for women (p_interaction<0.05), particularly for the highest risk categories of both variables. These associations with pre-diagnostic smoking were markedly stronger for second cancers known to be smoking-related than for others (p_homogeneity<0.001). Our findings for pre-diagnostic cigarette smoking indicated increased risk of second primary cancer for cancer sites considered smoking-related, highlighting the importance of assessing smoking habits in cancer survivors.     

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.     

Risk of second primary cancer associated with pre-diagnostic smoking,alcohol, and obesity in women with keratinocyte carcinoma

Keratinocyte carcinoma (KC), which includes basal-cell carcinoma (BCC) and squamous-cell cancer (SCC), has been associated with an increased risk of second primary cancers (SPCs), although the reason for this increase is unknown. We assessed the effects of smoking, alcohol, and obesity prior to the diagnosis of KC on the development of SPCs, as these are well-established risk factors for multiple cancers and may also contribute to the increased risk of SPCs among those with KC. A total of 15,628 women with self-reported KC were identified in the Nurses’ Health Study. Incident SPCs were assessed throughout the follow-up until June 2012. Cox proportional hazards models were used to calculate the hazard ratios (HRs) of SPC associated with pre-diagnostic smoking, alcohol and body mass index (BMI). We also compared these risk estimates to those for first cancers in all cohort participants. During 193,695 person-years of follow-up, we recorded 2839 SPC cases. Compared with never smokers, current smokers had a significantly elevated risk for SPC overall and specifically for lung, colorectal, and bladder cancers. We also found a positive association between higher BMI and risk for SPC overall as well as for endometrial and bladder SPCs. Women with KC who consumed alcohol ≥30 g/day had a marginally higher risk of SPC compared to non-drinkers. The associations between incident SPC risk among KC cases and smoking, alcohol, and obesity appeared similar to the associations between these risk factors and the incident first primary cancers in the whole cohort. Only in the heavy smoking (≥25 cigarettes/day) category was the HR for SPC after KC (2.34; 95% CI 1.98–2.76) slightly higher than that for the first cancer in the overall cohort (HR 1.86; 95% CI 1.75–1.98, P_{heterogeneity} = 0.01). In conclusion, pre-diagnostic smoking, alcohol and obesity prior to KC diagnosis were associated with risk of SPCs.     

Tobacco and alcohol as risk factors for oesophageal cancer in a high incidence area in South Africa

BackgroundThe Eastern Cape Province of South Africa, which includes the former Transkei has high rates of squamous cell oesophageal cancer (OC), thought to be caused mainly by nutritional deficiencies and fungal contamination of staple maize. A hospital-based case-control study was conducted at three of the major referral hospitals in this region to measure, among other suspected risk factors, the relative importance of tobacco smoking and alcohol consumption for the disease in this population.MethodsIncident cases (n = 670) of OC and controls (n = 1188) were interviewed using a structured questionnaire which included questions on tobacco and alcohol-related consumption. Odds ratios (ORs) with 95% confidence intervals for each of the risk factors were calculated using unconditional multiple logistic regression models.ResultsA monotonic dose-response was observed across the categories of each tobacco-related variable in both sexes. Males and females currently smoking a total of >14 g of tobacco per day were observed to have over 4-times the odds of developing OC (males OR = 4.36, 95% CI 2.24–8.48; females OR = 4.56, 95% CI 1.46–14.30), with pipe smoking showing the strongest effect. Similar trends were observed for the alcohol-related variables. The quantity of ethanol consumed was the most important factor in OC development rather than any individual type of alcoholic beverage, especially in smokers. Males and females consuming >53 g of ethanol per day had approximately 5-times greater odds in comparison to non-drinkers (males OR = 4.72, 95% CI 2.64–8.41; females OR = 5.24, 95% CI 3.34–8.23) and 8.5 greater odds in those who smoked >14 g tobacco daily. The attributable fractions for smoking and alcohol consumption were 58% and 48% respectively, 64% for both factors combined.ConclusionTobacco and alcohol use are major risk factors for OC development in this region.ImpactThis study provides evidence for further reinforcement of cessation of smoking and alcohol consumption to curb OC development.     

Examining the association between cigarette smoking and colorectal cancer using historical case–control data

Background: The majority of recent, well-designed studies have shown that long-term cigarette smoking increases colorectal cancer risk, but older studies with shorter durations of exposure often found no association. This study aimed to examine colorectal cancer risk by smoking exposure using data collected in the late-1950s and early-1960s. Methods: This case–control study examined colorectal cancer risk by lifetime smoking history. There were 1365 patients who visited Roswell Park Cancer Institute (RPCI) between 1957 and 1965 diagnosed with primary, incident colorectal cancers that were matched to 4096 malignancy-free controls on gender and age. Odds ratios were calculated using separate logistic regression models for each smoking exposure, while controlling for other tobacco use, county of residence, race, age, gender, and body mass index (BMI). Results: The adjusted OR for individuals who reported their greatest level of smoking to be more than 1 pack/day was 0.87 (95% CI = 0.67–1.15). Among those who smoked 42 or more years, the adjusted OR was 0.89 (95% CI = 0.68–1.15) compared to those who never smoked. For individuals who smoked more than 45 pack-years, the OR was 0.92 (95% CI = 0.72–1.19). The results did not differ significantly by gender, although men had considerably greater exposure compared to women. Results also did not differ by colorectal sub-site. Conclusion: No association was found between long-term cigarette smoking and colorectal cancer risk. These results are in accord with studies that followed cohorts throughout the 1950s and 1960s. Methodological limitations, such as missing data on covariates and the higher incidence of smoking-related illness in a hospital setting, may have contributed to the null results found in this study. Prolonged population exposure to cigarettes and perhaps a changing product may explain why more recent studies have reported a positive association between smoking and colorectal cancer.     

Smoking related risk involved in individuals carrying genetic variants of CYP1A1 gene in head and neck cancer

Background: CYP1A1 is one of the commonest genes which had been widely investigated to find the risk of various malignancies in different ethnic groups. The polymorphism in these genes with a combination of environmental exposure has been hypothesized to confer a differential risk of cancer for individuals carrying these genetic variants. Based on this model, individuals with higher CYP1A1 activity would be at increased risk of cancer when exposed to high levels of smoke components. The proposed mechanism involves cytochrome P450 1A1 (CYP1A1), a gene that is inducible by xenobiotics to produce genetic susceptibility for malignancies. Patients and procedures: We performed a case–control study in 205 cases with histopathologically confirmed squamous cell carcinoma of head and neck and reported habits of bidi or cigarettes smoking and 245 similar controls to investigate the role of CYP1A1 polymorphisms in the risk of head and neck cancers especially among smokers of Hyderabad Indian population. Venous blood samples (5 ml) were collected from patients and control groups; genomic DNA was extracted and used for polymerase chain reaction (PCR) to determine the genotypes. RFLP assays were designed to detect each of the variant CYP1A1 alleles. Results and discussion: CYP1A1m1/m1 genotype (OR = 8.12, 95% CI: 3.27–21.30) and CYP1A1w1/m1 showed elevated risk when compared with CYP1A1w1/w1. Similarly CYP1A1w2/m2 (OR = 1.58, 95% CI: 0.94–2.67) and CYP1A1m2/m2 (OR = 6.31, 95% CI: 2.74–18.69) genotypes also showed elevated risk when compared with CYP1A1w2/w2 genotype. This data demonstrated that smoking was a risk factor for head and neck cancers. The m2 mutations were in close linkage disequilibrium with the m1 mutations; 53% m1 mutants had the mutation in the m2 site. Conclusion: Those individuals carrying at least one CYP1A1 m1 or m2 variant allele were at a 2-fold elevated risk for head and neck cancer. Our data clearly demonstrates that CYP1A1 is an important determinant in susceptibility to tobacco-induced head and neck carcinogens and there is an association between genetic polymorphism in the CYP1A1 locus and elevated risk of the type of smoking among Indians. This appears to be a new and important prognostic and diagnostic marker for determining the risk of head and neck cancers genetically.     

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.     

Recreational physical activity and risk of papillary thyroid cancer among women in the California Teachers Study

Purpose: Little is known about the relationship between physical activity and thyroid cancer risk, and few cohort data on this association exist. Thus, the present study aimed to prospectively examine long-term activity and risk of papillary thyroid cancer among women. Methods: 116,939 women in the California Teachers Study, aged 22–79 years with no history of thyroid cancer at cohort entry, were followed from 1995–1996 through 2009; 275 were diagnosed with invasive papillary thyroid cancer. Cox proportional-hazards regression provided relative risk (RR) estimates and 95% confidence intervals (CI) for associations between thyroid cancer and combined strenuous and moderate recreational physical activity both in the long-term (high school through age 54 years or current age if younger than 54 years) and recently (during the three years prior to joining the cohort). Results: Overall, women whose long-term recreational physical activity averaged at least 5.5 MET-hours/week (i.e. were active) had a non-significant 23% lower risk of papillary thyroid cancer than inactive women (RR = 0.77, 95% CI: 0.57, 1.04). RR estimates were stronger among normal weight or underweight women (body mass index, BMI < 25.0 kg/m², trend p = 0.03) than among overweight or obese women (trend p = 0.35; homogeneity-of-trends p = 0.03). A similar pattern of risk was observed for recent activity (BMI < 25 kg/m², trend p = 0.11; BMI ≥ 25 kg/m², trend p = 0.16; homogeneity-of-trends p = 0.04). Associations for long-term activity did not appear to be driven by activity in any particular life period (e.g. youth, adulthood). Conclusions: Long-term physical activity may reduce papillary thyroid cancer risk among normal weight and underweight women.     

Survival trends of cancer amongst the south Asian and non-south Asian population under 30 years of age in Yorkshire, UK

Introduction: Several studies have shown differences in survival trends between ethnic groups across adults with cancer in the UK. It is unclear whether these differences exist exclusively in the older adult population or whether they begin to emerge in children and young adults. Methods: Subjects (n = 3534) diagnosed with cancer under 30 years of age in Yorkshire between 1990 and 2005 were analysed. Differences in survival rates for diagnostic subgroups were estimated by ethnic group (south Asian or not) using Kaplan–Meier estimation and Cox regression. Results: When compared to non-south Asians (all other ethnic groups excluding south Asians) a significant increased risk of death was seen for south Asians with leukaemia (hazard ratio (HR) = 1.75; 95% confidence interval (CI) = 1.11–2.76) and lymphoma (HR = 2.05; 95% CI = 1.09–3.87), whereas south Asians with solid tumours other than central nervous system tumours had a significantly reduced risk of death(HR = 0.50; 95% CI = 0.28–0.89). This was independent of socioeconomic deprivation. Conclusion: We found evidence of poorer survival outcomes for south Asians compared to non-south Asian children and young adults with leukaemia and lymphoma, but better outcomes for south Asian children and young adults with other solid tumours. This needs to be explained, and carefully addressed in the on-going development of cancer services.     

The importance of an exponential prostate-specific antigen decline after external beam radiotherapy for intermediate risk prostate cancer

Background: To study the influence of an exponential prostate-specific antigen (PSA) decline on biochemical failure after external-beam radiotherapy (EBRT). Methods: We analyzed 114 patients with intermediate risk prostate cancer (Gleason ≤ 6 and PSA 10–20 or Gleason 7 and PSA <10). Patients were randomized between EBRT doses of either 70.2 Gy or 79.2 Gy (1.8 Gy per day). All patients had a follow up of at least six PSA measurements post-EBRT. Exponential decline and PSA half life were included in a Cox regression analysis for factors associated with biochemical failure. Results: A total of 80/114 (70.2%) patterns were classified as having an exponential PSA decline. Both exponential decline (HR 0.115, 95%CI 0.03–0.44, p = 0.0016) and PSA half life ratio were statistically significant predictors (HR 1.03 (95% CI 1.01–1.06)) of biochemical failure. In the model predicting for exponential decline, none of the factors were significant. Conclusion: Patients with an exponential PSA decline show a better biochemical outcome in the long term.     

Polymorphisms in MSH2 gene and risk of gastric cancer, and interactions with lifestyle factors in a Chinese population

Background: Although polymorphisms in DNA mismatch repair (MMR) gene MSH2 have been associated with risks of many cancers, little is known about their etiology role in gastric cancer (GC) and the potential interacting role with lifestyle factors known to damage DNA. Methods: A population-based study was conducted in 3 counties (Jintan, Taixing and Huaian) of Jiangsu Province, the high-risk areas of GC in China. We investigated the association of polymorphisms IVS12?6T>C and IVS10+12G>A in MSH2 gene with the risk of GC and the potential gene–lifestyle interaction. Results: The risk of GC was found to be associated with the IVS12?6C allele (CC vs TT, OR = 2.34, 95% CI: 1.17–4.71) and IVS10+12A allele (GA or AA vs GG, OR = 1.55, 95% CI: 1.14–2.21; and GA vs GG, OR = 1.51, 95% CI: 1.04–2.17). Stratified analysis indicated that an increased risk of GC also was observed in: suspected familial subjects carrying the IVS12?6T>C (OR = 1.68, 95% CI: 1.27–2.66) or IVS10+12G>A (OR = 2.57, 95% CI: 1.53–4.10); or younger subjects carrying the IVS12?6T>C (OR = 2.15, 95% CI: 1.24–3.91) or IVS10+12G>A (OR = 2.23, 95% CI: 1.20–4.33); or male subjects carrying the IVS10+12G>A (OR = 1.64; 95% CI: 1.10–2.54). Furthermore, the combined IVS12?6CC and IVS10+12AA genotypes also significantly increased the risk of GC (OR = 2.12, 95% CI: 1.22–3.66). Statistically significant interactions were observed between: IVS10+12G>A and drinking, high pickled food or fried food intake (OR = 2.32; 95% CI: 1.43–3.78, OR = 2.55; 95% CI: 1.48–4.21 and OR = 2.88; 95% CI: 1.70–4.94, respectively); and IVS12?6T>C and high pickled food intake or fried food intake (OR = 2.65; 95% CI: 1.62–4.47 and OR = 2.48; 95% CI: 1.42–4.13, respectively). Conclusion: The IVS10+12G>A and IVS12?6T>C polymorphisms in MSH2 gene appear to be associated with risk of GC in this Chinese population. Risk for GC, stratified by related genotypes, was further modified by drinking, high pickled food or fried food intake. Larger prospective studies are needed to confirm these findings.     

Smoking and risk of meningioma: A meta-analysis

Objective: The relationship between smoking and the development of meningioma has been investigated in several epidemiological studies. However, the results of these studies are inconsistent. We conducted a meta-analysis in order to identify any potential association. Methods: PubMed, the Cochrane Library, and EMBASE databases were searched to identify relevant articles that investigated the risk of meningioma following cigarette smoking. Two researchers evaluated study eligibility and extracted the data independently, and disagreements were resolved by discussion. The variables used to estimate the pooled risk of smoking in meningioma development were the multivariate-adjusted risk estimates presented in the literature. Results: Seven case–control and two cohort studies were included in this meta-analysis. The pooled estimated risks associated with ever smoking for meningioma were 1.02 (95% confidence interval (CI): 0.85–1.21) in the case–control studies, 0.93 (95% CI: 0.83–1.04) in the cohort studies and 0.95 (95% CI: 0.87–1.05, P = 0.32) in all studies when the cohort and case–control data were combined. Subgroup analyses suggested that the risk estimates were 1.49 (95% CI: 1.06–2.09, P = 0.02), 0.86 (95% CI: 0.65–1.13), 0.79 (95% CI: 0.50–1.25) and 0.84 (95% CI: 0.69–1.03) for men, women, current and past smoking respectively. Sensitivity analyses restricted to studies with different adjustments for confounders yielded similar results. No evidence of publication bias was observed. Conclusion: Our meta-analysis suggests that there is no association between ever smoking and the risk of meningioma. However, a small but significant risk elevation is present among men smokers.     

Baseline alcohol consumption,type of alcoholic beverage and risk of colorectal cancer in the European Prospective Investigation into Cancer and Nutrition-Norfolk study

Excessive alcohol consumption has been associated with increased risk of colorectal cancer (CRC). However, the effect of modest alcohol consumption or of particular types of beverages on CRC risk remains unclear. We examined whether consumption of total alcohol or specific types of alcoholic beverages relate to overall or site-specific CRC risk in a prospective population study of 24,244 participants and 407 incident CRC cases after 11 years of follow-up. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. Consumption of specific alcoholic beverages at baseline was collected using a detailed health and lifestyle questionnaire. Total alcohol consumption was not associated with CRC risk before or after adjustment for age, sex, weight, height, and smoking status (HR: 0.80, 95% CI: 0.51–1.26 for alcohol consumption of ≥21 units/week compared with non-drinkers), and further adjustment for education level, exercise, family history of CRC, and dietary factors did not significantly alter the risk estimates (HR: 0.70, 95% CI: 0.44–1.13). No significant associations were observed between consumption of specific alcoholic beverages (beer, sherry, or spirits) and CRC risk when compared with non-drinkers after adjustment for lifestyle and dietary factors. Daily consumption of ≥1 unit of wine appeared inversely related to CRC risk (HR: 0.61, 95% CI: 0.40–0.94). No evidence was found for sex-specific relationships, and further exclusion of cases incident within 3 years of baseline did not change the associations observed. In this population-based UK cohort, we did not find any significant adverse effect of alcohol over the moderate range of intake on colorectal cancer risk.     

Effects of polymorphisms in translesion DNA synthesis genes on lung cancer risk and prognosis in Chinese men

PurposeTranslesion DNA synthesis (TLS) plays an important role in promoting replication through DNA lesions. Genetic polymorphisms in TLS genes may have potential roles in lung cancer development in humans.MethodsWe evaluated the association between genetic variants in six TLS genes and the risk and survival of lung cancer in a case–control study in China. Included in the study are 224 lung cancer patients and 448 healthy controls.ResultsCarriers of the G allele of POLκ rs5744724 had significantly reduced risk of lung cancer (odds ratio (OR) = 0.62, 95% confidence interval (CI): 0.44–0.89), comparing with those carrying the C allele, and the AA genotype of PCNA rs25406 was also associated with significantly decreased cancer risk compared with the major homozygote alleles (OR = 0.47, 95% CI: 0.25–0.86). Haplotype analysis showed that subjects with the POLκ C-G (rs5744533–rs5744724) haplotype had decreased risk of lung cancer (OR = 0.69, 95% CI: 0.49–0.98), comparing with those carrying the C-C haplotype. Besides, the heterozygote of REV1 rs3087386 and rs3792136 were independent prognostic factors for lung cancer survival with hazard radio (HR) 1.54 (95% CI: 1.12–2.12) and 1.44 (95% CI: 1.06–1.97) respectively.ConclusionsOur findings suggested that genetic variants in POLκ and PCNA genes may play roles in the susceptibility of lung cancer, and REV1 gene may have roles in lung cancer survival in Chinese men.     

Risk factors for multiple myeloma: A hospital-based case-control study in Northwest China

BackgroundThe distinctive racial/ethnic and geographic distribution of multiple myeloma (MM) suggests that both family history and environmental factors may contribute to its development.MethodsA hospital-based case–control study consisting of 220 confirmed MM cases and 220 individually matched patient controls, by sex, age and hospital was carried out at 5 major hospitals in Northwest China. A questionnaire was used to obtain information on demographics, family history, and the frequency of food items consumed.ResultsBased on multivariate analysis, a significant association between the risk of MM and family history of cancers in first degree relatives was observed (OR = 4.03, 95% CI: 2.50–6.52). Fried food, cured/smoked food, black tea, and fish were not significantly associated with the risk of MM. Intake of shallot and garlic (OR = 0.60, 95% CI: 0.43–0.85), soy food (OR = 0.52, 95% CI: 0.36–0.75) and green tea (OR = 0.38, 95% CI: 0.27–0.53) was significantly associated with a reduced risk of MM. In contrast, intake of brined vegetables and pickle was significantly associated with an increased risk (OR = 2.03, 95% CI: 1.41–2.93). A more than multiplicative interaction on the decreased risk of MM was found between shallot/garlic and soy food.ConclusionOur study in Northwest China found an increased risk of MM with a family history of cancer, a diet characterized by low consumption of garlic, green tea and soy foods, and high consumption of pickled vegetables. The effect of green tea in reducing the risk of MM is an interesting new finding which should be further confirmed.     

Risk factor for clear cell renal cell carcinoma in Chinese population: a case-control study

Background: Risk factors for clear cell renal cell carcinoma (ccRCC) differ among populations and remain controversial. We carried out a hospital-based case–control study to examine the effects of health status, lifestyle, and some genetic polymorphisms on ccRCC risk in Chinese subjects. Methods: Between 2007 and 2009, 250 newly diagnosed, histologically confirmed ccRCC cases and 299 sex-, age-matched healthy controls provided complete information including consumption of tea and alcohol, smoking, occupational exposure, body mass index (BMI), hypertension, diabetes, and urolithiasis by face-to-face interview in Shanghai. Genetic polymorphisms of cytochrome P450 mono-oxygenase (CYP1A1: 6235T>C, 4889A>G, and 4887C>A), glutathione S-transferase (GSTP1: 342A>G), and N-acetyltransferase (NAT2: 481C>T, 590G>A, and 857G>A) were identified by PCR-RFLP and DNA sequencing. Adjusted odds ratio (AOR) and 95% confidence interval (CI) were derived through multivariate logistic regression. Results: Green tea intake (≥500 ml/d) was inversely associated with ccRCC risk, with an AOR of 0.34 (95% CI 0.21–0.55). BMI (≥25 kg/m²), hypertension, and urolithiasis were independently associated with an increased risk of ccRCC, with AOR (95% CI) of 2.10 (1.32–3.34), 2.49 (1.57–3.93), and 3.33 (1.12–9.89), respectively. No association was observed between smoking, alcohol consumption, or occupational exposure with ccRCC risk. The polymorphisms and their interactions with the environmental exposures were mostly not associated with ccRCC risk. Conclusion: BMI (≥25 kg/m²), hypertension, and urolithiasis are independently associated with an increased risk, whereas green tea intake (≥500 ml/d) is independently associated with a decreased risk of ccRCC. The polymorphisms of the xenobiotic-metabolizing enzymes are weakly associated with ccRCC risk in Chinese subjects.     

Antihypertensive medications and survival in patients with cancer: A population-based retrospective cohort study

Background: The association between antihypertensive medications and survival in cancer patients remains unclear. Objectives: To explore the association between classes of antihypertensive drugs and survival in cancer patients. Methods: Provincial Cancer Registry data was linked with a Provincial Drug Program Information Network (DPIN) for patients with lung (n = 4241), colorectal (n = 3967), breast (n = 4019) or prostate (n = 3355) cancer between the years of 2004 and 2008. Cox regression analyses were used to compare survival of patients using beta blockers (BBs), angiotensin-converting enzyme inhibitors/receptor blockers (ACEi/ARB), calcium channel blockers (CCBs) or thiazide diuretics (TDs) to survival of patients who did not use any of these antihypertensive drugs. Survival of patients using only one class of antihypertensive drugs were compared to each other, with BBs as the reference class. Results: Compared to the antihypertensive drug non-user cohort, BBs had no effect on survival for any of the cancers. ACEi/ARBs use was weakly associated with increased deaths for breast cancer (HR: 1.22, 95% CI: 1.04–1.44) and lung cancer (HR: 1.11, 95% CI: 1.03–1.21) patients. Deaths were also increased with CCB use in patients with breast cancer (HR: 1.22, 95% CI: 1.02–1.47) and with TD use in lung cancer patients (HR: 1.1, 95% CI: 1.01–1.19). There was strong evidence (p-value <0.0001) of an increase in deaths with TD use for colorectal (HR: 1.28, 95% CI: 1.15–1.42), and prostate (HR 1.41, 1.2–1.65) cancer patients. When including only antihypertensive drug users prescribed one drug class, lung cancer patients receiving CCBs had improved survival compared to BBs (HR 0.79, 95% CI: 0.64–0.98). Conclusions: Some classes of antihypertensive agents are associated with a decreased survival in certain cancers. The decrease could be due to more comorbidities in antihypertensive drug users. However, CCB use was associated with improved survival in lung cancer patients.