N-Acetyltransferase-2, glutathione S-transferase M1 and T1 genetic polymorphisms, cigarette smoking and hepatocellular carcinoma: a case-control study

Our aim was to evaluate the role of N-acetyltransferase (NAT2) and glutathione S-transferase M1 and T1 (GSTM1 and GSTT1) polymorphisms in hepatocellular carcinoma (HCC) according to cigarette smoking, taking into account hepatitis B (HBV) and C (HCV) viral infection as well as alcohol consumption. A hospital-based case-control study was conducted in 2 areas of north Italy. Cases (n = 200) were patients hospitalized for HCC, and controls (n = 400) were patients admitted for reasons other than liver disease, neoplasms and tobacco- and alcohol-related diseases. Genotypes were determined using PCR and the PCR/restriction fragment length polymorphism-based method. The putative risk genotypes NAT2 slow acetylator, GSTM1 null and GSTT1 null were not associated with HCC (OR = 1.3, 95% CI 0.8-2.0; OR = 1.0, 95% CI 0.6-1.5; OR = 0.8, 95% CI 0.4-1.4, respectively). Although not statistically significant, an increase in HCC risk was observed among light smokers (1-20 pack-years) carrying GSTT1 null (OR = 1.7, 95% CI 0.6-4.7) and NAT2 slow acetylator (OR = 1.3, 95% CI 0.6-3.0) genotypes. In conclusion, there was no evidence for a gene-environment interaction in HCC risk for GSTM1, GSTT1 and NAT2 genotypes.     

Cigarette Smoking, Alcohol Consumption, and Endometrial Cancer Risk: A Population-based Study in Sweden

Objective: To assess effects of cigarette smoking and alcohol consumption on the risk of endometrial cancer among postmenopausal women. Methods: We performed a nationwide population-based case–control study among postmenopausal women aged 50–74 years in Sweden, including 709 incident endometrial cancer cases and 3368 controls. Results: Compared to never smokers, recent/current smokers had a decreased risk of endometrial cancer (multivariate OR 0.61, 95% CI 0.47–0.80), but former smokers presented no substantial difference in risk (multivariate OR 0.90, 95% CI 0.72–1.14). We observed a decreased risk of endometrial cancer for postmenopausal smoking, but there was no clear impact on risk for premenopausal smoking. The inverse association of smoking with risk was not explained by differences in body mass index between smokers and nonsmokers. Alcohol consumption was not clearly associated with risk of endometrial cancer. The multivariate OR for women consuming up to 1.6 g of alcohol per day was 1.12 (95% CI 0.88–1.44), and 0.92 (95% CI 0.70–1.20) for women consuming more than 4 g per day (p for trend over categories=0.44). Conclusions: Current cigarette smoking reduces the risk of postmenopausal endometrial cancer, but the inverse association dissipates after smoking cessation. Premenopausal smoking might not affect risk of postmenopausal endometrial cancer. Alcohol consumption is not materially associated with risk.     

<Emphasis Type="Italic">CYP1A1</Emphasis> polymorphisms and risk of lung cancer in non-smoking Chinese women: influence of environmental tobacco smoke exposure and <Emphasis Type="Italic">GSTM1/T1</Emphasis> genetic variation

Objective: We examined whether polymorphisms of CYP1A1, which plays a role in the metabolic activation of polycyclic aromatic hydrocarbons (PAHs), confer an increased risk of lung cancer in lifetime non-smoking Chinese women.Methods: A total of 126 incident lung cancer cases, of which 87.7 were pathologically confirmed, and 162 age-matched hospital controls were included. CYP1A1 MspI and Ile⁴⁶²Val polymorphisms were genotyped and tested for association with this disease.Results: An elevated risk of lung cancer was observed among individuals with the MspI CC (OR=1.7, 95 CI=0.9–3.3) and Ile⁴⁶²Val ValVal genotypes (OR=2.8, 95 CI=1.1–7.6). After stratifying by environmental tobacco smoke (ETS) exposure, the risk of lung cancer associated with both polymorphisms was higher among individuals with lower exposure to ETS, compared with those who reported at least weekly exposure. Individuals with the MspI CC genotype showed a two-fold higher risk of lung cancer if they were also null for either GSTM1 or T1 (OR=2.3, 95CI=1.0–5.0 and OR=2.7, 95 CI=1.1–6.9, respectively, compared to other genotype combinations combined).Conclusions: CYP1A1 is a susceptibility gene for lung cancer among non-smoking Asian women and this association can be influenced by ETS exposure and genetic variation at GST genes.     

Relation of serum insulin-like growth factor-I (IGF-I) and IGF binding protein-3 to risk of prostate cancer (United States)

Objective: Insulin-like growth factor I (IGF-I) exerts potent mitogenic and antiapoptotic effects on prostatic epithelial cells. Insulin-like growth factor binding protein-3 (IGFBP-3) modulates the effects of IGF-I, and independently induces apoptosis and inhibits cell growth. Previous studies have inconsistently associated IGF-I and IGFBP-3 with prostate cancer. To try and further clarify these potential associations, we undertook a sibling-matched case–control study. Methods: Serum IGF-I and IGFBP-3 were determined for 845 men (408 cases and 437 sibling controls). Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between the serum IGF levels and prostate cancer. Results: Among all study subjects, only the molar ratio of IGF-I to IGFBP-3 was associated with prostate cancer: comparing those in the highest to lowest quartiles gave an OR = 1.62 (95% CI = 1.02–2.57, trend-p = 0.04). Among men with clinically less aggressive disease, we observed positive associations between prostate cancer and high levels of IGF-I (OR = 2.78, 95% CI = 1.06–6.80, trend-p = 0.03), and IGFBP-3 (OR = 2.68, 95% CI = 1.08–6.80, trend-p = 0.04). Simultaneously modeling both left the IGF-I result essentially unchanged, while substantially weakening the IGFBP-3 association. Conclusions: We found that a high IGF-I to IGFBP-3 molar ratio was associated with an increased risk of prostate cancer. Furthermore, high IGF-I was associated with increased risk of prostate cancer among men with less advanced disease at diagnosis. These results lend support to the hypothesis that IGF-I, or the IGF-I to IGFBP-3 molar ratio, is an important risk factor for prostate cancer.     

Cigarette smoking,glutathione-s-transferase M1 and t1 genetic polymorphisms,and breast cancer risk (United States)

Objective: It has been suggested that functional polymorphisms in genes encoding tobacco carcinogen-metabolizing enzymes may modify the relationship between tobacco smoking and breast cancer risk. We sought to determine if there is a gene–environment interaction between GSTM1 (GSTM1A and GSTM1B), and GSTT1 genotypes and cigarette smoking in the risk of breast cancer. Methods: Cases and controls were recruited in a case–control study conducted in Connecticut from 1994 to 1998. Cases were histologically confirmed, incident breast cancer patients, and controls were randomly selected from women histologically confirmed to be without breast cancer. A total of 338 cases and 345 controls were genotyped for GSTM1 and GSTT1. Results: None of the GSTM1 genotypes, either alone or in combination with cigarette smoking, was associated with breast cancer risk. There was, however, a significantly increased risk of breast cancer among postmenopausal women with a GSTT1 null genotype (OR = 1.9, 95% CI 1.2–2.9). There were also indications of increased risk of breast cancer associated with cigarette smoking for postmenopausal women with GSTT1-null genotype, especially for those who commenced smoking before age 18 (OR = 2.9, 95% CI 1.0–8.8). Conclusion: Women with a GSTT1-null genotype may have an increased breast cancer risk, especially postmenopausal women who started smoking at younger ages.     

Glutathione S-transferase M1 and T1 genetic polymorphisms,alcohol consumption and breast cancer risk

Alcohol consumption has been inconsistently associated with breast cancer risk. Recent studies suggest that genetic polymorphisms of glutathione S-transferases (GSTs) may modify this relation. To determine if breast cancer risk is associated with GSTM1 and GSTT1 genetic polymorphisms, and to evaluate the effect modification between GST genotypes and alcohol consumption in the risk of breast cancer, we conducted a case-control study in the state of Connecticut in the period 1998 and 2001. Cases were histologically confirmed, incident breast cancer patients in New Haven County, CT. Controls were randomly selected from women histologically confirmed to be without breast cancer. The study results show that, while GSTM1 genotypes were not associated with breast cancer risk, GSTT1-null genotype was associated with a significant 90% increased risk for postmenopausal women (OR=1.9, 95% CI 1.2-3.0). Analysis by GST genotypes and alcohol consumption shows that GSTM1A ever-drinking women had a 2.5-fold (OR=2.5, 95% CI 1.1-5.5) increased risk of breast cancer compared to the GSTM1A never-drinkers, and the risk increases with duration and daily amount of alcohol consumption. Postmenopausal women with GSTT1-null genotype, who consumed a lifetime of >250 kg of spirit-equivalents, had an almost seven-fold increased risk (OR=6.8, 95% CI 1.4-33.9), and drinking commencing at younger ages appears to carry a higher risk. An OR of 8.2 (95% CI 1.2-57.4) was observed for those with GSTM1A, and GSTT1-null genotypes who had consumed a lifetime of >250 kg of spirit-equivalents. In conclusion, alcohol consumption may increase breast cancer risk among those who carry susceptible GST genotypes.     

Micronutrients and laryngeal cancer risk in Italy and Switzerland: a case-control study

Objective: To investigate the relation between various micronutrients and laryngeal cancer risk. Methods: A case–control study was conducted in Italy and Switzerland between 1992 and 2000. Cases were 527 patients with incident cancer of larynx, admitted to the major teaching and general hospitals of the study areas. Controls were 1297 subjects admitted for acute, non-neoplastic diseases to the same network of hospitals. Dietary habits were assessed using a validated food-frequency questionnaire. Odds ratios (OR) and their corresponding 95% confidence intervals (CI) were computed using multiple logistic regression. Results: Significant inverse relations emerged between laryngeal cancer risk and intake of vitamin C (OR = 0.2, for the highest versus the lowest intake quintile; 95% CI: 0.2–0.4), -carotene (OR = 0.2; 95% CI: 0.2–0.4), -carotene (OR = 0.3; 95% CI: 0.2–0.5), lutein/zeaxanthin (OR = 0.4; 95% CI: 0.3–0.6), vitamin E (OR = 0.4; 95% CI: 0.3–0.6), -criptoxanthin (OR = 0.4; 95% CI: 0.2–0.5), folic acid (OR = 0.4; 95% CI: 0.2–0.6), thiamin (OR = 0.4; 95% CI: 0.3–0.6), glutathione (OR = 0.5; 95% CI: 0.4–0.8), reduced glutathione (OR = 0.6; 95% CI: 0.4–0.8), vitamin B6 (OR = 0.6; 95% CI: 0.4–0.9) and potassium (OR = 0.6; 95% CI: 0.4–0.9). Direct associations were found with zinc (OR = 1.5; 95% CI: 1.0–2.2) and vitamin D (OR = 1.8; 95% CI: 1.2–2.6). Combining low intakes of vitamin C, carotene, vitamin E, and folate with heavy smoking and drinking led to ORs between 80 and 170. Conclusions: This study provides further support that, independently from smoking and alcohol consumption, the intake of several micronutrients, including selected antioxidants, is inversely related to laryngeal cancer risk.     

Olive oil,seed oils and other added fats in relation to ovarian cancer (Italy)

Objective: This study investigates the potential role of olive oil and other added fats used for seasoning or cooking on ovarian carcinogenesis. Methods: We analyzed data from a multicentre case–control study conducted between 1992 and 1999 in Italy, including a total of 1031 incident with a first diagnosis, histologically confirmed epithelial ovarian cancer cases and 2411 hospital controls with acute, non-malignant and non-gynecological conditions. The subjects' usual diet was investigated through a validated food-frequency questionnaire, including specific questions aimed at assessing added fat intake patterns. Results: After allowance for study centre, year at interview, age, education, parity, oral contraceptive use, and total energy intake, a reduced risk of ovarian cancer was observed for high intake of olive oil (odds ratio (OR) = 0.68, 95% confidence interval (CI) 0.50–0.93 for the highest quintile of intake, compared to the lowest one) and for a group of specific seed oils (i.e. sunflower, maize, peanut, and soya) (OR = 0.59, 95% CI 0.46–0.76). No significant associations were observed for mixed seed oils, butter, and margarine. Conclusions: The present study suggests a favorable effect of olive oil and other vegetable oils on ovarian cancer in this Italian population.     

GSTM1、GSTT1基因多态性和饮酒习惯与原发性肝癌发生的危险性

目的　研究GSTM 1和GSTT 1基因的多态性和饮酒习惯与原发性肝癌发生的危险性。方法　在肝癌高发区江苏省泰兴市进行了以人群为基础的病例对照研究 ,并应用多重PCR法检测了 2 0 7例原发性肝癌及其 1∶1配对的正常对照的GSTM 1和GSTT 1基因型。结果　GSTM 1空白基因型的频率 ,病例组为 5 8.94% ,对照组为 5 7.0 0 % ;GSTT 1空白基因型的频率 ,病例组和对照组分别为 5 2 .17%和 46.86% ,2组间无显著性差异。但GSTT 1的空白基因型与非空白基因型相比 ,当其长期饮用高度白酒达2 3年以上或月饮酒量大于 3 0 0 0 g时 ,患肝癌的危险性显著增高 (OR =2 .5 6,95 %CI为 1.0 8～ 6.0 5或OR =3 .48,95 %CI为 3 1.47～ 8.2 2 ) ;此外分析饮酒总量 (kg·年 )也得到同样的结果 (OR =3 .71,95 %为 1.5 1～ 9.12 )。结论　携带GSTT 1空白基因型且有长期大量饮酒习惯者 ,其患肝癌的危险性显著增高     

Glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) Polymorphisms and Lung Cancer Risk among a Select Group of Iranian People

Objective(s): Lung cancer, caused primarily by smoking, is one of the leading determinants of mortality throughoutthe world. Here we investigated the effects of polymorphisms in two enzymes, i.e., GSTT1 and GSTM1, related tothe antioxidant defense line against carcinogens associated with lung cancer among a select group of Iranian people.Materials and Methods: One hundred and twenty lung cancer patients from two referral centers in Tehran, Iran, wererecruited for comparison with 120 healthy controls. Genomic DNA was extracted from the FFPE tumor tissues ofthe select cases and peripheral blood buffy coats of healthy controls. The polymorphisms of GSTT1 and GSTM1 wereinvestigated by multiplex polymerase chain reaction. Results: With the 240 samples studied, no specific relationshipwith lung cancer was discerned for the GSTM1 (P=0.35; OR=1/33; 95% CI=0.79-2.25) polymorphism, but the GSTT1(P=0.005; OR=2.4; CI=1.32-4.35) gene polymorphism revealed a notable association on logistic regression, takinginto account age and sex factors. Furthermore, the GSTT1 genotype distribution in patients with LSCC was differentfrom that of healthy cases (P=0.006; OR=3.11; CI=1.38-7.04). The risk of developing lung cancer with the T0M1genotype was 3.46 times higher than with T1M1 genotype (P=0.002; OR=3.46; CI=1.61-7.46). Moreover, the risk ofdeveloping LSCC cancer in people with T0M1 genotypes was significantly elevated (P=0.004; OR=4.5; CI=1.62-12.52).Conclusion: Unlike GSTM1, the GSTT1 genotype distribution is associated with the incidence of lung cancer in Iranianpeople. Different types of lung cancer appear to show various correlations with GST polymorphisms in this regard.     

Glycemic index and load and risk of upper aero-digestive tract neoplasms (Italy)

Background: The ability of dietary carbohydrates to affect blood glucose and insulin levels by dietary carbohydrates is best measured by the glycemic index (GI) and glycemic load (GL) which have been directly associated with risk of several chronic conditions, including cancer. Patients and methods: Three case–control studies were conducted between 1992 and 2000 in Italy. The first one included 598 hospital patients with incident, histologically confirmed oral and pharyngeal cancer and 1491 controls admitted to the same hospital networks for acute, non-neoplastic diseases; the second study included 304 subjects with squamous cell oesophageal cancer and 743 controls; the third one included 460 cases with laryngeal cancer and 1088 controls. All subjects were interviewed using a validated food frequency questionnaire. Results: The odds ratios (OR) of upper aero-digestive tract neoplasms for the highest versus the lowest quintile of dietary GI and GL were 1.5 (95% confidence interval [CI]: 1.1–2.0) and 1.8 (95% CI: 1.1–2.9), respectively. The associations were in the same direction for various cancer sites. The ORs were apparently stronger in women, in those with high body mass index and reporting low alcohol consumption. Conclusions: This study supports the hypothesis that high dietary GI and GL are associated with cancers of the upper aero-digestive tract.     

Association of diabetes mellitus with prostate cancer: Nested case–control study (Prostate testing for cancer and Treatment study)

Observational studies suggest that diabetes is associated with a decreased risk of prostate cancer, but few are population based or have investigated associations with cancer stage or duration of diabetes. We report a case–control study nested within the population‐based Prostate testing for cancer and Treatment (ProtecT) study ISRCTN20141297. Men aged 50–69 years based around 9 UK cities were invited for a prostate‐specific antigen (PSA) test between June 2002 and November 2006. Amongst 55,215 PSA‐tested men, 1,966 had histologically confirmed prostate cancer; of these, 1,422 (72.3%) completed the questionnaire and 1,291 (65.7%) had complete data for analysis. We randomly selected 6,479 age‐ (within 5 years) and general practice‐matched controls. The prevalence of diabetes was 89/1,291 (6.9%) in cases and 555/6,479 (8.6%) in controls. Diabetes was associated with a reduced risk of prostate cancer (odds ratio = 0.78; 95% confidence interval: 0.61–0.99). There was weak evidence that the inverse association was greater for well‐ versus poorly differentiated cancers (p = 0.07). The magnitude of the inverse association did not change with increasing duration of diabetes (p for trend = 0.95). Diabetes is associated with a decreased risk of PSA‐detected prostate cancer. These data add to the evidence of the association of diabetes with prostate cancer in the PSA era.     

Association of NAT2 and smoking in relation to breast cancer incidence in a population-based case-control study (United States)

Objective: To evaluate the potential interaction between N-acetyltransferase 2 (NAT2) and smoking in breast cancer incidence. Methods: The data are derived from a population-based case–control study of women aged 20–69 years who were residents of Massachusetts or Wisconsin during 1997–1998. Incident cases of invasive breast cancer were identified through state tumor registries and age-similar controls were selected at random from population lists. Telephone interviews were conducted to obtain information on known and suspected risk factors including smoking history. Women provided oral mucosal DNA through the mail for genetic studies. Results: A total of 791 cases and 797 controls were included in the analysis. Overall, smoking was modestly associated with breast cancer risk (multivariate odds ratio (OR) for ever smoking: 1.37; 95% confidence interval (CI): 1.12–1.69), and there was a trend in risk for greater pack-years of smoking among postmenopausal women (p for trend = 0.02). Overall, NAT2 was not related to invasive breast cancer (multivariate OR: 1.11; 95% CI: 0.90–1.36). Associations of smoking with breast cancer tended to be somewhat stronger among the women with the slow acetylator genotype for NAT2: when compared to those who never smoked and were rapid acetylators, the OR for ever smoking was 1.50 (95% CI: 1.11–2.02) in slow acetylators, and OR: 1.24 (95% CI: 0.91–1.70) in rapid acetylators. However, tests for multiplicative interaction were not significant in case–control comparisons, or in case-only analyses. Conclusion: Results of the study are compatible with the majority of previous studies that indicate little or no association of NAT2, smoking, or their interaction with the occurrence of breast cancer.     

Alcohol consumption,variability in alcohol dehydrogenase genes and risk of renal cell carcinoma

Alcohol consumption has been associated inversely with renal cell carcinoma (RCC) risk; however, no study has examined effect modification by germline variation in alcohol‐metabolizing genes. We investigated whether the association between alcohol intake and RCC risk is modulated by germline variants in alcohol dehydrogenase genes in a large case–control study. Data from 652 RCC cases and 1,366 non‐cancer controls were analyzed. Alcohol intake was assessed using a standardized risk factor questionnaire. Three previously genotyped polymorphisms in ADH6 and ADH7 with the TaqMan assay were examined. Odds ratios (ORs) and 95% confidence interval (CI) were calculated using logistic regression, adjusting for covariates. Compared to non‐drinkers, ever consumption of alcohol was associated with lower RCC risk (OR = 0.52, 95% CI = 0.42–0.65). Analysis with cubic spline regression curve showed a “J‐shaped” relationship between alcohol drinks/day and RCC risk, such that there was no added benefit against RCC for consumption of more than two drinks/day. We observed effect modification by variation in rs1154454 (ADH7) (p_interaction = 0.007); a per unit increase in alcohol drink/day was associated with 35% lower RCC risk among non‐minor allele carriers, a 27% lower risk among those who carry one copy of the minor allele, but no association was observed among those with two copies of the minor allele. These findings indicate that alcohol consumption is associated with lower RCC risk. Consuming more than two drinks a day does not confer additional protection against RCC. The association between alcohol intake and RCC risk appears to be modulated by inter‐individual germline variation in alcohol‐metabolizing genes.     

Glutathione S-transferase M1 and T1 Polymorphisms,Cigarette Smoking and HPV Infection in Precancerous and Cancerous Lesions of the Uterine Cervix

Glutathione S-transferases (GSTs) play an important role in detoxification of carcinogenic electrophiles.The null genotypes in GSTM1 and GSTT1 have been implicated in carcinogenesis. Present study was planned toevaluate the influence of genetic polymorphisms of GSTM1 and GSTT1 gene loci in cervical carcinogenesis. Thestudy was conducted in Lok Nayak hospital, New Delhi. DNA from clinical scrapes of 482 women with minorgynaecologic complaints attending Gynaecology OPD and tumor biopsies of 135 cervical cancer cases attendingthe cancer clinic was extracted. HPV DNA was detected by standard polymerase chain reaction (PCR) usingL1 consensus primer pair. Polymorphisms of GSTM1 and GSTT1 were analysed by multiplex PCR procedures.Differences in proportions were tested using Pearson’s Chi-square test with Odds ratio (OR) and 95% confidenceinterval (CI). The risk of cervical cancer was almost three times in women with GSTM1 homozygous null genotype(OR-2.62, 95%CI, 1.77-3.88; p<0.0001). No association of GSTM1 or GSTT1 homozygous null genotypes wasobserved in women with normal, precancerous and cervical cancerous lesions among ≤35 or >35 years of agegroups. Smokers with null GSTT1 genotype had a higher risk of cervical cancer as compared to non-smokers(OR-3.01, 95% CI, 1.10-8.23; p=0.03). The results further showed that a significant increased risk of cervicalcancer was observed in HPV positive smoker women with GSTT1 (OR-4.36, 95% CI, 1.27-15.03; p=0.02) andGSTM1T1 (OR-3.87, 95% CI, 1.05-14.23; p=0.04) homozygous null genotypes as compared to HPV positive nonsmokers. The results demonstrate that the GST null genotypes were alone not associated with the developmentof cervical cancer, but interacted with smoking and HPV to exert effects in our Delhi population.     

Incidence of Transitional Cell Carcinoma of the Bladder and Arsenic Exposure in New Hampshire

OBJECTIVE: Arsenic is a known bladder carcinogen and populations exposed to high arsenic levels in their water supply have reported elevated bladder cancer mortality and incidence rates. To examine the effects of lower levels of arsenic exposure on bladder cancer incidence, we conducted a case-control study in New Hampshire, USA where levels above 10 micro/l are commonly found in private wells. METHODS: We studied 383 cases of transitional cell carcinoma of the bladder cancer, newly diagnosed between July 1, 1994 and June 30, 1998 and 641 general population controls. Individual exposure to arsenic was determined in toenail clippings using instrumental neutron activation analysis. RESULTS: Among smokers, an elevated odds ratio (OR) for bladder cancer was observed for the uppermost category of arsenic (OR: 2.17, 95% CI: 0.92-5.11 for greater than 0.330 mcg/g compared to less than 0.06 micro/g). Among never smokers, there was no association between arsenic and bladder cancer risk. CONCLUSIONS: These, and other data, suggest that ingestion of low to moderate arsenic levels may affect bladder cancer incidence, and that cigarette smoking may act as a co-carcinogen.     

Prospective study of plasma enterolactone and prostate cancer risk (Sweden)

Objectives: Enterolactone, a phytoestrogen produced by the intestinal microflora from precursors in plant foods, has been postulated to protect against hormone-dependent cancers. We studied the association between plasma enterolactone and risk of prostate cancer. Methods: In the Northern Sweden Health and Disease Cohort, enterolactone concentrations were measured by time-resolved fluoroimmunoassay in plasma taken from 265 men who were diagnosed with prostate cancer at a mean time of 5 years after blood collection, and in plasma from 525 control men, matched for age and date of blood collection. Results: There was no significant association between quartiles of plasma enterolactone and risk of prostate cancer. Odds ratios for prostate cancer, estimated by conditional logistic regression for increasing concentrations of enterolactone in quartiles were 1.00 (referent), 0.81 (95% confidence interval 0.52–1.27), 1.03 (0.67–1.58), and 1.22 (0.80–1.86). Adjustments for body mass index (BMI), smoking status and stratification for age, lag time, storage time and tumour characteristics did not materially alter risk estimates. Men with very low enterolactone levels, however, had significantly higher risk of prostate cancer, odds ratio for bottom decile versus all other deciles was 1.68 (1.03–2.74). Conclusions: Our results do not support the hypothesis that enterolactone formed from dietary lignans protects against prostate cancer.     

Alcohol Intake Interacts with Functional Genetic Polymorphisms of Aldehyde Dehydrogenase (ALDH2) and Alcohol Dehydrogenase (ADH) to Increase Esophageal Squamous Cell Cancer Risk

Introduction

Studies have reported alcohol consumption and genetic variants as major contributing factors for esophageal squamous cell carcinoma (ESCC). However, the complicated interactions between alcohol and genetic factors involved in alcohol metabolism have not been well elucidated with respect to augmented risk of ESCC.

Use of anti-inflammatory and non-narcotic analgesic drugs and risk of non-Hodgkin's lymphoma (NHL) (United States)

Objective: To examine whether exposures to anti-inflammatory and non-narcotic analgesic drugs are associated with risk of non-Hodgkin's lymphoma (NHL). Methods: A case–control study was conducted among women living in upstate New York. The study involved 376 cases of NHL identified through the New York State Cancer Registry and 463 controls randomly selected from the Medicare beneficiary files and New York State driver's license records. Information regarding use of common medications in the past 20 years and potential confounding variables was obtained by telephone interview. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using an unconditional logistic regression model. Results: There were non-significant increases in risk associated with ever use of cortisone injections and oral cortisone (OR = 1.44 (Cl 0.98–2.11) for injections and 1.21 (CI 0.73–2.00) for oral cortisone, although there was no clear dose–response relationship with either type. On the other hand, the risk of NHL progressively increased with the frequency of use of non-steroidal anti-inflammatory and non-narcotic analgesic drugs (NSAID/NNAD) (p-value for trend 0.008). Women who used any of these medications daily for more than 10 years had an OR of 1.90 (CI 1.01–3.57), compared with those who used it less than once a month on average. The risk associated with long-term use was most pronounced for ibuprofen, intermediate for aspirin, and least for acetaminophen. Conclusions: Because the population-attributable risk associated with NSAID/NNAD use is potentially large, our results need to be verified in further epidemiologic studies.