Opium: An emerging risk factor for gastric adenocarcinoma

Opium use has been associated with higher risk of cancers of the esophagus, bladder, larynx, and lung; however, no previous study has examined its association with gastric cancer. There is also little information on the associations between hookah (water pipe) smoking or the chewing of tobacco products and the risk of gastric cancer. In a case‐control study in Golestan Province of Iran, we enrolled 309 cases of gastric adenocarcinoma (118 noncardia, 161 cardia and 30 mixed‐location adenocarcinomas) and 613 matched controls. Detailed information on long‐term use of opium, tobacco products and other covariates were collected using structured and validated lifestyle and food frequency questionnaires. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were obtained using conditional logistic regression models. Opium use was associated with an increased risk of gastric adenocarcinoma, with an adjusted OR (95% CI) of 3.1 (1.9–5.1), and this increased risk was apparent for both anatomic subsites (cardia and noncardia). There was a dose‐response effect, and individuals with the highest cumulative opium use had the strongest association (OR: 4.5; 95% CI: 2.3–8.5). We did not find a statistically significant association between the use of any of the tobacco products and risk of gastric adenocarcinoma, overall or by anatomic subsite. We showed, for the first time, an association between opium use and gastric adenocarcinoma. Given that opium use is a traditional practice in many parts of the world, these results are of public health significance.     

Cancer risk among patients with coal workers' pneumoconiosis in Taiwan: A nationwide population‐based study

This study is aimed to evaluate the cancer risk among patients with coal workers' pneumoconiosis (CWP) using a nationwide population‐based dataset. Patients without previous cancer who had been diagnosed with CWP and followed‐up for more than 1 year between 1997 and 2006 were recruited from the Taiwan National Health Insurance database. Standardized incidence ratios (SIRs) of cancers in CWP patients were calculated and compared to the cancer incidence in the general population. Risk factors for cancer development were also analyzed. After a median follow‐up of 9.68 years, 954 cancers developed among 8,051 recruited CWP patients, with a follow‐up of 69,398 person‐years. The SIR for all cancers was 1.12 [95% confidence interval (CI) 1.04–1.18]. Males older than 80 years had a SIR of 1.27 (95% CI: 1.06–1.51). The SIRs of esophageal (1.76, 95% CI: 1.24–2.44), gastric (1.42, 95% CI: 1.13–1.76), liver and biliary tract (1.18, 95% CI: 1.01–1.37) and lung and mediastinal (1.45, 95% CI: 1.26–1.66) cancers were significantly higher in the CWP group than in the general population. Multivariate analysis showed that age ≥ 60 years [hazard ratio (HR) 1.70, 95% CI: 1.41–2.05), male gender (HR = 1.79, 95% CI: 1.44–2.23) and liver cirrhosis (HR = 3.99, 95% CI: 2.89–5.51) were significant predictors of cancer development in patients with CWP. We concluded that patients with CWP, especially elderly males, were at increased risk of cancer. Age, male gender and liver cirrhosis were independent risk factors for cancer development.     

Hookah Smoking and Lung Cancer in the Kashmir Valley of the Indian Subcontinent

Background: The literature about the causal relationship between lung cancer and tobacco smoking mostlyconcerns cigarettes. Hookah smoking is popular in the Kashmir valley of the Indian subcontinent, and is generallybelieved to be innocuous because of the passage of the smoke through water before inhalation. Objective: Todetermine the relationship of hookah smoking to lung cancer in Kashmir. Materials and Methods: In a casecontroldesign, 251 cases of lung cancer and 500 age-matched controls were studied. A predefined questionnairewas administered through a personal interview regarding various smoking and dietary patterns and the resultscompared through statistical analyses. Results: There were 194 (178 current) ever-smokers amongst the casesand 223 (134 current) amongst controls. Smokers had a 4.2 times risk of lung cancer compared to non smokers(OR 4.23, 95% CI 3.0-5.96, p<0.0001). There were 120 hookah smokers amongst the cases and 100 amongst thecontrols and hookah smokers were nearly six times at risk for lung cancer as compared to nonsmokers (OR 5.83,(95% CI 3.95-8.60, p< 0.0001). Cigarette smokers were commoner amongst cases (46 vs 64 in controls; OR 3.49,95% CI 2.18-5.60, p=0.000). The severity of smoking was associated with a higher risk of lung cancer (Chi-square72.09, p 0.000).The practice of changing water of the hookah after each session proved non-existent. Conclusion:Hookah smoking is associated with a significantly higher risk for lung cancer in Kashmiri population, with about6 fold elevated risk as compared to non-smoking controls.     

The association of soy food consumption with the risk of subtype of breast cancers defined by hormone receptor and HER2 status

Soy food intake has previously been associated with reduced breast cancer risk. Epidemiological evidence for subgroups of breast cancer, particularly by menopausal and hormone receptor status, is less consistent. To evaluate the role of hormone receptor and menopausal status on the association between soy food intake and breast cancer risk, we measured usual soy food intake in adolescence and adulthood via food frequency questionnaire in 70,578 Chinese women, aged 40–70 years, recruited to the Shanghai Women's Health Study (1996–2000). After a median follow‐up of 13.2 years (range: 0.01–15.0), 1,034 incident breast cancer cases were identified. Using Cox models, we found that adult soy intake was inversely associated with breast cancer risk [hazard ratio (HR) for fifth versus first quintile soy protein intake = 0.78; 95% confidence interval (CI):0.63–0.97]. The association was predominantly seen in premenopausal women (HR = 0.46; 95% CI:0.29‐0.74). Analyses further stratified by hormone receptor status showed that adult soy intake was associated with significantly decreased risk of estrogen receptor (ER)+/progesterone receptor (PR)+ breast cancer in postmenopausal women (HR = 0.72; 95% CI:0.53–0.96) and decreased risk of ER?/PR? breast cancer in premenopausal women (HR = 0.46; 95% CI:0.22–0.97). The soy association did not vary by human epidermal growth factor‐2 (HER2) status. Furthermore, we found that high soy intake during adulthood and adolescence was associated with reduced premenopausal breast cancer risk (HR = 0.53; 95% CI: 0.32–0.88; comparing third vs. first tertile) while high adulthood soy intake was associated with postmenopausal breast cancer only when adolescent intake was low (HR = 0.63; 95% CI: 0.43–0.91). Our study suggests that hormonal status, menopausal status and time window of exposure are important factors influencing the soy‐breast cancer association.     

Higher carbohydrate intake is associated with increased risk of all‐cause and disease‐specific mortality in head and neck cancer patients: results from a prospective cohort study

No studies have evaluated associations between carbohydrate intake and head and neck squamous cell carcinoma (HNSCC) prognosis. We prospectively examined associations between pre‐ and post‐treatment carbohydrate intake and recurrence, all‐cause mortality, and HNSCC‐specific mortality in a cohort of 414 newly diagnosed HNSCC patients. All participants completed pre‐ and post‐treatment Food Frequency Questionnaires (FFQs) and epidemiologic surveys. Recurrence and mortality events were collected annually. Multivariable Cox Proportional Hazards models tested associations between carbohydrate intake (categorized into low, medium and high intake) and time to recurrence and mortality, adjusting for relevant covariates. During the study period, there were 70 deaths and 72 recurrences. In pretreatment analyses, high intakes of total carbohydrate (HR: 2.29; 95% CI: 1.23–4.25), total sugar (HR: 3.03; 95% CI: 1.12–3.68), glycemic load (HR: 2.10; 95% CI: 1.15–3.83) and simple carbohydrates (HR 2.26; 95% CI 1.19–4.32) were associated with significantly increased risk of all‐cause mortality compared to low intake. High intakes of carbohydrate (HR 2.45; 95% CI: 1.23–4.25) and total sugar (HR 3.03; 95% CI 1.12–3.68) were associated with increased risk of HNSCC‐specific mortality. In post‐treatment analyses, medium fat intake was significantly associated with reduced risk of recurrence (HR 0.08; 95% CI 0.01–0.69) and all‐cause mortality (HR 0.27; 95% CI 0.07–0.96). Stratification by tumor site and cancer stage in pretreatment analyses suggested effect modification by these factors. Our data suggest high pretreatment carbohydrate intake may be associated with adverse prognosis in HNSCC patients. Clinical intervention trials to further examine this hypothesis are warranted.     

Family history of cancer in first-degree relatives and risk of gastric cancer and its precursors in a Western population

Background

Family history may inform risks of gastric cancer and preneoplastic lesions.

Methods

We examined associations with history of cancer in first-degree relatives for 307 incident gastric cancer cases among 20,720 male smokers in a prospective study in Finland. Cox regression was used to calculate gastric cancer hazard ratios (HR) and 95% confidence intervals (95% CI). Logistic regression was used to estimate odds ratios (OR) and 95% CIs for low serum pepsinogen, a marker of gastric atrophy.

Results

Gastric cancer risk was associated with gastric cancer history in first-degree relatives overall (HR 1.56, 95% CI 1.15–2.12), in fathers (HR 1.67, 95% CI 1.09–2.55) and in siblings (HR 2.05, 95% CI 1.25–3.38). Associations were significant for noncardia (HR 1.83, 95% CI 1.30–2.57) but not cardia (HR 0.93, 95% CI 0.46–1.87) cancers, and marginal for both intestinal—(HR 1.53, 95% CI 0.92–2.55) and diffuse-type (HR 1.47, 95% CI 0.72–3.03) histologies. Family history of other cancer types was not associated with gastric cancer risk. Family history of gastric cancer was associated with low pepsinogen (OR 1.29, 95% CI 1.11–1.50).

Conclusions

Family history of gastric cancer is strongly associated with specific subtypes of gastric cancer as well as with gastric atrophy, a risk factor for developing this malignancy.

     

Positive association between Toll-like receptor 4 gene +896A/G polymorphism and susceptibility to gastric carcinogenesis: a meta-analysis

Several studies have investigated the association between the Toll-like receptor 4 (TLR4) gene +896A/G polymorphism and gastric carcinogenesis, including gastric cancer and precancerous gastric lesions. However, published results are inconsistent. So, we performed a meta-analysis to assess whether the TLR4 +896A/G single-nucleotide polymorphism (SNP) is a risk factor in gastric cancer development. We searched PubMed and Embase databases for studies that reported the odds ratio (OR) and 95 % confidence interval (CI) for the association between the TLR4 +896A/G SNP and the risk of gastric cancer and/or precancerous lesions with the last update of November 2012. Data were analyzed using Review Manager (Version 5.1), and publication bias was estimated. We included 10 study populations, comprising 2,233 cases and 2,849 controls from 8 publications. The pooled OR was 2.00 (95 % CI?=?1.59–2.53) for the G allelic model. Analysis stratified by different stages and anatomic sites of neoplasia resulted in a significantly increased risk associated with gastric cancer (OR?=?1.87, 95 % CI?=?1.44–2.44), especially the non-cardia subtype (OR?=?2.03, 95 % CI?=?1.51–2.72). Besides, the G allele emerged as a strong risk factor for precancerous gastric lesions (OR?=?2.47, 95 % CI?=?1.57–3.88). A subsequent subgroup analysis by Helicobacter pylori-positive ratio in cases (>80 %) indicated an enhancement in the association with precancerous lesions (OR?=?3.43, 95 % CI?=?1.92–6.13). The TLR4 +896A/G SNP is a risk factor in gastric carcinogenesis, especially in H. pylori-infected patients with precancerous lesions.     

Opium Use and Head and Neck Cancers: A Matched Case-Control Study in Iran

Background: Head and Neck (H and N) cancers include malignant tumors of the nasal cavity, pharynx, paranasal sinuses, oral cavity, larynx and salivary glands. Opium use might be related to these cancers. The aim of this study was to investigate the relation between Opium and its Derivatives (O and D) use and the incidence of H and N cancers. Methods: In this case-control study conducted in Kerman, 140 patients with H and N cancers and 280 healthy controls (matched for age, gender, and place of residence) were included. Information about their use of O and D, cigarette smoking, alcohol and diet were collected using a structured questionnaire. Conditional logistic regression was used to investigate the relation between variables. Results: The use of opioids was associated with an increased risk of HandN cancers (Adjusted OR: 8.13; CI: 4.08-16.2). A significant dose-response relation between O and D use was observed, with high use Adjusted OR=8.91; 95% CI: 4.03-19.65 and low use Adjusted OR=6.52; 95% CI: 3.18- 13.36. This dose-response association was stronger in patients with laryngeal cancer and opioids use, with high use Adjusted OR = 11.17; 95% CI=4.48-28.09 and low use Adjusted OR = 9.46; 95% CI= 3.97- 22.52. Conclusion: The results show that opium use can be considered as an important risk factor for H and N cancers. Also in Iran, opium seems to play a more important role than cigarette smoking.     

Reproductive factors,hormone use and gastric cancer risk: The Singapore Chinese Health Study

Gastric cancer incidence varies greatly worldwide, but is consistently twice as high in men than in women. The hormone‐related factors hypothesized to be associated with lower risk of gastric cancer in women have not been fully explored in populations with a high background risk of gastric cancer. The Singapore Chinese Health Study (SCHS) is a prospective cohort study in which 34,022 of the participants enrolled between 1993 and 1998 were women between 45 and 74 years of age. Information on reproductive histories, hormone replacement therapy (HRT) and oral contraceptive (OC) use was collected through in‐person interviews at baseline. As of December 31, 2013, 269 incident gastric cancer cases were identified. Multivariable‐adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated to evaluate gastric cancer risk associations. Older age at natural menopause (≥55 versus <45 years: HR = 0.50, 95% CI: 0.25–0.99), type of menopause (other versus natural: HR = 0.48, 95% CI: 0.27–0.87) and greater years of menstrual cycling (fourth versus first quartile: HR = 0.67, 95% CI: 0.46–0.96) were associated with a decreased risk of gastric cancer. Ever use of OCs and HRT was also associated with reduced risk of gastric cancer; the multivariable‐adjusted HRs (95% CIs) were 0.40 (0.17–0.90) for use of HRT >3 years and 0.67 (0.47–0.94) for ever use of OCs, compared with never use. Reproductive factors associated with a longer window of fertility and the use of exogenous hormones were shown to reduce gastric cancer development in a cohort of Chinese women with a high background risk of gastric cancer.     

Dietary glycemic index and glycemic load and risk of colorectal cancer: results from the EPIC‐Italy study

A carbohydrate‐rich diet, resulting in high blood glucose and insulin, has been hypothesized as involved in colorectal cancer etiology. We investigated dietary glycemic index (GI) and glycemic load (GL), in relation to colorectal cancer, in the prospectively recruited EPIC‐Italy cohort. After a median 11.7 years, 421 colorectal cancers were diagnosed among 47,749 recruited adults. GI and GL were estimated from validated food frequency questionnaires. Multivariable Cox modeling estimated hazard ratios (HRs) for associations between colorectal cancer and intakes of total, high GI and low GI carbohydrate and GI and GL. The adjusted HR of colorectal cancer for highest versus lowest GI quartile was 1.35; 95% confidence interval (CI) 1.03–1.78; p trend 0.031. Increasing high GI carbohydrate intake was also significantly associated with increasing colorectal cancer risk (HR 1.45; 95% CI 1.04–2.03; p trend 0.034), whereas increasing low GI carbohydrate was associated with reducing risk (HR 0.73; 95% CI 0.54–0.98; p trend 0.033). High dietary GI and high GI carbohydrate were associated with increased risks of cancer at all colon sites (HR 1.37; 95% CI 1.00–1.88, HR 1.80; 95% CI 1.22–2.65, respectively), whereas high GI carbohydrate and high GL were associated with increased risk of proximal colon cancer (HR 1.94; 95% CI 1.18–3.16, HR 2.01; 95% CI 1.08–3.74, respectively). After stratification for waist‐to‐hip ratio (WHR), cancer was significantly associated with GI, and high GI carbohydrate, in those with high WHR. These findings suggest that high dietary GI and high carbohydrate intake from high GI foods are associated with increased risk of colorectal cancer.     

Prospective cohort study of general and central obesity,weight change trajectory and risk of major cancers among Chinese women

General obesity, typically measured using body mass index (BMI), has been associated with an increased risk of several cancers. However, few prospective studies have been conducted in Asian populations. Although central obesity, often measured using waist–hip ratio (WHR), is more predictive for type 2 diabetes and cardiovascular diseases (CVD) risk than BMI, knowledge of its association with cancer incidence is limited. In a cohort of 68,253 eligible Chinese women, we prospectively investigated the association of BMI, WHR and weight change during adulthood with risk of overall cancer and major site‐specific cancers using multivariate Cox proportional hazard models. Compared to the BMI group of 18.5–22.9 kg/m², obese (BMI ≥ 30 kg/m²) women were at an increased risk of developing overall cancer (hazard ratio = 1.36, 95% confidence interval = 1.21–1.52), postmenopausal breast cancer (HR: 2.43, 95% CI: 1.73–3.40), endometrial cancer (HR: 5.34, 95% CI: 3.48–8.18), liver cancer (HR: 1.93, 95% CI: 1.14–3.27) and epithelial ovarian cancer (HR: 2.44, 95% CI: 1.37–4.35). Weight gain during adulthood (per 5 kg gain) was associated with increased risk of all cancers combined (HR: 1.05, 95% CI: 1.03–1.08), postmenopausal breast cancer (HR: 1.17, 95% CI: 1.10–1.24) and endometrial cancer (HR: 1.37, 95% CI: 1.27–1.48). On the other hand, WHR was not associated with cancer risk after adjustment for baseline BMI. These findings suggest that obesity may be associated with cancer risk through different mechanisms from those for type 2 diabetes and CVD and support measures of maintaining health body weight to reduce cancer risk in Chinese women.     

Adolescent and mid‐life diet and subsequent risk of thyroid cancer in the NIH‐AARP diet and health study

Although thyroid cancer is suspected to have a nutritional etiology, prospective studies examining the relationship between diet and thyroid cancer are lacking. During 1996–1997, NIH‐AARP Diet and Health Study participants, ages 51–72 years, completed a 37‐item food frequency questionnaire about diet at ages 12–13 years (adolescence) and 10 years before baseline (mid‐life). Over a median 10 years of follow‐up, 325 individuals (143 men and 182 women) were diagnosed with thyroid cancer. Multivariable‐adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated for intakes of foods and food groups comparing the highest to the lowest quartiles. Adolescent intakes of chicken/turkey (HR = 1.59, 95% CI: 0.97–2.60; p_trend < 0.01) and sweet baked goods (HR = 1.59, 95% CI: 1.09–2.34; p_trend = 0.04) were positively associated with thyroid cancer risk, while intake of butter/margarine was inversely associated with risk (HR = 0.64, 95% CI: 0.44–0.91; p_trend < 0.02). Similar to adolescent diet, mid‐life intake of sweet baked goods was nonsignificantly associated with an increased risk of thyroid cancer (HR = 1.39, 95% CI: 0.96–2.00; p_trend = 0.11), but intake of butter/margarine was inversely associated with risk (HR = 0.66, 95% CI: 0.46–0.95; p_trend = 0.03). Among men, higher adolescent consumption of canned tuna was positively associated with risk of thyroid cancer (HR = 1.69, 95% CI: 1.01–2.83; p_trend = 0.03), and greater mid‐life intake of broccoli was associated with a twofold increased risk (HR = 2.13, 95% CI: 1.13–3.99; p_trend < 0.01). This large prospective study suggests that several components of the adolescent and mid‐life diet, including iodine‐rich foods and goitrogens, may influence thyroid cancer risk.     

Cancer incidence in relation to body fatness among 0.5 million men and women: Findings from the China Kadoorie Biobank

High body mass index (BMI) has been associated with an increased risk of several cancers. Evidence relating body fatness, especially based on different anthropometric measures, to risk of major cancers in China from prospective cohort studies is lacking. The prospective China Kadoorie Biobank study recruited 0.5 million adults aged 30–79 years from 10 diverse areas across China during 2004–2008, recording 21,474 incident cancers during 8.95 years of follow-up. BMI, body fat percentage (BFP), waist circumference (WC) and waist-to-hip ratio (WHR) were measured at baseline. We assessed the associations of body fatness with 15 major cancers by calculating Cox regression yielded adjusted hazard ratios (HRs). Each 5 kg/m² increase in BMI was associated with an increased risk of endometrial (HR, 2.01; 95% CI, 1.72–2.35), postmenopausal breast (HR, 1.29; 95% CI, 1.18–1.40), colorectal (HR, 1.17; 95% CI, 1.10–1.25) and cervical (HR, 1.15; 95% CI, 1.03–1.29) cancer, whereas it was associated with a reduced risk of esophageal (HR, 0.73; 95% CI, 0.67–0.79), lung (HR, 0.78; 95% CI, 0.74–0.82), liver (HR, 0.85; 95% CI, 0.79–0.92) and gastric (HR, 0.88; 95% CI, 0.82–0.94) cancer. Significant linear trends of BMI-cancer associations were observed, excluding for lung, gastric and cervical cancer (both overall and nonlinear p < 0.05). The relation between BFP, WC and WHR and the above cancers was similar to that of BMI. Our study indicates that either high or low body fatness contributes to the incidence of different types of cancer in China.     

Effects of dietary factors and the NAT2 acetylator status on gastric cancer in Koreans

Environmental dietary carcinogens and genetic polymorphisms in metabolic enzymes have been reported to be the risk factors for gastric cancer. This study was undertaken to investigate the effects of the diet, the N‐acetyltransferase (NAT) 2 acetylation status and their interaction on gastric cancer risk. The study population consisted of 471 gastric cancer patients and 471 age‐ and sex‐matched control subjects. NAT2 genotypes were identified using single‐nucleotide primer extension reaction methods. Thirty‐one alleles related to 12 polymorphism sites were assayed in this study. Significantly increased odds ratios were observed in former smokers (OR = 2.39, 95% CI = 1.57–3.62), heavy drinkers (OR = 1.28, 95% CI = 1.06–1.55) and individuals who eat well‐done meat (OR = 1.24, 95% CI = 1.09–1.41). The odds ratios (95% CI) for high intake of kimchi, stews and soybean paste were 3.27 (2.44–4.37), 1.96 (1.50–2.58) and 1.63 (1.24–2.14), respectively. The NAT2 genotype alone was not associated with gastric cancer risk. A significant gene–environment interaction was observed between environmental carcinogens and NAT2 genotypes. The odds ratios for kimchi, stews and soybean paste were higher in slow/intermediate acetylators than in rapid acetylators. The odds ratios for slow/intermediate acetylators were 2.28 (95% CI: 1.29–4.04) for light smokers and 3.42 (95% CI: 2.06–5.68) for well‐done meat intake. The NAT2 acetylator genotype may be an important modifier of the effects of environmental factors on gastric cancer risk. © 2009 UICC     

Vitamin E intake and the lung cancer risk among female nonsmokers: A report from the Shanghai Women's Health Study

Vitamin E includes several tocopherol isoforms, which may reduce lung cancer risk, but past studies evaluating the association between vitamin E intake and lung cancer risk were inconsistent. We prospectively investigated the associations between tocopherol intake from diet and from supplements with lung cancer risk among 72,829 Chinese female nonsmokers aged 40–70 years and participating in the Shanghai Women's Health Study (SWHS). Dietary and supplement tocopherol exposure was assessed by a validated food‐frequency questionnaire at baseline and reassessed for change in intake during follow‐up. Cox proportional hazards models with time‐dependent covariates were used to calculate multivariate‐adjusted hazard ratios (HRs) and 95% confidence interval (CIs) for lung cancer. After 12.02 years of follow‐up, 481 women were diagnosed with lung cancer. Total dietary tocopherol was inversely associated with lung cancer risk among women meeting dietary guidelines for adequate intake (AI) of tocopherol (14 mg/day or more: HR: 0.78; 95% CI 0.60–0.99; compared with the category less than AI). The protective association between dietary tocopherol intake and lung cancer was restricted to women exposed to side‐stream smoke in the home and workplace [HR = 0.53 (0.29–0.97), p‐trend = 0.04]. In contrast, vitamin E supplement use was associated with increased lung cancer risk (HR: 1.33; 95% CI: 1.01–1.73), more so for lung adenocarcinoma risk (HR: 1.79; 95% CI: 1.23–2.60). In summary, dietary tocopherol intake may reduce the risk of lung cancer among female nonsmokers; however, supplements may increase lung adenocarcinoma risk and requires further investigation.     

Hormonal and reproductive factors and risk of upper gastrointestinal cancers in men: A prospective cohort study within the UK Biobank

Incidence of upper gastrointestinal cancers of the oesophagus and stomach show a strong unexplained male predominance. Hormonal and reproductive factors have been associated with upper gastrointestinal cancers in women but there is little available data on men. To investigate this, we included 219,425 men enrolled in the UK Biobank in 2006–2010. Baseline assessments provided information on hormonal and reproductive factors (specifically hair baldness, number of children fathered, relative age at first facial hair and relative age voice broke) and incident oesophageal or gastric cancers were identified through linkage to U.K. cancer registries. Unadjusted and adjusted hazard ratios (HR) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. During 8 years of follow‐up, 309 oesophageal 210 gastric cancers occurred. There was some evidence that male pattern baldness, was associated with gastric cancer risk (adjusted HR 1.35, 95% CI 0.97, 1.88), particularly for frontal male pattern baldness (adjusted HR 1.52, 95% CI 1.02, 2.28). There was little evidence of association between other hormonal and reproductive factors and risk of oesophageal or gastric cancer, overall or by histological subtype. In the first study of a range of male hormonal and reproductive factors and gastric cancer, there was a suggestion that male pattern baldness, often used as a proxy of sex hormone levels, may be associated with gastric cancer. Future prospective studies that directly test circulating sex steroid hormone levels in relation to upper gastrointestinal cancer risk are warranted.     

Diabetes mellitus and risk of cancer in Takayama: A population‐based prospective cohort study in Japan

Diabetes mellitus (DM) has been reported to be associated with an increased risk of site‐specific cancers; however, few studies have assessed associations of DM with both total and site‐specific cancers in Japan. We examined the association of a history of DM with cancer incidence in a population‐based prospective cohort study in Japan. A total of 14 173 men and 16 547 women over 35 years old, who completed a self‐administered baseline questionnaire in 1992, were followed up for cancer incidence from September 1992 to March 2008. At baseline, 6.3% men and 2.9% women had a history of diabetes. A total of 1974 men and 1514 women were identified as newly diagnosed with cancer. Hazard ratios (HR) and 95% confidence intervals (CI) were determined using Cox proportional hazards models. After controlling for potential confounders, men with DM had a modest risk increase of total cancer occurrence compared with those without DM (HR, 1.09; 95% CI, 0.93–1.29). Increased risk of cancer of the liver (HR, 2.18; 95% CI, 1.27–3.74), bile duct (HR, 2.17; 95% CI, 1.01–4.66), and larynx (HR, 3.61; 95% CI, 1.16–11.2) in diabetic men were observed. In women, significant increased risk of total cancer (HR, 1.35; 95% CI, 1.06–1.73) and stomach cancer (HR, 2.15; 95% CI, 1.30–3.54) were observed among diabetic subjects. These data suggest that people with DM may be at increased risk of both total and some site‐specific cancers.     

Consumption of fruits,vegetables and fruit juices and differentiated thyroid carcinoma risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study

Fruit and vegetable (F&V) intake is considered as probably protective against overall cancer risk, but results in previous studies are not consistent for thyroid cancer (TC). The purpose of this study is to examine the association between the consumption of fruits, vegetables, fruit juices and differentiated thyroid cancer risk within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. The EPIC study is a cohort including over half a million participants, recruited between 1991 and 2000. During a mean follow‐up of 14 years, 748 incident first primary differentiated TC cases were identified. F&V and fruit juice intakes were assessed through validated country‐specific dietary questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression models adjusted for potential confounding factors. Comparing the highest versus lowest quartile of intake, differentiated TC risk was not associated with intakes of total F&V (HR: 0.89; 95% CI: 0.68–1.15; p‐trend = 0.44), vegetables (HR: 0.89; 95% CI: 0.69–1.14; p‐trend = 0.56), or fruit (HR: 1.00; 95% CI: 0.79–1.26; p‐trend = 0.64). No significant association was observed with any individual type of vegetable or fruit. However, there was a positive borderline trend with fruit juice intake (HR: 1.23; 95% CI: 0.98–1.53; p‐trend = 0.06). This study did not find any significant association between F&V intakes and differentiated TC risk; however a positive trend with fruit juice intake was observed, possibly related to its high sugar content.     

Italian mediterranean index and risk of colorectal cancer in the Italian section of the EPIC cohort

Colorectal cancer is among the commonest cancers worldwide. Dietary factors have been linked to colorectal cancer risk, however, few studies have evaluated the relationship between a priori dietary patterns and colorectal cancer risk. We evaluated the effect of adherence to a Mediterranean dietary pattern, as measured by the Italian Mediterranean Index, on the risk of colorectal cancer in the 45,275 participants of the Italian section of the EPIC study who completed a dietary questionnaire. Hazard ratios (HRs) with 95% confidence intervals (CIs) for colorectal cancer in relation to categories of Italian Mediterranean Index score were estimated by multivariate Cox models adjusted for known risk factors, on the whole cohort, on men and women and according to cancer subsite. During a mean follow‐up of 11.28 years, 435 colorectal cancer cases were identified. The Italian Mediterranean Index was inversely associated with colorectal cancer risk (HR: 0.50; 95% CI: 0.35–0.71 for the highest category compared to the lowest, P‐trend: 0.043). Results did not differ by sex. Highest Italian Mediterranean Index score was also significantly associated with reduced risks of any colon cancer (HR: 0.54, 95% CI: 0.36–0.81), distal colon cancer (HR: 0.44, 95% CI: 0.26–0.75) and rectal cancer (HR: 0.41, 95% CI: 0.20–0.81), but not of proximal colon cancer. These findings suggest that adherence to a Mediterranean diet (as measured by the Italian Mediterranean Index) protects against colorectal cancer in general but not against cancer developing in the proximal colon.     

Lycopene,tomato products and prostate cancer‐specific mortality among men diagnosed with nonmetastatic prostate cancer in the Cancer Prevention Study II Nutrition Cohort

While dietary lycopene and tomato products have been inversely associated with prostate cancer incidence, there is limited evidence for an association between consumption of lycopene and tomato products and prostate‐cancer specific mortality (PCSM). We examined the associations of prediagnosis and postdiagnosis dietary lycopene and tomato product intake with PCSM in a large prospective cohort. This analysis included men diagnosed with nonmetastatic prostate cancer between enrollment in the Cancer Prevention Study II Nutrition Cohort in 1992 or 1993 and June 2011. Prediagnosis dietary data, collected at baseline, were available for 8,898 men, of whom 526 died of prostate cancer through 2012. Postdiagnosis dietary data, collected on follow‐up surveys in 1999 and/or 2003, were available for 5,643 men, of whom 363 died of prostate cancer through 2012. Cox proportional hazards regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for PCSM. Neither prediagnosis nor postdiagnosis dietary lycopene intake was associated with PCSM (fourth vs. first quartile HR = 1.00, 95% CI 0.78–1.28; HR = 1.22, 95% CI 0.91–1.64, respectively). Similarly, neither prediagnosis nor postdiagnosis consumption of tomato products was associated with PCSM. Among men with high‐risk cancers (T3–T4 or Gleason score 8–10, or nodal involvement), consistently reporting lycopene intake ≥ median on both postdiagnosis surveys was associated with lower PCSM (HR = 0.41, 95% CI 0.17–0.99, based on ten PCSM cases consistently ≥ median intake) compared to consistently reporting intake < median. Future studies are needed to confirm the potential inverse association of consistently high lycopene intake with PCSM among men with high‐risk prostate cancers.