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There is evidence that diet and nutrition are modifiable risk factors for several cancers, but associations may be flawed due to inherent biases. Nutritional epidemiology studies have largely relied on a single assessment of diet using food frequency questionnaires. We conduct an umbrella review of meta-analyses of observational studies to evaluate the strength and validity of the evidence for the association between food/nutrient intake and risk of developing or dying from 11 primary cancers. It is estimated that only few single food/nutrient and cancer associations are supported by strong or highly suggestive meta-analytic evidence, and future similar research is unlikely to change this evidence. Alcohol consumption is positively associated with risk of postmenopausal breast, colorectal, esophageal, head & neck and liver cancer. Consumption of dairy products, milk, calcium and wholegrains are inversely associated with colorectal cancer risk. Coffee consumption is inversely associated with risk of liver cancer and skin basal cell carcinoma., Diet and food intake have been associated with a risk of developing different types of cancer but individual nutritional epidemiology studies are prone to inherent bias. Here, the authors perform an umbrella review of meta-analyses of observational studies and show the level of evidence for associating food and nutrients to cancer risk.

Background In the 2007 World Cancer Research Fund/American Institute for Cancer Research Second Expert Report, the expert panel judged that there was strong evidence that alcoholic drinks and body fatness increased esophageal cancer risk, whereas fruits and vegetables probably decreased its risk. The judgments were mainly based on case–control studies. As part of the Continuous Update Project, we updated the scientific evidence accumulated from cohort studies in this topic. Methods We updated the Continuous Update Project database up to 10 January 2017 by searching in PubMed and conducted dose–response meta-analyses to estimate summary relative risks (RRs) and 95% confidence intervals (CIs) using random effects model. Results A total of 57 cohort studies were included in 13 meta-analyses. Esophageal adenocarcinoma risk was inversely related to vegetable intake (RR per 100 g/day: 0.89, 95% CI: 0.80–0.99,n = 3) and directly associated with body mass index (RR per 5 kg/m2: 1.47, 95% CI: 1.34–1.61,n = 9). For esophageal squamous cell carcinoma, inverse associations were observed with fruit intake (RR for 100 g/day increment: 0.84, 95% CI: 0.75–0.94,n = 3) and body mass index (RR for 5 kg/m2 increment: 0.64, 95% CI: 0.56–0.73,n = 8), and direct associations with intakes of processed meats (RR for 50 g/day increment: 1.59, 95% CI: 1.11–2.28,n = 3), processed and red meats (RR for 100 g/day increment: 1.37, 95% CI: 1.04–1.82,n = 3) and alcohol (RR for 10 g/day increment: 1.25, 95% CI: 1.12–1.41,n = 6). Conclusions Evidence from cohort studies suggested a protective role of vegetables and body weight control in esophageal adenocarcinomas development. For squamous cell carcinomas, higher intakes of red and processed meats and alcohol may increase the risk, whereas fruits intake may play a protective role.

Purpose There is no published dose–response meta-analysis on the association between height and colorectal cancer risk (CRC) by sex and anatomical sub-site. We conducted a meta-analysis of prospective studies on the association between height and CRC risk with subgroup analysis and updated evidence on the association between body fatness and CRC risk. Methods PubMed and several other databases were searched up to November 2016. A random effects model was used to calculate dose–response summary relative risks (RR’s). Results 47 studies were included in the meta-analyses including 50,936 cases among 7,393,510 participants. The findings support the existing evidence regarding a positive association of height, general and abdominal body fatness and CRC risk. The summary RR were 1.04 [95% (CI)1.02–1.05, I² = 91%] per 5 cm increase in height, 1.02 [95% (CI)1.01–1.02, I² = 0%] per 5 kg increase in weight, 1.06 [95% (CI)1.04–1.07, I² = 83%] per 5 kg/m2 increase in BMI, 1.02 [95% (CI)1.02–1.03, I² = 4%] per 10 cm increase in waist circumference, 1.03 [95% (CI)1.01–1.05, I² = 16%] per 0.1 unit increase in waist to hip ratio. The significant association for height and CRC risk was similar in men and women. The significant association for BMI and CRC risk was stronger in men than in women. Conclusion The positive association between height and risk of CRC suggests that life factors during childhood and early adulthood might play a role in CRC aetiology. Higher general and abdominal body fatness during adulthood are risk factors of CRC and these associations are stronger in men than in women. Electronic supplementary material The online version of this article (doi:10.1007/s00394-017-1557-1) contains supplementary material, which is available to authorized users.

Background: Colorectal adenomas are known as precursors for the majority of colorectal carcinomas. While weight gain during adulthood has been identified as a risk factor for colorectal cancer, the association is less clear for colorectal adenomas. We conducted a systematic review and meta-analysis to quantify the evidence on this association. Methods: : We searched MEDLINE up to September 2016 to identify observational (prospective, cross-sectional and retrospective) studies on weight gain during adulthood and colorectal adenoma occurrence and recurrence. We conducted meta-analysis on high weight gain versus stable weight, linear and non-linear dose-response meta-analyses to analyze the association. Summary odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using a random effects model. Results: For colorectal adenoma occurrence, the summary OR was 1.39 (95% CI: 1.17-1.65; I 2 :43%, N =9 studies, cases=5,507) comparing high (midpoint: 17.4 kg) versus stable weight gain during adulthood and with each 5 kg weight gain the odds increased by 7% (2%-11%; I 2 :65%, N =7 studies). Although there was indication of non-linearity ( Pnon-linearity

Purpose The purpose of the present study was to systematically review the complex associations between energy balance-related factors and breast cancer risk, for which previous evidence has suggested different associations in the life course of women and by hormone receptor (HR) status of the tumor. Methods Relevant publications on adulthood physical activity, sedentary behavior, body mass index (BMI), waist and hip circumferences, waist-to-hip ratio, and weight change and pre- and postmenopausal breast cancer risk were identified in PubMed up to 30 April 2017. Random-effects meta-analyses were conducted to summarize the relative risks across studies. Results One hundred and twenty-six observational cohort studies comprising over 22,900 premenopausal and 103,000 postmenopausal breast cancer cases were meta-analyzed. Higher physical activity was inversely associated with both pre- and postmenopausal breast cancers, whereas increased sitting time was positively associated with postmenopausal breast cancer. Although higher early adult BMI (ages 18–30 years) was inversely associated with pre- and postmenopausal breast cancers, adult weight gain and greater body adiposity increased breast cancer risk in postmenopausal women, and the increased risk was evident for HR+ but not HR− breast cancers, and among never but not current users of postmenopausal hormones. The evidence was less consistent in premenopausal women. There were no associations with adult weight gain, inverse associations with adult BMI (study baseline) and hip circumference, and non-significant associations with waist circumference and waist-to-hip ratio that were reverted to positive associations on average in studies accounting for BMI. No significant associations were observed for HR-defined premenopausal breast cancers. Conclusion Better understanding on the impact of these factors on pre- and postmenopausal breast cancers and their subtypes along the life course is needed.

Carotenoids and retinol are considered biomarkers of fruits and vegetables intake, and are of much interest because of their anti‐inflammatory and antioxidant properties; however, there is inconsistent evidence regarding their protective effects against lung cancer. We conducted a meta‐analysis of prospective studies of blood concentrations of carotenoids and retinol, and lung cancer risk. We identified relevant prospective studies published up to December 2014 by searching the PubMed and several other databases. We calculated summary estimates of lung cancer risk for the highest compared with lowest carotenoid and retinol concentrations and dose–response meta‐analyses using random effects models. We used fractional polynomial models to assess potential nonlinear relationships. Seventeen prospective studies (18 publications) including 3603 cases and 458,434 participants were included in the meta‐analysis. Blood concentrations of α‐carotene, β‐carotene, total carotenoids, and retinol were significantly inversely associated with lung cancer risk or mortality. The summary relative risk were 0.66 (95% confidence interval [CI]: 0.55–0.80) per 5 μg/100 mL of α‐carotene (studies [n] = 5), 0.84 (95% CI: 0.76–0.94) per 20 μg/100 mL of β‐carotene (n = 9), 0.66 (95% CI: 0.54–0.81) per 100 μg/100 mL of total carotenoids (n = 4), and 0.81 (95% CI: 0.73–0.90) per 70 μg/100 mL of retinol (n = 8). In stratified analysis by sex, the significant inverse associations for β‐carotene and retinol were observed only in men and not in women. Nonlinear associations were observed for β‐carotene, β‐cryptoxanthin, and lycopene, with stronger associations observed at lower concentrations. There were not enough data to conduct stratified analyses by smoking. In conclusion, higher blood concentrations of several carotenoids and retinol are associated with reduced lung cancer risk. Further studies in never and former smokers are needed to rule out confounding by smoking.

We conducted a systematic literature review to explore the association between circulating C-reactive protein (CRP), a low-grade inflammation biomarker, and breast cancer risk. Relevant prospective studies in women were identified in PubMed and Web of Science until February 2015. Random-effects dose–response meta-analysis was conducted, overall and in postmenopausal women. Twelve out of 15 studies identified were included in the meta-analysis on any breast cancers (3,522 cases; 69,610 women) and nine on postmenopausal breast cancer (2,516 cases; 36,847 women). For each doubling of CRP concentration, a 7% [95% confidence interval (CI), 2%–12%] and 6% (95% CI, 1%–11%) increased risk was observed (I2 = 47% and 32%; Pheterogeneity = 0.04 and 0.17), respectively. The association was linear over most of the range of CRP concentrations. Positive associations remained in the studies that examined the exclusion of early years of follow-up. Associations were attenuated in studies adjusted for lifestyle factors, which partly explained the significant heterogeneity between studies in the overall analysis. On average, the associations in studies adjusted or not adjusted for body mass index were similar. Low-grade inflammation may have a role in breast cancer development. Additional prospective studies are needed to better understand confounding and effect modification from lifestyle factors. Cancer Epidemiol Biomarkers Prev; 24(10); 1439–49. ©2015 AACR.

Use of dietary supplements is rising in countries where colorectal cancer is prevalent. We conducted a systematic literature review and meta-analyses of prospective cohort studies on dietary supplement use and colorectal cancer risk. We identified relevant studies in Medline, Embase and Cochrane up to January 2013. Original and peer-reviewed papers on dietary supplement use and colorectal cancer, colon cancer, or rectal cancer incidence were included. "Use-no use"(U-NU), "highest-lowest"(H-L) and "dose-response"(DR) meta-analyses were performed. Random-effects models were used to estimate summary estimates. In total, 24 papers were included in the meta-analyses. We observed inverse associations for colorectal cancer risk and multivitamin (U-NU: RR = 0.92; 95% CI: 0.87,0.97) and calcium supplements (U-NU: RR = 0.86; 95% CI: 0.79,0.95; H-L: RR = 0.80; 95% CI: 0.70,0.92; DR: for an increase of 100 mg/day, RR = 0.96; 95% CI: 0.94,0.99). Inconsistent associations were found for colon cancer risk and supplemental vitamin A and vitamin C, and for colorectal cancer risk and supplemental vitamin D, vitamin E, garlic and folic acid. Meta-analyses of observational studies suggest a beneficial role for multivitamins and calcium supplements on colorectal cancer risk, while the association with other supplements and colorectal cancer risk is inconsistent. Residual confounding of lifestyle factors might be present. Before recommendations can be made, an extensive assessment of dietary supplement use and a better understanding of underlying mechanisms is needed.

Objective: As part of the World Cancer Research Fund International Continuous Update Project, we updated the systematic review and meta-analysis of prospective studies to quantify the dose-response between foods and beverages intake and colorectal cancer risk. Data Sources: PubMed and several databases up to May 31 st 2015. Study selection: Prospective studies reporting adjusted relative risk estimates for the association of specific food groups and beverages and risk of colorectal, colon and rectal cancer. Data synthesis: Dose-response meta-analyses using random effect models to estimate summary relative risks (RRs). Results: Results: 400 individual study estimates from 111 unique cohort studies were included. Overall, the risk increase of colorectal cancer is 12% for each 100g/day increase of red and processed meat intake (95%CI=4-21%, I2 =70%, pheterogeneity (ph)

In the World Cancer Research Fund/American Institute for Cancer Research report from 2007 the evidence relating body fatness to ovarian cancer risk was considered inconclusive, while the evidence supported a probably causal relationship between adult attained height and increased risk. Several additional cohort studies have since been published, and therefore we conducted an updated meta-analysis of the evidence as part of the Continuous Update Project. We searched PubMed and several other databases up to December 2013. Summary relative risks (RRs) were calculated using a random effects model. The summary relative risk for a 5 unit increment in BMI was 1.07 (95% CI: 1.02-1.11, I2=53%, n=26 studies). There was evidence of a nonlinear association, pnonlinearity

Background: We conducted a systematic review and meta-analysis of existing data from observational studies to assess the strength of the association of alcohol drinking with second primary cancer risk in patients with upper aerodigestive tract (UADT; oral cavity, pharynx, larynx, and esophagus) cancer. Methods: PubMed and Embase were searched up to July 2012 and the reference lists of studies included in the analysis were examined. Random-effects models were used to estimate summary relative risks (RR) and 95% confidence interval (CI). Results: Nineteen studies, 8 cohort and 11 case–control studies, were included. In highest versus lowest meta-analyses, alcohol drinking was associated with significantly increased risk of UADT second primary cancers (RR, 2.97; 95% CI, 1.96–4.50). Significantly increased risks were also observed for UADT and lung combined (RR, 1.90; 95% CI, 1.16–3.11) and all sites (RR, 1.60; 95% CI, 1.22–2.10) second primary cancers. For an increase in the alcohol intake of 10 grams per day, dose–response meta-analysis resulted in a significantly increased RR of 1.09 (95% CI, 1.04–1.14) for UADT second primary cancers. Conclusions: Alcohol drinking in patients with UADT cancer is associated with an increased risk of second primary cancers. Studies conducted in alcohol drinking patients with UADT cancer and evaluating the effect of alcohol cessation on second primary cancer and other outcomes are needed. Impact: Our results emphasize the importance of prevention policies aiming to reduce alcohol drinking. Health-care professionals should encourage alcohol drinking patients with UADT cancer to reduce their consumption and reinforce the surveillance of this at-risk subpopulation. Cancer Epidemiol Biomarkers Prev; 23(2); 324–31. ©2013 AACR.

Background: In 2007, the World Cancer Research Fund (WCRF) and the American Institute for Cancer Research (AICR) issued recommendations on diet, physical activity, and weight management for cancer prevention on the basis of the most comprehensive collection of available evidence. Objective: We investigated whether concordance with WCRF/AICR recommendations is related to risk of death. Design: The current study included 378,864 participants from 9 European countries enrolled in the European Prospective Investigation into Cancer and Nutrition study. At recruitment (1992-1998), dietary, anthropometric, and lifestyle information was collected. A WCRF/AICR score, which incorporated 6 of the WCRF/AICR recommendations for men [regarding body fatness, physical activity, foods and drinks that promote weight gain, plant foods, animal foods, and alcoholic drinks (score range: 0-6)] and 7 WCRF/AICR recommendations for women [plus breastfeeding (score range: 0-7)], was constructed. Higher scores indicated greater concordance with WCRF/AICR recommendations. Associations between the WCRF/AICR score and risks of total and cause-specific death were estimated by using Cox regression analysis. Results: After a median follow-up time of 12.8 y, 23,828 deaths were identified. Participants within the highest category of the WCRF/AICR score (5-6 points in men; 6-7 points in women) had a 34% lower hazard of death (95% CI: 0.59, 0.75) compared with participants within the lowest category of the WCRF/AICR score (0-2 points in men; 0-3 points in women). Significant inverse associations were observed in all countries. The WCRF/AICR score was also significantly associated with a lower hazard of dying from cancer, circulatory disease, and respiratory disease. Conclusion: Results of this study suggest that following WCRF/AICR recommendations could significantly increase longevity. Am J Clin Nutr 2013;97:1107-20.

Current evidence indicates that red and processed meat intake increases the risk of colorectal cancer; however, the association with colorectal adenomas is unclear. To conduct a systematic review and meta-analysis of epidemiological studies of red and processed meat intake and risk of colorectal adenomas as part of the Continuous Update Project of the World Cancer Research Fund. PubMed and several other databases were searched for relevant studies from their inception up to 31 December 2011. Summary relative risks (RRs) were estimated using a random effects model. Nineteen case–control studies and seven prospective studies were included in the analyses. The summary RR per 100 g/day of red meat was 1.27 (95 % CI 1.16–1.40, I 2 = 5 %, n = 16) for all studies combined, 1.20 (95 % CI 1.06–1.36, I 2 = 0 %, n = 6) for prospective studies, and 1.34 (95 % CI 1.12–1.59, I 2 = 31 %, n = 10) for case–control studies. The summary RR per 50 g/day of processed meat intake was 1.29 (95 % CI 1.10–1.53, I 2 = 27 %, n = 10) for all studies combined, 1.45 (95 % CI 1.10–1.90, I 2 = 0 %, n = 2) for prospective studies, and 1.23 (95 % CI 0.99–1.52, I 2 = 37 %, n = 8) for case–control studies. There was evidence of a nonlinear association between red meat (p nonlinearity

Epidemiological evidence of red meat and processed meat consumption and colorectal cancer risk has accumulated during the past decades. Meta-analyses of case-control and prospective cohort studies have shown a moderate increased risk, but the association is controversial. Because diet is one of the modifiable lifestyle factors for colorectal cancer prevention, the relationship has an important public health perspective. Three prospective cohort studies and one case-control study of total red meat and processed meat and colorectal cancer were published in 2011 and 2012. The findings were in general supportive of an increased risk with higher consumption. The same applies to the four studies each on fresh red meat and processed meat. Associations with dietary heterocyclic amines, nitroso-compounds, and heme iron intake are inconsistent, but evidence suggested a positive association between heme iron intake and colorectal cancer risk.

Background: Measurement errors in the dietary assessment of fruit and vegetable intake may attenuate associations with breast cancer risk and might explain the weak associations observed in epidemiologic studies. Carotenoid concentrations in blood are biomarkers of fruit and vegetable intake; however, no systematic assessment has compared dietary intake with blood concentrations of carotenoids and breast cancer risk. Objective: We conducted a systematic review and meta-analysis of prospective studies of dietary intake and blood concentrations of carotenoids and breast cancer risk. Design: We searched PubMed and several other databases for relevant studies up to 31 August 2011. Random-effects models were used to estimate summary estimates. Results: Of the 6 dietary carotenoids assessed, only intake of b-carotene was significantly associated with a reduced breast cancer risk (summary RR: 0.95; 95% CI: 0.91, 0.99; I 2 : 0%) per 5000 mg/d (n = 10). In contrast, the summary RR for blood concentrations of carotenoids was 0.78 (95% CI: 0.61, 0.99; I 2 : 53%) per 100 mg total carotenoids/dL (n = 7), 0.74 (95% CI: 0.57, 0.97; I 2 : 43%) per 50 mg b-carotene/dL (n = 13), 0.82 (95% CI: 0.73, 0.92, I 2 : 3%) per 10 mg a-carotene/dL (n = 12), and 0.68 (95% CI: 0.52, 0.89; I 2 : 0%) per 25 mg lutein/dL (n = 6). Conclusions: Blood concentrations of carotenoids are more strongly associated with reduced breast cancer risk than are carotenoids assessed by dietary questionnaires. Our results suggest that the use of certain biomarkers may clarify inconsistent and weak results between dietary intake and breast cancer risk. Am J Clin Nutr doi: 10.3945/ajcn.112.034165.

Background: In 2007 the World Cancer Research Fund (WCRF) and the American Institute of Cancer Research (AICR) issued 8 recommendations (plus 2 special recommendations) on diet, physical activity, and weight management for cancer prevention on the basis of the most comprehensive collection of available evidence. Objective: We aimed to investigate whether concordance with the WCRF/AICR recommendations was related to cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Design: The present study included 386,355 EPIC participants from 9 European countries. At recruitment, dietary, anthropometric, and lifestyle information was collected. A score was constructed based on the WCRF/AICR recommendations on weight management, physical activity, foods and drinks that promote weight gain, plant foods, animal foods, alcoholic drinks, and breastfeeding for women; the score range was 0-6 for men and 0-7 for women. Higher scores indicated greater concordance with WCRF/AICR recommendations. The association between the score and cancer risk was estimated by using multivariable Cox regression models. Results: Concordance with the score was significantly associated with decreased risk of cancer. A 1-point increment in the score was associated with a risk reduction of 5% (95% Cl: 3%, 7%) for total cancer, 12% (95% CI: 9%, 16%) for colorectal cancer, and 16% (95% CI: 9%, 22%) for stomach cancer. Significant associations were also observed for cancers of the breast, endometrium, lung, kidney, upper aerodigestive tract, liver, and esophagus but not for prostate, ovarian, pancreatic, and bladder cancers. Conclusion: Adherence to the WCRF/AICR recommendations for cancer prevention may lower the risk of developing most types of cancer. Am J Clin Nutr 2012;96:150-63.

Item does not contain fulltext BACKGROUND & AIMS: The association between fruit and vegetable intake and colorectal cancer risk has been investigated by many studies but is controversial because of inconsistent results and weak observed associations. We summarized the evidence from cohort studies in categorical, linear, and nonlinear, dose-response meta-analyses. METHODS: We searched PubMed for studies of fruit and vegetable intake and colorectal cancer risk that were published until the end of May 2010. We included 19 prospective studies that reported relative risk estimates and 95% confidence intervals (CIs) of colorectal cancer-associated with fruit and vegetable intake. Random effects models were used to estimate summary relative risks. RESULTS: The summary relative risk for the highest vs the lowest intake was 0.92 (95% CI: 0.86-0.99) for fruit and vegetables combined, 0.90 (95% CI: 0.83-0.98) for fruit, and 0.91 (95% CI: 0.86-0.96) for vegetables (P for heterogeneity=.24, .05, and .54, respectively). The inverse associations appeared to be restricted to colon cancer. In linear dose-response analysis, only intake of vegetables was significantly associated with colorectal cancer risk (summary relative risk=0.98; 95% CI: 0.97-0.99), per 100 g/d. However, significant inverse associations emerged in nonlinear models for fruits (Pnonlinearity

The objective of the present study was to conduct the first systematic review and meta-analysis of prospective studies investigating the associations between total cholesterol (TC), HDL-cholesterol (HDL-C) and LDL-cholesterol (LDL-C) levels and the risk of breast cancer. Relevant studies were identified in PubMed (up to January 2014). Inclusion criteria were original peer-reviewed publications with a prospective design. Random-effects models were used to estimate summary hazard ratios (HR) and 95 % CI. Distinction was made between studies that did or did not exclude cancer cases diagnosed during the first years of follow-up, thereby eliminating potential preclinical bias. Overall, the summary HR for the association between TC and breast cancer risk was 0·97 (95 % CI 0·94, 1·00; dose–response per 1 mmol/l increment, thirteen studies), and that between HDL-C and breast cancer risk was 0·86 (95 % CI 0·69, 1·09; dose–response per 1 mmol/l increment, six studies), with high heterogeneity (I2= 67 and 47 %, respectively). For studies that eliminated preclinical bias, an inverse association was observed between the risk of breast cancer and TC (dose–response HR 0·94 (95 % CI 0·89, 0·99), seven studies, I2= 78 %; highest v. lowest HR 0·82 (95 % CI 0·66, 1·02), nine studies, I2= 81 %) and HDL-C (dose–response HR 0·81 (95 % CI 0·65, 1·02), five studies, I2= 30 %; highest v. lowest HR 0·82 (95 % CI 0·69, 0·98), five studies, I2= 0 %). There was no association observed between LDL-C and the risk of breast cancer (four studies). The present meta-analysis confirms the evidence of a modest but statistically significant inverse association between TC and more specifically HDL-C and the risk of breast cancer, supported by mechanistic plausibility from experimental studies. Further large prospective studies that adequately control for preclinical bias are needed to confirm the results on the role of cholesterol level and its fractions in the aetiology of breast cancer.

Obesity not only is an independent risk factor of postmenopausal breast cancer (BC), and in particular estrogen receptor-positive/progesterone receptor-positive BC, it is also a prognostic factor of the disease. Substantial evidence has shown that obesity, as measured by body mass index (BMI) is linked to BC outcomes. All-cause and BC-specific mortality risk increase for each BMI unit increase in pre- and postmenopausal BC survivors is estimated to range from 8 to 29 %, depending on when BMI is ascertained. The positive associations in pre- and postmenopausal BC and in hormone receptor-positive and hormone receptor-negative BC are not significantly different. Furthermore, the negative impact of abdominal obesity on BC survival highlights the need of using fat distribution (waist circumference, waist-hip-ratio) as well as general obesity (BMI) to evaluate prognosis in the clinical setting. More research is needed to elucidate possible differential associations in pre- and postmenopausal BC that are defined by hormone receptor and/or human epidermal growth factor receptor (HER), and in advanced tumors; for which the data are limited and less clear. Current evidence on treatment toxicity supports the guidelines from the American Society for Clinical Oncology, which recommends the use of full weight-based chemotherapy to treat obese cancer patients. Several studies have shown that lifestyle interventions are feasible and safe; more research is needed on specific diets for health maintenance and weight loss in BC survivors. Being physically active (≥150 min/week of moderate intensity activity) helps manage body weight (normal BMI 18.5-24.9 kg/m(2)), improves survival, and has secondary health benefits. Oncologists should recommend their patients to be physically active and control body weight when the conditions of the patient allow it.

Smoking is estimated to cause about half of all bladder cancer cases. Case-control studies have provided evidence of an inverse association between fruit and vegetable intake and bladder cancer risk. As part of the World Cancer Research/American Institute for Cancer Research Continuous Update Project, we conducted a systematic review and meta-analysis of prospective studies to assess the dose-response relationship between fruit and vegetables and incidence and mortality of bladder cancer. We searched PubMed up to December 2013 for relevant prospective studies. We conducted highest compared with lowest meta-analyses and dose-response meta-analyses using random effects models to estimate summary relative risks (RRs) and 95% confidence intervals (CIs), and used restricted cubic splines to examine possible nonlinear associations. Fifteen prospective studies were included in the review. The summary RR for an increase of 1 serving/day (80 g) were 0.97 (95% CI: 0.95-0.99) I(2) = 0%, eight studies for fruits and vegetables, 0.97 (95% CI: 0.94-1.00, I(2) = 10%, 10 studies) for vegetables and 0.98 (95% CI: 0.96-1.00, I(2) = 0%, 12 studies) for fruits. Results were similar in men and women and in current, former and nonsmokers. Amongst fruits and vegetables subgroups, for citrus fruits the summary RR for the highest compared with the lowest intake was 0.87 (95% CI: 0.76-0.99, I(2) = 0%, eight studies) and for cruciferous vegetables there was evidence of a nonlinear relationship (P = 0.001). The current evidence from cohort studies is not consistent with a role for fruits and vegetables in preventing bladder cancer.

Background: Dairy product and calcium intakes have been associated with increased prostate cancer risk, but whether specific dairy products or calcium sources are associated with risk is unclear. Objective: In the Continuous Update Project, we conducted a meta-analysis of prospective studies on intakes of dairy products and calcium and prostate cancer risk. Design: PubMed and several other databases were searched up to April 2013. Summary RRs were estimated by using a random-effects model. Results: Thirty-two studies were included. Intakes of total dairy products [summary RR: 1.07 (95% CI: 1.02, 1.12; n = 15) per 400 g/d], total milk [summary RR: 1.03 (95% CI: 1.00, 1.07; n = 14) per 200 g/d], low-fat milk [summary RR: 1.06 (95% CI: 1.01, 1.11; n = 6) per 200 g/d], cheese [summary RR: 1.09 (95% CI: 1.02, 1.18; n = 11) per 50 g/d], and dietary calcium [summary RR: 1.05 (95% CI: 1.02, 1.09; n = 15) per 400 mg/d] were associated with increased total prostate cancer risk. Total calcium and dairy calcium intakes, but not nondairy calcium or supplemental calcium intakes, were also positively associated with total prostate cancer risk. Supplemental calcium was associated with increased risk of fatal prostate cancer. Conclusions: High intakes of dairy products, milk, low-fat milk, cheese, and total, dietary, and dairy calcium, but not supplemental or nondairy calcium, may increase total prostate cancer risk. The diverging results for types of dairy products and sources of calcium suggest that other components of dairy rather than fat and calcium may increase prostate cancer risk. Any additional studies should report detailed results for subtypes of prostate cancer.

The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) current dietary recommendations for cancer prevention include “eating at least five portions/servings of a variety of non-starchy vegetables and or fruits every day”. The most recent report coordinated by WCRF/AICR (2007) concluded that the evidence of a protective effect of fruits and vegetables on cancer was either “probable”—mouth, pharynx and larynx, oesophagus stomach, lung- or “limited suggestive”—nasopharynx, lung, colorectum, ovary, endometrium, pancreas, liver-. In a previous report published by WCRF/AICR in 1997, the evidence of the association of fruits and vegetables with cancer risk was considered convincing. This judgement was based mainly on the results of case-control studies. The association of fruit and vegetable intake and the risk of colorectal, breast and pancreatic cancer was re-examined in the Continuous Update Project (CUP) and the results were quantitatively summarised in meta-analyses. The CUP, with more data available, has confirmed the conclusion of the WCRF/AICR second expert report that there is no convincing evidence that fruits and vegetables play a role on cancer aetiology. On the other hand, evidence that is more consistent has been collected in the CUP about the role of dietary fibre and colorectal cancer. The evidence on the role of dietary fibre in colorectal cancer aetiology has been recently upgraded by the CUP expert panel from probable to convincing.

International audience; Several observational studies have investigated the role of body mass index (BMI) in second primary cancer incidence in women with breast cancer. We conducted a systematic review and meta-analysis of the evidence to assess the strength of this association. PubMed and Embase were searched for observational studies up to May 2012, and the reference lists of studies included in the analysis were examined. Random effects models were used to estimate summary relative risks (RRs) and 95 % confidence intervals (CIs). Thirteen prospective studies, five cohort and eight nested case-control studies, were included. In categorical meta-analyses of BMI, obesity was associated to significantly increased risks of contralateral breast (RR = 1.37, 95 % CI: 1.20-1.57), breast (RR = 1.40, 95 % CI: 1.24-1.58), endometrial (RR = 1.96, 95 % CI: 1.43-2.70), and colorectal (RR = 1.89, 95 % CI: 1.28-2.79) second primary cancers. For a BMI increase of 5 kg/m(2), dose-response meta-analyses resulted in significantly increased RRs of 1.12 (95 % CI: 1.06-1.20) and 1.14 (95 % CI: 1.07-1.21) for contralateral breast and breast second primary cancers, respectively. The summary RR for endometrial second primary cancers was 1.46 (95 % CI: 1.17-1.83) for a 5-unit increment. This result emphasizes the importance of prevention policies aiming to reduce overweight and obesity prevalence. Clinical trials in breast cancer patients with excess body weight evaluating the effect of normal weight restoration on second primary cancer incidence are needed.

Greater height has been associated with increased risk of several cancers, but epidemiological data on height and pancreatic cancer are inconclusive. We conducted a systematic review and meta-analysis of prospective studies to clarify these results.PubMed and several other databases were searched up to September 2011. Prospective studies of height and pancreatic cancer were included. Summary relative risks were estimated by the use of a random effects model.We identified twelve cohort studies that were included in the meta-analysis. The summary RR per 5-cm increase in height was 1.07 (95 % CI: 1.03-1.12, I (2) = 57 %). The results were similar among men and women. The summary estimate was attenuated when we included results from two pooled analyses together with these studies, summary RR = 1.03 (95 % CI: 1.00-1.07, I (2) = 44 %).This meta-analysis of cohort studies provides further evidence that greater adult attained height is associated with increased pancreatic cancer risk. However, given the unexplained heterogeneity, further studies are needed before a conclusion can be drawn.

Item does not contain fulltext OBJECTIVE: To investigate the association between intake of dietary fibre and whole grains and risk of colorectal cancer. DESIGN: Systematic review and meta-analysis of prospective observational studies. DATA SOURCES: PubMed and several other databases up to December 2010 and the reference lists of studies included in the analysis as well as those listed in published meta-analyses. STUDY SELECTION: Prospective cohort and nested case-control studies of dietary fibre or whole grain intake and incidence of colorectal cancer. RESULTS: 25 prospective studies were included in the analysis. The summary relative risk of developing colorectal cancer for 10 g daily of total dietary fibre (16 studies) was 0.90 (95% confidence interval 0.86 to 0.94, I(2)=0%), for fruit fibre (n=9) was 0.93 (0.82 to 1.05, I(2)=23%), for vegetable fibre (n=9) was 0.98 (0.91 to 1.06, I(2)=0%), for legume fibre (n=4) was 0.62 (0.27 to 1.42, I(2)=58%), and for cereal fibre (n=8) was 0.90 (0.83 to 0.97, I(2)=0%). The summary relative risk for an increment of three servings daily of whole grains (n=6) was 0.83 (0.78 to 0.89, I(2)=18%). CONCLUSION: A high intake of dietary fibre, in particular cereal fibre and whole grains, was associated with a reduced risk of colorectal cancer. Further studies should report more detailed results, including those for subtypes of fibre and be stratified by other risk factors to rule out residual confounding. Further assessment of the impact of measurement errors on the risk estimates is also warranted.

Contains fulltext : 98290.pdf (Publisher’s version ) (Open Access) BACKGROUND: The evidence that red and processed meat influences colorectal carcinogenesis was judged convincing in the 2007 World Cancer Research Fund/American Institute of Cancer Research report. Since then, ten prospective studies have published new results. Here we update the evidence from prospective studies and explore whether there is a non-linear association of red and processed meats with colorectal cancer risk. METHODS AND FINDINGS: Relevant prospective studies were identified in PubMed until March 2011. For each study, relative risks and 95% confidence intervals (CI) were extracted and pooled with a random-effects model, weighting for the inverse of the variance, in highest versus lowest intake comparison, and dose-response meta-analyses. Red and processed meats intake was associated with increased colorectal cancer risk. The summary relative risk (RR) of colorectal cancer for the highest versus the lowest intake was 1.22 (95% CI = 1.11-1.34) and the RR for every 100 g/day increase was 1.14 (95% CI = 1.04-1.24). Non-linear dose-response meta-analyses revealed that colorectal cancer risk increases approximately linearly with increasing intake of red and processed meats up to approximately 140 g/day, where the curve approaches its plateau. The associations were similar for colon and rectal cancer risk. When analyzed separately, colorectal cancer risk was related to intake of fresh red meat (RR(for 100 g/day increase) = 1.17, 95% CI = 1.05-1.31) and processed meat (RR (for 50 g/day increase) = 1.18, 95% CI = 1.10-1.28). Similar results were observed for colon cancer, but for rectal cancer, no significant associations were observed. CONCLUSIONS: High intake of red and processed meat is associated with significant increased risk of colorectal, colon and rectal cancers. The overall evidence of prospective studies supports limiting red and processed meat consumption as one of the dietary recommendations for the prevention of colorectal cancer.

Background: Leukemia is the most frequently occurring cancer in children. Although its etiology is largely unknown, leukemia is believed to result from an interaction between genetic and environmental factors. Among different potential risk factors, the possible role of maternal alcohol consumption during pregnancy has been questioned. Methods: To assess the association between maternal alcohol consumption during pregnancy and childhood leukemia, a systematic review and meta-analysis of published studies was done. Results: Twenty-one case-control studies were included in categorical and dose-response meta-analyses. No cohort study was identified. Analyses were conducted by type of leukemia, children's age at diagnosis, and type of alcoholic beverage and trimester of pregnancy at alcohol use. Alcohol intake during pregnancy (yes versus no) was statistically significantly associated with childhood acute myeloid leukemia (AML) [odds ratio (OR), 1.56; 95% confidence interval (CI), 1.13-2.15] but not with acute lymphoblastic leukemia (OR, 1.10; 95% CI, 0.93-1.29). Heterogeneity between studies was observed. The OR of AML for an increase of a drink per week was 1.24 (95% CI, 0.94-1.64). The association of alcohol intake during pregnancy with AML was observed for cancers diagnosed at age 0 to 4 years (OR, 2.68; 95% CI, 1.85-3.89) in five studies without heterogeneity (I2 ≤ 0.1%). Conclusions: The results of case-control studies indicate that maternal alcohol consumption during pregnancy is associated with a significantly increased risk of AML in young children. Impact: Avoidance of maternal alcohol drinking during pregnancy might contribute to a decrease in the risk of childhood AML. Cancer Epidemiol Biomarkers Prev; 19(5); 1238–60. ©2010 AACR.

Introduction Several case-control studies have suggested inverse associations between whole grain intake and colorectal cancer risk, but few cohort studies have been published on the subject. As part of the Continuous Update Project of the World Cancer Research Fund we conducted a systematic review and meta-analysis of whole grain intake and colorectal cancer risk. Methods We searched the Pubmed database for prospective cohort and nested case-control studies of whole grain intake and risk of incident colorectal cancer, up to December 2010. Summary RRs were calculated using a random effects model. Results Seven cohort studies reported results for total whole grain intake and colorectal cancer risk. The summary RR for high vs low intake of whole grain was 0.79 (95% CI 0.72 to 0.86), with no significant heterogeneity, I 2 =0%. The summary RR for a 3 servings per day increment was 0.81 (95% CI 0.75 to 0.88), with little heterogeneity, I 2 =15%. A similar reduction in risk was also found for colon cancer (summary RR=0.81, 95% CI 0.70 to 0.95, I 2 =0%), but the result for rectal cancer was not statistically significant and there was substantial heterogeneity (summary RR=0.75, 95% CI 0.53 to 1.08, I 2 =87%). Conclusion Our results support the hypothesis that whole grain consumption protects against colorectal cancer.

Introduction The association between fruit and vegetable intake and colorectal cancer risk has been investigated by many studies, but remains a controversial issue because of inconsistent results and weak observed associations. We summarise the evidence from cohort studies in categorical, linear and non-linear dose-response meta-analyses. Methods We searched PubMed for studies of fruit and vegetable intake and colorectal cancer risk up to May 2010. Prospective studies that reported RR estimates and 95% CIs of colorectal cancer associated with fruit and vegetable intake were included. Random effects models were used to estimate summary RRs. Results Nineteen cohort studies were included in the meta-analysis. The summary RR for the highest vs the lowest intake was 0.92 (95% CI 0.86 to 0.99) for fruit and vegetables combined, 0.90 (95% CI 0.83 to 0.98) for fruit and 0.91 (95% CI 0.86 to 0.96) for vegetables. The inverse associations appear to be restricted to colon cancer. In linear dose-response analysis only intake of vegetables was significantly associated with colorectal cancer risk, summary RR 0.98 (95% CI 0.97 to 0.99) per 100 g per day. However, significant inverse associations emerged in non-linear models for fruits (p non-linearity non-linearity =0.001). The greatest risk reduction was observed when increasing intake from very low levels of intake. There was generally little evidence of heterogeneity in the analyses and there was no evidence of small-study bias. Conclusion This meta-analysis indicates that there is a weak, but statistically significant non-linear inverse association between fruit and vegetable intake and colorectal cancer risk.

Introduction In the WCRF/AICR 2 nd expert report, it was concluded that foods containing dietary fibre probably decreases colorectal cancer risk. As part of the WCRF Continuous Update Project, we updated the associations between dietary intake of total fibre and by dietary sources, and colorectal cancer incidence. Methods Relevant prospective studies were identified in PubMed until May 2010. Random effect dose-response meta-analyses were performed on total dietary fibre, and specifically fruit, vegetable, legume, and cereal fibres and colorectal cancer risk. Heterogeneity between studies was assessed by I 2 statistic. Results Total dietary fibre intake was inversely and statistically significantly associated with colorectal cancer. The summary RR for 10 g/day increase was 0.90 (95% CI 0.86 to 0.94, 15 studies). Similar association was observed in cereal fibre (RR 10g/day =0.90, 95% CI 0.83 to 0.97, 8 studies) but not in fruit fibre (RR 10g/day =0.93, 95% CI 0.82 to 1.05, 9 studies), vegetable fibre (RR 10g/day =0.98, 95% CI 0.91 to 1.06, 9 studies), and legume fibre (RR 10g/day =0.62, 95% CI 0.27 to 1.42, 4 studies). There was no evidence of heterogeneity between studies. Conclusion The overall results of cohort studies indicate that high intake of dietary fibre is inversely associated with decreased colorectal cancer risk. The protective effect is more evident for fibre from cereal sources. More studies in different populations are needed to confirm this observation.