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Cholesterol and breast cancer risk: a systematic review and meta-analysis of prospective studies.
Touvier, M, Fassier, P, His, M, Norat, T, Chan, DS, Blacher, J, Hercberg, S, Galan, P, Druesne-Pecollo, N, Latino-Martel, P
The British journal of nutrition. 2015;(3):347-57
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Abstract
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.
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Alcohol drinking and second primary cancer risk in patients with upper aerodigestive tract cancers: a systematic review and meta-analysis of observational studies.
Druesne-Pecollo, N, Keita, Y, Touvier, M, Chan, DS, Norat, T, Hercberg, S, Latino-Martel, P
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 2014;(2):324-31
Abstract
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.
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Excess body weight and second primary cancer risk after breast cancer: a systematic review and meta-analysis of prospective studies.
Druesne-Pecollo, N, Touvier, M, Barrandon, E, Chan, DS, Norat, T, Zelek, L, Hercberg, S, Latino-Martel, P
Breast cancer research and treatment. 2012;(3):647-54
Abstract
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.
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Beta-carotene supplementation and cancer risk: a systematic review and metaanalysis of randomized controlled trials.
Druesne-Pecollo, N, Latino-Martel, P, Norat, T, Barrandon, E, Bertrais, S, Galan, P, Hercberg, S
International journal of cancer. 2010;(1):172-84
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Abstract
The effect of beta-carotene supplementation on cancer incidence has been investigated in several randomized controlled trials. The objective was to review the effect of beta-carotene supplementation on cancer incidence in randomized trials by cancer site, beta-carotene supplementation characteristics and study population. Relevant trials were retrieved by searching PubMed (up to April 2009). Authors involved in selected studies were contacted for additional information. Thirteen publications reporting results from 9 randomized controlled trials were included. Overall, no effect of beta-carotene supplementation was observed on the incidence of all cancers combined (RR, 1.01; 95% CI, 0.98-1.04), pancreatic cancer (RR, 0.99; 95% CI, 0.73-1.36), colorectal cancer (RR, 0.96; 95% CI, 0.85-1.09), prostate cancer (RR, 0.99; 95% CI, 0.91-1.07), breast cancer (RR, 0.96; 95% CI, 0.85-1.10), melanoma (RR, 0.98; 95% CI, 0.65-1.46) and non melanoma skin cancer (RR, 0.99; 95% CI, 0.93-1.05). The incidence of lung and stomach cancers were significantly increased in individuals supplemented with beta-carotene at 20-30 mg day(-1) (RR, 1.16; 95% CI, 1.06-1.27 and RR, 1.34; 95% CI, 1.06-1.70), in smokers and asbestos workers (RR, 1.20; 95% CI, 1.07-1.34 and RR, 1.54; 95% CI, 1.08-2.19) compared to the placebo group. Beta-carotene supplementation has not been shown to have any beneficial effect on cancer prevention. Conversely, it was associated with increased risk not only of lung cancer but also of gastric cancer at doses of 20-30 mg day(-1), in smokers and asbestos workers. This study adds to the evidence that nutritional prevention of cancer through beta-carotene supplementation should not be recommended.