Dairy products, calcium and prostate cancer risk

In a prospective study of 10 011 men with 815 prostate cancer cases, despite plausible biological mechanisms, neither increasing intake levels of dairy products nor calcium from dairy products (P trend; 0.23 and 0.64, respectively), or calcium supplements was associated with prostate cancer risk (relative risk, 1.05; 95% confidence interval, 0.84–1.31)

Animal products, calcium and protein and prostate cancer risk in the Netherlands Cohort Study

Prostate cancer risk in relation to consumption of animal products, and intake of calcium and protein was investigated in the Netherlands Cohort Study. At baseline in 1986, 58,279 men aged 55-69 years completed a self-administered 150-item food frequency questionnaire and a questionnaire on other risk factors for cancer. After 6.3 years of follow-up, 642 prostate cancer cases were available for analysis. In multivariate case-cohort analyses adjusted for age, family history of prostate cancer and socioeconomic status, no associations were found for consumption of fresh meat, fish, cheese and eggs. Positive trends in risk were found for consumption of cured meat and milk products (P-values 0.04 and 0.02 respectively). For calcium and protein intake, no associations were observed. The hypothesis that dietary factors might be more strongly related to advanced prostate rumours could not be confirmed in our study. We conclude that, in this study, animal products are not strongly related to prostate cancer risk

Can weight loss prevent cancer?

We review and update evidence on obesity, weight gain and weight loss in relation to leading cancers since the International Agency for Research on Cancer report of 2002. Emphasis is placed on the time course of disease and implications for weight control to prevent cancer. We conclude that weight loss could prevent a major portion of common cancers

A review and meta-analysis of prospective studies of red and processed meat intake and prostate cancer

Over the past decade, several large epidemiologic investigations of meat intake and prostate cancer have been published. Therefore, a meta-analysis of prospective studies was conducted to estimate potential associations between red or processed meat intake and prostate cancer. Fifteen studies of red meat and 11 studies of processed meat were included in the analyses. High vs. low intake and dose-response analyses were conducted using random effects models to generate summary relative risk estimates (SRRE). No association between high vs. low red meat consumption (SRRE = 1.00, 95% CI: 0.96-1.05) or each 100 g increment of red meat (SRRE = 1.00, 95% CI: 0.95-1.05) and total prostate cancer was observed. Similarly, no association with red meat was observed for advanced prostate cancer (SRRE = 1.01, 95% CI: 0.94-1.09). A weakly elevated summary association between processed meat and total prostate cancer was found (SRRE = 1.05, 95% CI: 0.99-1.12), although heterogeneity was present, the association was attenuated in a sub-group analysis of studies that adjusted for multiple potential confounding factors, and publication bias likely affected the summary effect. In conclusion, the results of this meta-analysis are not supportive of an independent positive association between red or processed meat intake and prostate cancer

A reproducible brain tumour model established from human glioblastoma biopsies

<p>Abstract</p> <p>Background</p> <p>Establishing clinically relevant animal models of glioblastoma multiforme (GBM) remains a challenge, and many commonly used cell line-based models do not recapitulate the invasive growth patterns of patient GBMs. Previously, we have reported the formation of highly invasive tumour xenografts in nude rats from human GBMs. However, implementing tumour models based on primary tissue requires that these models can be sufficiently standardised with consistently high take rates.</p> <p>Methods</p> <p>In this work, we collected data on growth kinetics from a material of 29 biopsies xenografted in nude rats, and characterised this model with an emphasis on neuropathological and radiological features.</p> <p>Results</p> <p>The tumour take rate for xenografted GBM biopsies were 96% and remained close to 100% at subsequent passages <it>in vivo</it>, whereas only one of four lower grade tumours engrafted. Average time from transplantation to the onset of symptoms was 125 days ± 11.5 SEM. Histologically, the primary xenografts recapitulated the invasive features of the parent tumours while endothelial cell proliferations and necrosis were mostly absent. After 4-5 <it>in vivo </it>passages, the tumours became more vascular with necrotic areas, but also appeared more circumscribed. MRI typically revealed changes related to tumour growth, several months prior to the onset of symptoms.</p> <p>Conclusions</p> <p><it>In vivo </it>passaging of patient GBM biopsies produced tumours representative of the patient tumours, with high take rates and a reproducible disease course. The model provides combinations of angiogenic and invasive phenotypes and represents a good alternative to <it>in vitro </it>propagated cell lines for dissecting mechanisms of brain tumour progression.</p

Is alcohol consumption a risk factor for prostate cancer? A systematic review and meta-analysis.

Background: Research on a possible causal association between alcohol consumption and risk of prostate cancer is inconclusive. Recent studies on associations between alcohol consumption and other health outcomes suggest these are influenced by drinker misclassification errors and other study quality characteristics. The influence of these factors on estimates of the relationship between alcohol consumption and prostate cancer has not been previously investigated. Methods: PubMed and Web of Science searches were made for case–control and cohort studies of alcohol consumption and prostate cancer morbidity and mortality (ICD–10: C61) up to December 2014. Studies were coded for drinker misclassification errors, quality of alcohol measures, extent of control for confounding and other study characteristics. Mixed models were used to estimate relative risk (RR) of morbidity or mortality from prostate cancer due to alcohol consumption with study level controls for selection bias and confounding. Results: A total of 340 studies were identified of which 27 satisfied inclusion criteria providing 126 estimates for different alcohol exposures. Adjusted RR estimates indicated a significantly increased risk of prostate cancer among low (RR = 1.08, P 1.3, <24 g per day). This relationship is stronger in the relatively few studies free of former drinker misclassification error. Given the high prevalence of prostate cancer in the developed world, the public health implications of these findings are significant. Prostate cancer may need to be incorporated into future estimates of the burden of disease alongside other cancers (e.g. breast, oesophagus, colon, liver) and be integrated into public health strategies for reducing alcohol related disease

Breast cancer risk associated with different HRT formulations: a register-based case-control study

BACKGROUND: Previous epidemiological studies have inconsistently shown a modestly increased breast cancer risk associated with hormone replacement therapy (HRT). Limited information is available about different formulations – particularly concerning different progestins. METHODS: A case-control study was performed within Germany in collaboration with regional cancer registries and tumor centers. Up to 5 controls were matched breast cancer cases. Conditional logistic regression analysis was applied to estimate crude and adjusted odds ratios (OR) and 95% confidence intervals (95% CI). Stratified analyses were performed to compare the risk of different estrogens, progestins, and combinations. RESULTS: A total of 3593 cases of breast cancer were identified and compared with 9098 controls. The adjusted overall risk estimate for breast cancer (BC) associated with current or past use of HRT was 1.2 (1.1–1.3), and almost identical for lag times from 6 months to 6 years prior to diagnosis. No significant trend of increasing BC risk was found with increasing duration of HRT use, or time since first or last use in aggregate. Many established BC risk factors significantly modified the effect of HRT on BC risk, particularly first-degree family history of BC, higher age, lower education, higher body mass index (BMI), and never having used oral contraceptives (OCs) during lifetime. Whereas the overall risk estimates were stable, the numbers in many of the sub-analyses of HRT formulation groups (estrogens, progestins, and combinations) were too small for strong conclusions. Nevertheless, the BC risk seems not to vary much across HRT formulation subgroups. In particular, no substantial difference in BC risk was observed between HRT containing conjugated equine estrogens (CEE) or medroxyprogesterone acetate (MPA) and other formulations more common in Europe. CONCLUSION: The BC risk of HRT use is rather small. Low risk estimates for BC and a high potential for residual confounding and bias in this observational study do not permit causal conclusions. Apparently, there is not much variation of the BC risk across HRT formulations (estrogens, progestins). However, the small numbers and the overlapping nature of some of the subgroups suggest cautious interpretation