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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostate cancer is the most frequently occurring form of cancer in German men with an incidence of 49.000 in the year 2002. Epidemiological studies indicate diet and physical activity may play major roles in both incidence and progression of the disease. Obesity may increase both primary risk and biochemical (increase in prostate specific antigen) or clinical recurrence. Among individual food groups/nutrients a high consumption of total fat, saturated fats, meat, dairy, and calcium are related to an increased risk. Tomato products, soy, lycopene, selenium, marine omega-3-fatty acids and vitamin E in smokers may inversely be associated with prostate cancer. Interventional studies with supplemental tomato products and selenium also showed a delay in disease progression. Evidence from experimental studies and clinical experience suggest that application of selenium during chemotherapy and/or radiotherapy may decrease therapy related toxicities and increases the effect of the standard therapy on cancer cells. For expert patients it is essential to participate in decisions concerning their standard as well as complementary therapy by developing individual self-help concepts. These often include both changing dietary habits and taking dietary supplements. Physicians should consider these needs when they counsel cancer patients.
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PMID:[Nutrition and prostate cancer--what is the scientific evidence?]. 1705 96

Increasing prostate volume contributes to urinary tract symptoms and may obscure prostate cancer detection. We investigated the association between obesity and prostate volume, prostate-specific antigen (PSA) and PSA density among 753 men referred for prostate biopsy. Among men with a negative biopsy, prostate volume significantly increased approximately 25% from the lowest to highest body mass index (BMI), waist or hip circumference or height categories. PSA was 0.7 ng/ml lower with a high waist-to-hip ratio. These associations were less consistent among subjects diagnosed with high-grade prostatic intraepithelial neoplasia or cancer. Our data suggest that obesity and height are independently associated with prostate volume..
Prostate Cancer Prostatic Dis 2007
PMID:The association between body size, prostate volume and prostate-specific antigen. 1717 79

Clifton Leaf, in his article "Why We're Losing the War on Cancer," presents criticisms of past research approaches and the small impact of this research thus far on producing cures or substantially extending the life of many cancer patients. It is true that gains in long-term survival for people with advanced cancers have been modest, hindered in part by the heterogeneity of tumors, which allows the cancers to persist using alternate molecular pathways and so evade many cancer therapeutics. In contrast, clinical trials have demonstrated that it is possible to reduce the incidence or improve cancer survival through prevention and early detection. Strides have been made in preventing or detecting early the four deadliest cancers in the United States (i.e., lung, breast, prostate, and colorectal). For example, 7-year follow-up data from the Breast Cancer Prevention Trial (BCPT) provides evidence that tamoxifen reduces the occurrence of invasive breast tumors by more than 40%; recent studies using aromatase inhibitors and raloxifene are also promising. The Prostate Cancer Prevention Trial (PCPT) showed that finasteride reduced prostate cancer incidence by 25%, and the ongoing Selenium and Vitamin E Cancer Prevention Trial (SELECT) is investigating selenium and vitamin E for prostate cancer prevention based on encouraging results from earlier studies. Living a healthy lifestyle, including regular physical activity, avoiding obesity, and eating primarily a plant-based diet has been associated with a lower risk of colorectal cancer. In addition, noninvasive stool DNA tests for early detection are being studied, which may lessen the reluctance of people to be screened for colorectal polyps and cancer. Behavioral and medical approaches for smoking prevention are ways to reduce the incidence of lung cancer, with antinicotine vaccines on the horizon that may help former smokers to avoid relapse. The US National Lung Screening Trial is testing whether early detection via spiral CT screening will reduce lung cancer mortality. Prevention and earlier detection offer efficient and practical strategies to reduce the cancer burden. Several of the suggestions Mr. Leaf makes, such as developing interdisciplinary collaborations and allocating resources to research earlier in the process of carcinogenesis, have become an integral strategy in the National Cancer Institute's (NCI) approach in the past decade, specifically in the realm of cancer prevention and early detection. For example, an aggressive program to identify biomarkers for earlier detection of cancer--the NCI's Early Detection Research Detection (EDRN)--has identified three promising biomarkers since its establishment in 2000. It collaborates with the National Institute of Standards and Technology and extramural scientists to develop validation standards and to identify the best technologies to use for systematic investigations. If these biomarkers can be validated, they might help to reduce cancer mortality.
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PMID:A favorable view: progress in cancer prevention and screening. 1730 81

Although cancer is a common disease, there is only a limited number of effective measures for prevention and early detection. The European Cancer Code gives valid recommendations for behavioural changes, of which not smoking, eating "healthily" and avoiding obesity are probably the most important ones. As for the most frequent cancer types, there is evidence that screening programmes for early detection of colorectal, breast and cervix cancer can reduce morbidity and mortality. For lack of such evidence, no screening programmes for lung and prostate cancer can be recommended at this time.
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PMID:[Cancer prevention and early detection: what does make sense?]. 1732 66

The relationship between obesity and prostate cancer remains unclear. We investigated the effect of prostate volume on the obesity and prostate cancer association. With a multi-centered, rapid-recruitment protocol, weight and body size measurements were collected prior to diagnosis, and medical charts were reviewed for pathology results (n = 420 controls, 119 high-grade prostatic intraepithelial neoplasia (PIN) cases, and 286 cancer cases (41% Gleason > 6). In multivariable logistic regression models adjusting for age, PSA levels and history, DRE results, and number of cores at biopsy, the association between BMI and cancer was restricted to men with a smaller prostate volume (volume < 40 cm(3): OR(BMI > or = 30) = 2.17 (1.09, 4.32), p (trend) = 0.02; volume > or = 40 cm(3): OR(BMI > or = 30) = 0.77 (0.34, 1.77), p (trend) = 0.17; p (interaction) = 0.03). Similarly, the WHR and PIN association was significantly modified by prostate volume (volume < 40 cm(3): OR((WHR: Tertile 3 vs. T1)) = 3.76 (1.54, 9.21) (p (trend) < 0.01); volume > or = 40 m(3): OR((WHR: T3 vs. T1)) = 0.63 (0.32, 1.23) (p (trend) = 0.17); p (interaction) < 0.01). In conclusion, prostate volume acts as a modifier, and BMI and WHR are significantly associated with prostate cancer or PIN, respectively, in the absence of biopsy sampling error derived from obesity-related prostate enlargement.
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PMID:Prostate volume modifies the association between obesity and prostate cancer or high-grade prostatic intraepithelial neoplasia. 1733 11

The 2006 annual American Urological Association (AUA) meeting took place in Atlanta from 20-25th of May. Four hundred and seventy nine abstracts (27.8%) were dedicated to the prostate cancer. The aim of this study is to summarise the most debated topics and to highlight the most original research. The main topics this year were obesity, ethnicity, PSA kinetic, surgical margins, robot and adjuvant therapy.
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PMID:[Prostate cancer: synopsis of the American Urological Association (AUA) 2006]. 1735 16

Studies on obesity and prostate cancer risk are inconsistent, perhaps because of differential effects on aggressive and nonaggressive cancers. Participants included 34,754 men residing in Washington State (aged 50-76 years at baseline) in a prospective cohort study who were recruited between 2000 and 2002; 383 developed aggressive (regional/distant stage or Gleason sum 7-10) and 437 developed nonaggressive disease through December 2004. Compared with normal-weight men (body mass index (kg/m(2)) <25), obese men (> or = 30 kg/m(2)) had a reduced risk of nonaggressive disease (hazard ratio = 0.69, 95% confidence interval: 0.52, 0.93; p for trend = 0.01). Overweight men (25-29.9 kg/m(2)) had an increased risk of aggressive disease (hazard ratio = 1.4, 95% confidence interval: 1.1, 1.8), but there was no increased risk for obese men (p for trend = 0.69). Body mass index of >25 at age 18 years was associated with increased risk of aggressive prostate cancer; obesity at ages 30 and 45, but not 18, years was associated with reduced risk of nonaggressive prostate cancer. Height (fourth vs. first quartile) was associated with an increased risk of total prostate cancer (hazard ratio = 1.3, 95% confidence interval: 1.1, 1.6), which did not differ by aggressiveness. There were no associations of prostate cancer with age at which maximum height was reached. Results from this study demonstrate the complexity of prostate cancer epidemiology and the importance of examining risk factors by tumor characteristics.
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PMID:Anthropometrics and prostate cancer risk. 1739 97

Many investigators suggested that obesity predisposes to adverse prostate cancer characteristics and outcomes. We tested the effect of obesity on the rate of aggressive prostate cancer at either prostate biopsy or radical prostatectomy (RP). Clinical and pathological data were available for 1,814 men. Univariable and multivariable logistic regression models addressed the rate of high grade prostate cancer (HGPCa) at either biopsy or final pathology. Clinical stage, prostate-specific antigen (PSA), percentage of free PSA and prostate volume were the base predictors. All models were fitted with and without body mass index (BMI), which quantified obesity. BMI and its reciprocal (InvBMI) were coded as cubic splines to allow nonlinear effects. Predictive accuracy (PA) was quantified with area under curve estimates, which were subjected to 200 bootstrap re-samples to reduce overfit bias. Gains in PA related to the inclusion of BMI were compared using the Mantel-Haenszel test. HGPCa at biopsy was detected in 562 (31%) and HGPCa at RP pathology was present in 931 (51.3%) men. In either univariable or multivariable models predicting HGPCa at biopsy, BMI or InvBMI failed to respectively reach statistical significance or add to multivariable PA (BMI gain = 0%, p = 1.0; InvBMI gain = -0.2%, p = 0.9). Conversely, in models predicting HGPCa at RP, BMI and InvBMI represented independent predictors but failed to increase PA (BMI gain = 0.7%, p = 0.6; InvBMI gain = 0.5, p = 0.7%). Obesity does not predispose to more aggressive prostate cancer at biopsy. Similarly, obesity does not change the ability to identify those who may harbor HGPCa at RP.
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PMID:Obesity does not predispose to more aggressive prostate cancer either at biopsy or radical prostatectomy in European men. 1745 51

Both obesity and prostate cancer are epidemic in Western society. Although initial epidemiologic data appeared conflicting, recent studies, especially large prospective studies published in the past 6-12 months, have clarified the association between obesity and prostate cancer. The aim of this paper is to review the epidemiologic data linking obesity and prostate cancer, with an emphasis on new data published since 2005. A PubMed search was done on the keywords, "prostate cancer" and "obesity." Relevant articles and their references were reviewed for data on the association between obesity and prostate cancer. Recent data suggest that obesity is associated with reduced risk of nonaggressive disease but increased risk of aggressive disease. This may in part be explained by an inherent bias in our ability to detect prostate cancer in obese men (lower prostate-specific antigen values and larger sized prostates making biopsy less accurate for finding an existing cancer). Ultimately, this leads to increased risk of cancer recurrence after primary therapy and increased risk of prostate cancer mortality. The biologic causes of these associations are likely multifactorial, although the lower testosterone levels among obese men appear to be one of the most promising explanations. The association between obesity and prostate cancer is complex. Emerging data suggest a differential effect of obesity by disease aggressiveness: obesity may reduce the risk of nonaggressive disease while it may promote aggressive disease.
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PMID:Obesity and prostate cancer: making sense out of apparently conflicting data. 1747 39

The aim of this study was to examine the influence of hormonal therapy (HT) on glucose metabolism in prostate cancer (PCa) patients. Fifty-two PCa patients receiving HT with gonadotropin-releasing hormone (GnRH) analogues and/or antiandrogen drugs were enrolled in this study. Both blood and urine samples were taken a few hours after breakfast before and after HT, and glucose levels in the blood and urine were measured. Elevations of blood glucose levels of 30-50, 50-100 and over 100 mg/dl after HT as compared with the levels before HT were observed in two, eight and five patients, respectively. Urine examination revealed deterioration of glucosuria in seven patients. The mean blood glucose level after HT was significantly higher than that measured before HT. The elevation of blood glucose level significantly correlated with concurrence of diabetes mellitus (DM) and higher body mass index (BMI) before HT. Deterioration of glucosuria significantly correlated with the concurrence of DM. HT for PCa patients, especially with concurrent DM or obesity, induces elevation of the blood glucose level and deterioration of glucosuria. Therefore, glucose intolerance should be considered during HT for PCa.
Prostate Cancer Prostatic Dis 2007
PMID:Glucose intolerance during hormonal therapy for prostate cancer. 1748 9


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