Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine whether endogenous androgens influence the occurrence of prostate cancer, we conducted a nested case-control study among participants enrolled in the Carotene and Retinol Efficacy Trial. We analyzed serum samples of 300 cases diagnosed between 1987 and 1998, and 300 matched controls. Higher concentrations of testosterone (T) were not associated with increased prostate cancer risk. Relative to men with levels in the lowest fourth of the distribution, men in the upper fourth of total T had a risk of 0.82 [95% confidence interval (CI), 0.52-1.29]. The corresponding relative risks for free T (0.72; 95% CI, 0.45-1.14), percentage of free T (0.74; 95% CI, 0.46-1.19), and total T:sex hormone binding globulin ratio (0.52; 95% CI, 0.32-0.83) similarly were not elevated. Higher concentrations of androstenedione, dehydroepiandrosterone sulfate, and 3 alpha-androstanediol glucuronide were weakly associated with risk. Relative risks associated with being in the highest fourth for androstenedione, dehydroepiandrosterone sulfate, and 3 alpha-androstanediol glucuronide were 1.20 (95% CI, 0.76-1.89), 1.38 (95% CI, 0.86-2.21), and 1.27 (95% CI, 0.80-2.00), respectively. Men in the upper fourth of total estradiol (E2), free E2 and percentage of free E2 had relative risks of 0.71 (95% CI, 0.42-1.13), 0.52 (95% CI, 0.33-0.82), and 0.65 (95% CI, 0.40-1.05), respectively. The inverse association between E2 and prostate cancer risk was largely restricted to men with blood collection within 3 years of diagnosis. Our results add to the evidence that serum testosterone is unrelated to prostate cancer incidence. The suggestions that intraprostatic androgen activity may increase risk and that serum estrogens may decrease risk, warrant additional study.
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PMID:Endogenous sex hormones and prostate cancer risk: a case-control study nested within the Carotene and Retinol Efficacy Trial. 1469 30

Several studies have evaluated the possible association between intakes of retinoids and carotenoids and the risk of prostate cancer, but the evidence is still inconsistent. Further, only a few studies have investigated the role of specific carotenoids other than beta-carotene. We have thus considered the association between retinol and various carotenoids using data from a multicentric case-control study conducted in Italy between 1991 and 2002. This included 1,294 incident, histologically confirmed prostate cancer cases below age 75 years admitted to major teaching and general hospitals in the areas under study, and 1,451 controls below age 75 years selected among patients admitted to the same hospitals as cases for a wide spectrum of acute nonneoplastic conditions not related to long-term modifications of diet. Subjects' usual diet was investigated by means of a validated food-frequency questionnaire. Multivariate odds ratios and the corresponding 95% confidence intervals were estimated using unconditional logistic regression models. The risk of prostate cancer tended to decrease with increasing intake of retinol (OR=0.79 for the highest versus the lowest quintile of intake), carotene (OR=0.70), alpha-carotene (OR=0.85) and beta-carotene (OR=0.72), although the estimates were significant for carotene and beta-carotene only. No meaningful associations emerged for nonprovitamin A carotenoids, such as lycopene (OR=0.94) and lutein/zeaxanthin (OR=0.91). No systematic heterogeneity was observed across strata of age, education and body mass index. Thus, our study supports the hypothesis of a weak protective effect of carotene, particularly beta-carotene, on the risk of prostate cancer, while it indicates that other carotenoids, including lycopene, and retinol are not appreciably related to the risk of this neoplasm.
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PMID:Retinol, carotenoids and the risk of prostate cancer: a case-control study from Italy. 1538 52

Biomarkers of trans-fatty acid consumption have been associated with increased risks of breast and colon cancer, although no studies have examined their associations with prostate cancer risk. Using data from the beta-Carotene and Retinol Efficacy Trial, this nested case-control study examined the relationships between serum phospholipid trans-fatty acids and prostate cancer incidence in 272 case and 426 control men. Trans-fatty acids were measured using organic extraction followed by separations with TLC and gas chromatography. Adjusted odds ratios for risk of prostate cancer with increasing levels of trans-fatty acids were calculated using logistic regression. There were consistent trends for increasing prostate cancer risk with higher levels of C18 but not C16 trans-fatty acids, although only trends for Delta11t 18:1 trans-vaccenic and Delta9c,12t 18:2 fatty acids reached statistical significance. Odds ratios (95% confidence interval) contrasting low versus high quartiles for these fatty acids were 1.69 (1.03-2.77) and 1.79 (1.02-3.15), respectively. There were no consistent differences in associations between low-grade and high-grade cancer among the subset of 209 cases with information on tumor grade. Additional studies are needed to confirm these findings and better control for factors, such as use of prostate-specific antigen screening, which may confound this association.
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PMID:Serum trans-fatty acids are associated with risk of prostate cancer in beta-Carotene and Retinol Efficacy Trial. 1582 75

The relationship between lipid soluble antioxidant vitamins, lipid peroxidation, disease stage and the systemic inflammatory response were examined in healthy subjects (n = 14), patients with benign prostate hyperplasia BPH (n = 20), localized (n = 40) and metastatic (n = 38) prostate cancer. Prostate cancer patients had higher concentrations of malondialdehyde (p < 0.05) and lower circulating concentrations of lutein (p < 0.05), lycopene (p < 0.001) and beta-carotene (p < 0.05). Patients with metastatic prostate cancer, when compared with patients having localized disease, had a higher Gleason score (p < 0.01) and had more hormonal treatment, but lower concentrations of PSA (p < 0.05), alpha-tocopherol (p < or = 0.05), retinol (p < 0.01), lutein (p < 0.05) and lycopene (p < 0.01). In the prostate cancer patients, PSA was correlated with the concentrations of the lipid peroxidation product, malondialdehyde (rs= 0.353, p = 0.002). C-reactive protein was not correlated with the vitamin antioxidants nor malondialdehyde. In contrast, there was a negative correlation between malondialdehyde concentrations and both lutein (rs= -0.263, p = 0.020) and lycopene (rs= -0.269, p = 0.017). These results indicate that lower concentrations of carotenoids, in particular, lycopene reflect disease progression rather than the systemic inflammatory response in patients with prostate cancer.
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PMID:Vitamin antioxidants, lipid peroxidation and the systemic inflammatory response in patients with prostate cancer. 1610 18

Prostate cancer, the most commonly diagnosed cancer among American men, develops slowly over many years. The long latent period of 20 to 30 years, involved in the multistep process of carcinogenesis, provides an important opportunity to block or reverse progression to a malignant state. Vitamin A (retinoids) and vitamin D not only have the ability to block steps in the process of carcinogenesis but they can also modulate or reverse some malignant characteristics of cancer cells. However, at high levels, vitamins A and D have undesirable side effects, thus, limiting effective dose levels and efficacy. Therefore, combination treatment at low doses, to increase efficacy and avoid toxicity, is of special interest. This study examines the effects of the synthetic retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) in combination with cholecalciferol (vitamin D3) on growth, and on the expression of vimentin, matrix metalloproteinase-2 (MMP-2), and retinoid and vitamin D receptor expression, using the non-tumorigenic, human prostate epithelial cell line RWPE-1. Treatment with 4-HPR and cholecalciferol resulted in synergistic growth inhibition when compared to that caused by each agent alone. A decrease in vimentin expression and MMP-2 activity, and up-regulation of vitamin D receptor (VDR) and some of the retinoid-X (RXRs) and retinoic acid receptor (RARs) subtypes, was observed. These results suggest that combined treatment with 4-HPR and cholecalciferol, at doses lower than what might be effective with single agents, increases their efficacy and suggest that this may serve as an effective strategy for chemoprevention and treatment of prostate cancer.
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PMID:Cholecalciferol (vitamin D3) and the retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) are synergistic for chemoprevention of prostate cancer. 1702 72

Prostate cancer risk was examined in relation to intakes of fruit, vegetables, beta-carotene and retinol. Subjects were a cohort of 1985 men previously to asbestos who participated in a cancer prevention programme of beta-carotene and retinol supplements that commenced in July 1990. Diet was assessed at entry to the programme. Ninety-seven cases of prostate cancer were identified during follow-up until the end of 2004. A decreased prostate cancer risk was observed with increasing intakes of vitamin C-rich vegetables, including bell peppers and broccoli. Fruit, other vegetables and vitamin A intakes did not appear to be strong factors in the development of prostate cancer in this study.
Prostate Cancer Prostatic Dis 2008
PMID:Fruit, vegetable, vitamin A intakes, and prostate cancer risk. 1751 26

Oxidative stress, associated with aging and inflammation, is likely to play a role in the etiology of prostate cancer. We evaluated potential associations between gene variants that result in reduced neutralization of reactive oxygen species (ROS; MnSOD Ala-16Val, CAT -262 C>T, and GPX1 Pro200Leu) and prostate cancer risk among 724 men with incident prostate cancer who participated in the Carotene and Retinol Efficacy Trial (CARET) cohort, a randomized trial for the prevention of lung cancer among men with a history of smoking and/or asbestos exposure. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by logistic regression. Nested case-control analyses included study participants with available DNA (n = 533 cases and 1,470 controls), matched for race, age, and length of follow-time. Overall, there were no associations between genotypes of MnSOD, CAT, and GPX1 and prostate cancer risk, although among men diagnosed before age 65, CAT TT genotype was associated with increased risk (OR, 2.0; 95% CI, 0.97-3.95). Further analyses stratified by factors related to environmental oxidative stress exposures did not modify associations. When calculating the number of risk alleles of MnSOD, CAT, and GPX1 hypothetically related to reduced protection against ROS, there was a nonsignificant relationship between prostate cancer and carriage of five or more risk alleles, in comparison to men with less than five risk alleles (OR, 2.0; 95% CI, 0.90-4.42). In conclusion, it does not seem that variants in MnSOD, CAT, or GPX1 have an influence on prostate cancer risk in this cohort of men who were smokers or exposed to asbestos, although it is possible that cumulative defects in protection from oxidative stress may result in increased risk of the disease.
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PMID:Polymorphisms in oxidative stress-related genes are not associated with prostate cancer risk in heavy smokers. 1754 72

Previous studies offer suggestive, but not definitive, evidence that total fat or specific fats may increase prostate cancer risk. This study investigates associations of dietary fat, meat, and dairy foods with prostate cancer risk among 12,025 men in the Carotene and Retinol Efficacy Trial (CARET). After 11 y of follow-up, 890 incident prostate cancers were reported and confirmed. Diet was assessed by a biannual FFQ. Cox proportional hazards models were used to estimate multivariate-adjusted hazard ratios (HR) of intake of fat and fat-related foods (meat and dairy) with prostate cancer incidence. Multiplicative interaction terms tested whether associations differed by family history, race, or smoking. Overall, fat was not associated with total, nonaggressive or aggressive prostate cancer. In subgroup analyses the HR for men with a family history of prostate cancer were 2.47 (95%CI = 0.96-6.37) and 2.61 (95% CI = 1.01-6.72) for total polyunsaturated fat (PUFA) and (n-6) PUFA for the 4th vs. 1st quartiles of intake, respectively. Red meat was not associated with total or aggressive prostate cancer. However, higher dairy intake had a statistically significant reduced risk of aggressive prostate cancer than lower dairy intake (HR = 0.59, 95% CI = 0.40-0.85). Dairy foods also protected current, but not former, smokers against aggressive cancer (HR = 0.42, 95% CI = 0.25-0.70). Our findings suggest that associations of dietary fat with prostate cancer risk may vary by type of fat or fat-containing food, and that risk may vary by host factors, including family history and smoking.
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PMID:(n-6) PUFA increase and dairy foods decrease prostate cancer risk in heavy smokers. 1758 37

Despite recent comprehensive review articles concluding that supplemental antioxidants do not undermine the effectiveness of cytotoxic therapies, the use of antioxidants during cancer treatment remains controversial. Many oncologists take the position that antioxidants by their nature undermine the free radical mechanism of chemotherapy and radiotherapy and should therefore generally be avoided during treatment. For their part, many integrative practitioners believe that antioxidants taken during cancer treatment not only alleviate some of the adverse effects of that treatment but also enhance the efficacy of cancer therapy. Until recently, research attention has focused primarily on the interaction of antioxidants with chemotherapy; relatively little attention has been paid to the interaction of antioxidants with radiotherapy. This article reviews the clinical literature that has addressed whether antioxidants do in fact interfere with radiation therapy. Studies have variously investigated the use of alpha-tocopherol for the amelioration of radiation-induced mucositis; pentoxifylline and vitamin E to correct the adverse effects of radiotherapy; melatonin alongside radiotherapy in the treatment of brain cancer; retinol palmitate as a treatment for radiation-induced proctopathy; a combination of antioxidants (and other naturopathic treatments) and external beam radiation therapy as definitive treatment for prostate cancer; and the use of synthetic antioxidants, amifostine, dexrazoxane, and mesna as radioprotectants. With few exceptions, most of the studies draw positive conclusions about the interaction of antioxidants and radiotherapy. Although further studies are needed, the preponderance of evidence supports a provisional conclusion that dietary antioxidants do not conflict with the use of radiotherapy in the treatment of a wide variety of cancers and may significantly mitigate the adverse effects of that treatment.
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PMID:Do antioxidants interfere with radiation therapy for cancer? 1776 41

Fenretinide, N-(4-hydroxyphenyl)retinamide (4-HPR) is an aminophenol-containing synthetic retinoid derivative of all-trans-retinoic acid, which is a potent chemopreventive and antiproliferative agent against various cancers. Clinical studies of 4-HPR have shown side effects consisting of night blindness and ocular toxicity. To maintain potent anticancer activity without side effects, p-dodecylaminophenol (p-DDAP) was designed based on structure-activity relationships of 4-HPR. In our study, we investigate whether p-DDAP shows anticancer activity against human prostate cancer cell line PC-3 when compared with 4-HPR. p-DDAP inhibited PC-3 cell growth progressively from low to high concentration in a dose-dependent manner. p-DDAP was the most potent antiproliferative agent in vitro among 6 p-alkylaminophenols and 3 4-hydroxyphenyl analogs examined including 4-HPR. Cells treated with p-DDAP were shown to undergo apoptosis, based on condensation nuclei, cytofluorimetric analysis, propidium iodide staining and the expression of bcl-2 and caspase 3. p-DDAP arrested the S phase of the cell cycle, while 4-HPR arrested the G(0)/G(1) phase. In addition, both the i.v. and i.p. administration of p-DDAP suppressed tumor growth in PC-3-implanted mice in vivo. p-DDAP showed no effects on blood retinol concentrations, in contrast to reductions after 4-HPR administration. These results indicate that p-DDAP exhibits excellent anticancer efficacy against hormonal independent prostate cancer in vitro and in vivo, and it may have great potential for clinical use in the treatment of prostate cancer with reduced side effects.
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PMID:p-Dodecylaminophenol derived from the synthetic retinoid, fenretinide: antitumor efficacy in vitro and in vivo against human prostate cancer and mechanism of action. 1795 89


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