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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of the various basement membrane (BM) components (type IV collagen, laminin and heparan sulphate proteoglycan) was studied in fetal, adult normal, hyperplastic and neoplastic prostates in formalin- and ethanol-fixed paraffin-embedded specimens. Stromal, epithelial and neoplastic BMs expressed differential susceptibility to pepsin treatment, suggesting conformational differences in the expression of epitopes on BM proteins in distinct anatomical structures and various lesions of the human prostate. In fetal prostate the acinar BM was regular and continuous in contrast to normal adult prostate and various hyperplastic conditions where the acinar BM was locally thickened or unreactive to the anti-BM antibodies. The localization pattern of BM components in grade I and grade II phases of prostatic cancer did not differ essentially from those found in various hyperplastic lesions. Regardless of the histopathological grade of malignancy, prostatic carcinoma cells were surrounded by distinct pericellular and periacinar membranes which were present even at points of contact with the stroma. This suggests that stroma invasion is invariably associated with neoplastic BM formations. Immunohistochemical evidence of the stromal or epithelial origin of neoplastic BMs could not be found. However, the consistent extracellular distribution of neoplastic BM components in contact with the stroma indicates that the elaboration of BM material requires a stromal influence.
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PMID:Basement membranes in fetal, adult normal, hyperplastic and neoplastic human prostate. 203 51

Using a monoclonal antibody to bromodeoxyuridine and immunohistochemistry, we measured the incorporation of this thymidine analogue into the deoxyribonucleic acid of human prostate adenocarcinoma cells exposed in situ. Fifteen patients with prostate cancer were given an intravenous infusion of 500 mg. bromodeoxyuridine at needle biopsy to label tumor cells in the deoxyribonucleic acid synthesis phase (S phase). The tumor specimens were fixed with 70 per cent ethanol, embedded in paraffin, sectioned and stained by an indirect immunoperoxidase method using anti-bromodeoxyuridine monoclonal antibody as the first antibody. The results showed that this method demonstrated bromodeoxyuridine-labeled nuclei satisfactorily in tissue section. The bromodeoxyuridine labeling index, S phase fraction, was determined by counting the number of bromodeoxyuridine-labeled cells in the tissue sections. Grade 3 tumors averaged 4.37 +/- 0.48 per cent labeling versus 2.41 +/- 0.49 per cent in grade 2 tumors, and grade 1 tumor in the series had an S phase fraction of 1.36 +/- 0.39 per cent. The average S phase fractions for single gland, cribriform, fused and medullary were 1.16, 2.30, 3.74 and 4.95 per cent, respectively. The results obtained with S phase fraction measured with bromodeoxyuridine labeling proved to be comparable to the results of histological grade and growth pattern. Thus, the higher S phase fraction may indicate biological malignancy. Moreover, the degree of heterogeneity concerning S phase fraction distribution within prostate cancer tissue could be compared to the morphological appearance. Our preliminary results suggest that the measurement of bromodeoxyuridine labeling index in prostate cancer may prove to be a new objective and quantitative assay of biological potential of individual tumor.
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PMID:Immunocytochemical demonstration of S phase cells by anti-bromodeoxyuridine monoclonal antibody in human prostate adenocarcinoma. 264 26

Vitamin E (tocopherol) enhances the growth inhibitory effects of adriamycin (ADR) on a variety of cancer cells in vitro. The role of vitamin E (d-alpha-tocopheryl) acid succinate in adjuvant chemotherapy with ADR was assessed in DU-145 human prostatic carcinoma cells in culture. Adriamycin produced a dose-dependent growth inhibition of DU-145 cells. The ID50 of DU-145 cells on the criteria: of clonal assay was 13 ng./ml. and of cell count assay was 14 ng./ml. Vitamin E succinate also inhibited the growth of DU-145 human prostatic carcinoma cells in a dose-dependent manner. 4.4 micrograms./ml. and 5.4 micrograms./ml. vitamin E succinate in the culture medium produced inhibition of growth to 50 per cent of control (ID50) in the clonal and the cell count assays respectively. When adriamycin and vitamin E succinate were used in combination, both additive and synergistic effects were observed, depending on the concentration of vitamin E succinate used. Doses of vitamin E succinate greater than its ID50 had a synergistic effect while doses smaller than its ID50 had an additive effect. In either case, the presence of vitamin E succinate caused an enhancement of tumor cell cytotoxicity of adriamycin while decreasing its ID50. Equivalent concentrations of sodium succinate and ethanol used to dissolve vitamin E succinate did not have any effect on DU-145 cells. Thus, it is concluded that the effect of vitamin E succinate is due to vitamin E and not due to succinate or ethanol. These results suggest that vitamin E may have a role in the treatment of human prostatic cancer as an adjuvant agent to adriamycin.
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PMID:Vitamin E enhances the chemotherapeutic effects of adriamycin on human prostatic carcinoma cells in vitro. 373 28

The majority of human cancers have multifactorial environmental causes stemming mainly from lifestyle factors such as use of tobacco products through cigarette smoking, snuff dipping, or chewing, and specific nutritional elements and dietary practices. The mechanisms of these lifestyle factors can be analyzed in terms of specific genotoxic carcinogens, and of epigenetic agents or promoting factors. Tobacco and tobacco smoke contain not only genotoxic carcinogens but also, with a more important ultimate effect, cocarcinogens and promoters. Alcohol acts as a cocarcinogen with tobacco, possibly by modifying the metabolism of carcinogens in select organs. Genotoxic carcinogens as nutritional factors may be found in pickled, salted, and smoked foods and may be responsible for gastric cancer. Vitamins C and E and other antioxidants are effective inhibitors. Other types of genotoxic carcinogens are mutagenic chemicals found in broiled and fried foods, and these may be involved in cancer of the colon, breast, and prostate. Promoting effects derive from a high level of dietary fat, which has been linked epidemiologically and through laboratory studies to a higher risk for these cancers. Possible mechanisms by which fat exerts its effects are an increased concentration of bile acids in the stool, as related to colon cancer, and which may be countered by a high cereal fiber diet, to increase stool bulk. In relation to breast or prostate cancer, fat may exert its effect on complex hormonal balances, and also on membrane composition. These promoting effects, whether associated with tobacco smoke or nutrition, are highly dose-dependent, and provided the insult is not too far advanced, reversible. Thus, lowering the dosage, or eliminating the effect as in smoking cessation should have an appreciable effect in reducing overt disease development, and do so fairly promptly. This may apply also to a reduction of second disease in cases where a first occurrence has been successfully treated by conventional means.
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PMID:The role of genotoxic carcinogens and of promoters in carcinogenesis and in human cancer causation. 638 22

A rapid, sensitive and specific high-performance liquid chromatographic (HPLC) assay was developed for the determination of estramustine and its 17-keto metabolite in plasma. The assay involves extraction of the compounds into hexane from plasma buffered to pH 9.0, the residue obtained by evaporation of the hexane extract is dissolved in the mobile phase hexane-ethanol (92.5:7.5) with HPLC analysis performed on a 5-micrograms silica gel column using a fluorescence detector with excitation at 195 nm and emission at wavelengths greater than 250 nm. The overall recoveries and limits of sensitivity for estramustine and the 17-keto metabolite are 74.7% and 40 ng/ml of plasma and 85.1% and 50 ng/ml of plasma, respectively. The method was used to obtain plasma concentration-time profiles in three subjects with prostatic cancer following oral administration of a single 7 mg/kg dose of estramustine phosphate.
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PMID:Determination of estramustine and its 17-keto metabolite in plasma by high-performance liquid chromatography. 739 Nov 81

The value of serum acid phosphatase (S-ACP) as a marker of transurethral resection (TUR) syndrome was studied in 105 patients undergoing TURP. In ten patients who developed TUR syndrome the elevation of S-ACP was statistically significantly higher than in the rest of the patients. In seven patients prostatic cancer was diagnosed in the resection chips, but there were no differences in the S-ACP levels during TURP between these patients and the rest of the group. According to the present study, S-ACP seems to be a reliable and cheap marker of TUR syndrome, but the method is slow as compared to ethanol, which restricts its use.
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PMID:Serum acid phosphatase in TUR syndrome. 750 9

Alcohol consumption and cigarette smoking have been suggested as possible causes of prostate cancer. We therefore examined this relation in a cohort of 43,432 men who were members of a prepaid health plan in northern California (United States) and who had received a health examination in the period from 1979 through 1985. Detailed information on demographic variables, alcohol consumption, smoking habits, medical complaints and conditions, occupation, and surgery (including vasectomy) was assessed. Symptoms of prostatism and a history of sexually transmitted diseases were abstracted from the medical records of all prostate cancer patients and of a matched subsample of randomly selected control-subjects. Alcohol consumption was associated with no elevated prostate cancer risk for the 238 men in our study in whom prostate cancer developed, but smoking one or more packs of cigarettes per day was associated with an adjusted relative risk (RR) of 1.9 (95 percent confidence interval [CI] = 1.2-3.1). Prostate cancer risk for Black men was 2.2 (CI = 1.6-3.1) when compared with that for White men, and education level was associated positively in an increasing trend (P < 0.020) up to an RR of 1.4 (CI = 0.9-2.1) among men with postgraduate education. Symptoms of prostate hypertrophy were not associated with elevated risk of prostate cancer if they occurred two or more years before the diagnosis. The finding that smoking increased the risk of prostate cancer confirms the observations of others but needs cautious interpretation because we were unable to adjust for the potential confounding effect of dietary and hormonal factors.
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PMID:Alcohol consumption, smoking, and other risk factors and prostate cancer in a large health plan cohort in California (United States). 751 Jan 34

Prostate cancer is the most common malignancy in US men (more than 165,000 cases per annum) and occurs substantially more frequently in blacks than in whites. The causes of this disease are, however, poorly understood. Alcohol consumption, which has been clearly related to malignancies of the upper aerodigestive tract, may also increase risk of cancer at other sites, including the prostate. The authors investigated alcohol use as a risk factor for prostate cancer among US blacks and whites. A population-based, case-control study was carried out among 981 men (479 blacks and 502 whites) with pathologically confirmed prostate cancer diagnosed between August 1, 1986, and April 30, 1989, and 1,315 controls (594 blacks and 721 whites) who resided in Atlanta, Georgia; Detroit, Michigan; and 10 counties in New Jersey, geographic areas covered by three population-based cancer registries. In-person interviews elicited information on alcohol use and other factors possibly related to prostate cancer. Compared with never-users, risk for prostate cancer increased with amount of alcohol drunk (chi2 (trend), p < 0.001), with significantly elevated risks seen for those who had 22-56 drinks per week (odds ratio = 1.4; 95% confidence interval 1.0-1.8) and 57 or more drinks per week (odds ratio = 1.9; 95% confidence interval 1.3-2.7). The finding was consistent among blacks (chi2 (trend), p < 0.01) and whites (chi2 (trend), p < 0.05), and among young and old subjects; it was not restricted to a specific type of alcoholic beverage. In this first large study among US blacks and whites, increased risk for prostate cancer was associated with increased alcohol use. The risk was similar for whites and blacks and could not be attributed to tobacco use or to a number of other potential confounders.
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PMID:Alcohol use and prostate cancer risk in US blacks and whites. 865 Dec 31

Prostate epithelial cell growth is under the control of both steroid and peptide factors. Human prostate cancer cell lines have been used to investigate similar agents in malignancy. Activins are dimeric peptides structurally related to transforming growth factor-beta and produced in the gonads and a wide array of extragonadal tissues. The activins act at the pituitary to regulate the synthesis and secretion of FSH. At other sites, such as bone marrow, liver, and gonads, activin may play an important role in the regulation of cell growth and differentiation. It was the purpose of the current study to determine whether activin had similar actions on prostate cancer cells, specifically the androgen-responsive LNCaP and the androgen-resistant PC-3 cell lines. Using reverse transcription-PCR, messenger RNAs for type I and type II activin receptor subunits as well as the activin-binding protein follistatin were detected in both cell lines. Activin treatment rapidly (<24 h) inhibited LNCaP, but not PC-3, cell growth. The effects of activin were evident at low levels, with a concentration of 5 ng/ml being effective at 24 h, and a concentration of 0.5 ng/ml being effective at 48 h. These results contrasted with the actions of transforming growth factor-beta, which inhibited only PC-3 cells and required a greater treatment duration (96 h) to be effective. To determine whether these prostate cancer cell lines were also producing activin, LNCaP and PC-3 cells were treated with follistatin. Again, only the LNCaP cells responded, with growth acceleration noted by 24 h. As PC-3 cell responses to activin could be independent of cell proliferation, we transfected LNCaP and PC-3 cells with a known activin-responsive promoter/reporter gene construct (p3TP-Lux) and treated cells with activin. Only LNCaP cells produced a measurable response in luciferase activity. Finally, we attempted to determine whether the PC-3 cell resistance to activin was mediated via a transferable factor. PC-3 conditioned medium was added to LNCaP cells in the absence or presence of exogenous activin and had a small, but statistically nonsignificant (P < 0.09), action to blunt the actions of activin. We conclude that activin is a potent growth inhibitor of LNCaP cell growth. Moreover, these cells also produce activin, suggesting that locally derived activin may play a role in regulating cell proliferation. Despite expressing messenger RNAs for activin receptors, PC-3 cells are resistant to activin, perhaps the result of the production of an activin-blocking factor or a defective activin response system. These cell lines will thus serve as useful models in which to further study the cellular basis of activin action.
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PMID:Activin inhibition of prostate cancer cell growth: selective actions on androgen-responsive LNCaP cells. 894 Mar 39

The complex process of carcinogenesis is mainly due to environmental factors and therefore preventable. Diet may account for about 35% of cancer cases; risk factors and protective factors are discussed. Accordingly, obesity is associated with an increased risk of endometrial and postmenopausal breast cancers. Less clear is the relationship with colorectal and prostate cancer. The observed inverse association of body weight with lung cancer risk is most probably confounded by smoking habits and/or the effect of preclinical cancer. The risk factor fat has been studied mainly in relation to colorectal, breast and prostate cancer; the results are controversial. More consistent are the associations between (red) meat consumption and risk of colorectal and prostate cancer. Alcohol is a risk factor for tumors of the upper gastrointestinal tract, the hepatocellular carcinoma and the (distal) colorectal cancer. Even small amounts of alcohol seem to increase the risk of breast cancer. Residues, contaminants, mycotoxins and additives like benzopyrene, nitrosamine(s), and aflatoxine are associated with a smaller risk of cancer than "overnutrition". High intake of fruit and vegetables is related to a reduced risk of lung cancer and cancer of the upper gastrointestinal tract. What the specific chemicals in fruits and vegetables are that are responsible for this association are still unclear. Despite only weak associations between dietary factors and cancer risk, for potential protective effects it is recommendable to increase the consumption of fruit and vegetables, to avoid obesity, to reduce the intake of fat, meat and alcohol and to avoid cured, pickled, smoked, and mouldy food.
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PMID:[The significance of nutrition in primary prevention of cancer]. 938 16


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