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)

The growth of DU-145 human prostate carcinoma cells is reduced to 50% of control by 1 X 10(-6) M to 2 X 10(-6) M selenium and to 2% of control at 10(-4)M selenium. These cells show greater sensitivity to inhibition of growth or DNA synthesis by selenium than human W1-38 and HeLa cells and mouse mammary tumor cells. It has been shown that selenium inhibits carcinogenesis and reduces the incidence of chemical carcinogen and virus-induced tumors of a variety of organs in animals. Selenium may also inhibit the growth of certain tumor cells of non-human origin. To our knowledge, this is the first study on the effects of selenium on the growth of human tumor cells. From extrapolation, it is deduced that selenium serum levels in humans living in high selenium areas may be as high as 10(-6) M and could be effective in inhibiting the growth of tumor cells in vivo. These findings have implications in the prevention and intervention of prostate cancer in man.
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PMID:Inhibitory effects of selenium on the growth of DU-145 human prostate carcinoma cells in vitro. 402 50

Weekly intragastric treatment with N-nitrosobis(2-oxopropyl)amine or N-nitrosobis(2-hydroxypropyl)amine induced hyperplastic, preneoplastic and neoplastic prostatic changes in greater than 80% of MRC rats. The lesions initially appeared as focal or multifocal proliferations of alveolar epithelium in a cribriform pattern which, in all but one case, underwent progressive changes, often tending toward squamous cell formation. Tumors, found primarily in the ventral prostate, demonstrated various degrees of differentiation and invasive growth. A few neoplasms developed in the seminal vesicles; however all were of a glandular type. The sequential alteration of induced lesions is described and the possible reasons for the squamous cell character of most tumors discussed. Prostatic cancer induction by systemic application of specific nitrosamines could provide a unique tool for investigating important aspects of the disease.
Carcinogenesis 1983
PMID:Prostatic cancer induced in MRC rats by N-nitrosobis(2-oxopropyl)-amine and N-nitrosobis(2-hydroxypropyl)amine. 618 48

In untreated male ACI/Seg rats, the incidence of microscopic cancer of the ventral prostate is zero below the age of 16 months but increases to greater than 80% by 36 months of age, while the incidence of grossly manifest cancer of the ventral prostate is zero before the age of 20 months and increases to 16% by 36 months of age. In contrast, in untreated male Copenhagen rats, the incidence of microscopic prostatic cancer is only 10%, and the incidence of grossly manifest prostatic cancer is less than 1% even at 36 months of age. Analysis of the relationship between ACI/Seg host age and the incidence of microscopic versus grossly manifest prostatic cancer suggests that microscopic prostatic cancer is the result of a multistep process and that additional events are required for the progression of microscopic to grossly manifest prostatic cancer. Comparison of the serum levels of sex steroid hormones between aging male ACI/Seg and Copenhagen rats reveals substantial differences, suggesting that alterations in the serum testosterone:estrogen ratio may be one of the factors involved in prostatic carcinogenesis in the ACI/Seg rat. Chronic elevation of serum testosterone levels in these male ACI/Seg rats by means of exogenous testosterone treatment alone, however, does not induce the precocious development of microscopic prostatic cancer in young (i.e., less than 1 year of age) animals, suggesting that other factors, in addition to alterations in serum levels of testosterone, are required for prostatic carcinogenesis in the male ACI/Seg rat.
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PMID:The aging ACI/Seg versus Copenhagen male rat as a model system for the study of prostatic carcinogenesis. 649 39

In this paper, studies by a large series of independent investigators are reviewed with regard to the basic structure and function of the prostate in an attempt to examine their relationship to prostatic cancer etiology. These studies demonstrate that the functional activities of the prostate involve secretion, transport, and reabsorption of a variety of materials into and out of the glandular lumen and that these activities are directly related to the basic structural organization of the gland. These functional activities are constantly occurring in the prostate even under basal (ie, nonejaculating) conditions. Due to these functional activities, the prostatic fluid in the glandular lumen is a complex mixture of a variety of components derived, not only from the synthetic activity of the glandular epithelial cells of the gland itself, but also from the blood serum. The levels of these components are continuously modulated, not only by the frequency of active ejaculation, but also, under basal conditions by the continuous interaction with the glandular prostatic cells lining the acinar lumen and ducts. A concept is presented that the initiation and/or promotion of prostatic carcinogenesis may well involve the chronic modulation/interaction of the prostatic glandular cells with their lumenal fluid.
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PMID:Prostatic structure and function in relation to the etiology of prostatic cancer. 686 50

The aim of this study is to present our preliminary experience in treating BPH-related urine retention, resistant to other medical treatment, with transurethral brachytherapy. We also deal with dosimetric analysis so as to eliminate ethical concerns about the exposure of patients not suffering from cancer to a certain level of body irradiation. Patients suffering from BPH-related urethral obstruction were treated with two transurethral applications (three weeks apart) of Cs137 MDR, which delivered a total of 16 Gy, at 0.5 cm from the urethral walls (dose rate 5-7 Gy/h). The application was done under ultrasonographic observation. Dosimetric calculation of the radiation exposure of the human body during transurethral radiotherapy (TURT) was performed for patients suffering from prostate cancer and treated with external beam radiotherapy and a boost dose through transurethral brachytherapy. For this purpose we used TLDs on skin surface and dosimetric analysis of X-ray films. Five patients treated for BPH urethral obstruction presented no sign of acute toxicity. All of them were weaned of their indwelling catheter immediately after the end of the first application. Obstruction did not recur within 12-18 months of follow-up. The dose delivered outside the prostate ranges from 1-7 cG, depending upon location. Proximal rectal and bladder walls received 1-2 Gy, a dose that is far from inducing acute or late toxicity. The estimated risk for carcinogenesis is negligible, and the expected benefit for the quality of life transcends the risks. No ethical concern is justified for testing transurethral radiotherapy for BPH-related urethral obstruction. TURT seems to be effective and provides durable results. Further investigation is required.
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PMID:Transurethral radiotherapy for benign prostatic hypertrophy-related urethral obstruction. Dosimetry, ethics, and preliminary results. 752 61

Epidemiological studies have shown an association between a high-fat diet and a high mortality rate from breast, colon, and prostate cancer. However, the promotional effect of a high-fat diet on experimental carcinogenesis has not been fully established for the prostate. In this study, the effect on prostatic carcinogenesis of two-generation exposure to a high-fat diet was investigated using ACI/Seg rats, a strain with high incidence of spontaneous prostate cancer. A high-fat diet (20% corn oil) or a low-fat diet (5% corn oil) was given to mother rats during pregnancy and the newborn male rats were fed the same diets for 60 or 100 weeks after weaning. At 100 weeks, atypical hyperplasia and adenocarcinoma of the prostate were respectively found in 73.3% (11/15) and 20.0% (3/15) of the high-fat diet group and in 20.0% (3/15) and 0% (0/15) of the low-fat diet group. There was a significant increase of atypical hyperplasia in the high-fat diet group (P < 0.05). The serum concentrations of sex hormones and the prostatic proliferative activity as measured by flow cytometry or bromodeoxyuridine labeling were not significantly affected by diet. These results showed that feeding a high-fat diet before conception and from the beginning of organogenesis had a marked promotional effect on the early stage of prostate carcinogenesis in rats.
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PMID:Promotional effect of two-generation exposure to a high-fat diet on prostate carcinogenesis in ACI/Seg rats. 752 54

In search of biomarkers that predict of human prostate cancer progression, we hypothesized that these markers must be expressed in prostatic epithelial cells during multi-step prostate carcinogenesis. Since both genetic and epigenetic factors have been implicated in human prostate cancer development, two osseous-metastatic experimental models were developed in our laboratory, one based on gene transfection and the other on stromal-epithelial interaction studies. In the genetic model, PC-3 cells transfected with point-mutated c-erbB-2/neu oncogene subsequently acquired the potential to metastasize from the prostate to soft tissues and the skeleton. In the epigenetic model, sublines derived from the parental androgen-dependent LNCaP cell line metastasized from the primary tumor to the lymph node and bone. Cells with known lineage relationships were cloned from both the primary and the metastatic tumors and were characterized extensively using cellular, biochemical, immunohistochemical, and molecular techniques. Relevant stage-specific biomarkers associated with prostate cancer progression in these two models were defined and used to evaluate human prostate tissues obtained from the clinic. In this communication, we focused our discussion on the potential importance of c-erbB-2/neu oncogene, vimentin, hepatocyte growth factor/scatter factor and its receptor, c-met oncogene, tumor angiogenesis and neuroendocrine factors as biomarkers for human prostate cancer progression.
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PMID:Biomarkers associated with prostate cancer progression. 752 53

Prostate cancer is the most common noncutaneous malignancy diagnosed in American men, and in 1994 it will pass lung cancer as the most common cancer diagnosed in the United States, with an estimated 200,000 new cases. The molecular biology of prostate carcinogenesis is rapidly advancing, and it is clear that, to a degree, prostate cancer is a heritable disease. The use of serum prostate-specific antigen (PSA) as a screening tool has been widely accepted by the medical community, although the evidence to support the efficacy of screening is not yet available. The curative approaches to organ-confined, clinically localized prostate cancer include radiation therapy, radical prostatectomy, and close observation in selected patients. The absence of well-designed clinical trials contributes to the confusion surrounding which curative treatment is the best option in individual patients. The standard approach to patients with evidence of extracapsular spread without distant metastases has been external-beam radiotherapy, although the results with radiation therapy alone in these patients has left considerable room for improvement. Innovative combined-modality approaches are currently being investigated at a number of institutions for these poor-prognosis patients. Three-dimensional conformal radiation therapy is currently being investigated at multiple institutions and offers some hope for improved results. The treatment of metastatic disease remains hormonal manipulation, although the exact nature of optimal androgen deprivation is currently a matter of considerable debate. In patients with hormone-refractory disease newer regimens using novel chemotherapy regimens offer some promise.
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PMID:Prostate cancer. 753 41

Prostatic cancer is the second most frequent cancer in men in France. It is a serious disease with a relative 5-year survival of 42%. Although the incidence of latent forms appears to be constant throughout the world, the incidence of clinical forms varies from country to country and according to race. These aspects are in favour of a dual mechanism of prostatic carcinogenesis: initiation of a cellular modification, which may be transmitted genetically according to an autosomal dominant mode, but whose expression may be influenced by the environment, and successive steps of transformation (epigenetic factors) which are essentially environment-dependent. The main identified risk factors essentially consist of a direct family history, age and a diet rich in animal fats. In contrast, neither the presence of benign prostatic hypertrophy, nor the characteristics of the sex life or a history of vasectomy appear to influence the incidence of prostatic cancer. The main epidemiological data currently available are presented.
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PMID:[Cancer of the prostate. 1. Epidemiology]. 753 26

The authors have studied DNA base damage and activities of antioxidant enzymes in human benign prostatic hyperplasia (BPH) tissues and surrounding disease-free tissues removed from prostate glands of 15 patients. In these tissues, endogenous levels of various typical hydroxyl radical-induced products of DNA bases and activities of catalase and superoxide dismutase were measured. The majority of patients had higher levels of DNA base lesions and lower activities of enzymes in BPH tissues than in normal prostate tissues. When activities of both enzymes were lower in BPH tissues than in normal tissues, the increases in the amounts of DNA base lesions over control levels were most prominent. In the case of similar enzyme activities in both BPH and normal tissues, no changes in levels of DNA base lesions were observed. These results suggest a possible association between antioxidant enzyme activities and levels of DNA base lesions in BPH tissues. Some of the identified DNA lesions are known to be premutagenic and may play a role in carcinogenesis. Although a possible link between BPH and prostate cancer is controversial, BPH patients with both decreased antioxidant enzyme activities and increased levels of DNA lesions may be at risk of developing prostate cancer.
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PMID:DNA base modifications and antioxidant enzyme activities in human benign prostatic hyperplasia. 753 80


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