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)

Specific receptors for dihydrotestosterone and estradiol-17-beta have been identified in cytosols of the human and baboon prostate. Binding of radioactive estradiol-17-beta to the 0.4 M potassium chloride extractable component of human prostate nuclei also was demonstrated. Cyproterone acetate and diethylstilbestrol, agents of known high affinity for dihydrotestosterone and estradiol-17-beta receptors, respectively, did not bind significantly to sex hormone binding globulin and, therefore, were useful as competitors in distinguishing binding of dihydrotestosterone and estradiol-17-beta to sex hormone binding globulin and to their specific receptors. Displacement of [3H]-estradiol-17-beta binding by diethylstilbestrol in cytosols of 11 needle biopsy specimens (mean equals 16.8 mg.) from prostatic cancer patients was analyzed. These preliminary data indicated a trend towards greater competition by diethylstilbestrol for high affinity binding sites in differentiated tumor specimens from men who were not receiving estrogen therapy. Objective and subjective responses to hormone therapy were recorded in these patients, whereas the disease in those men with low displacement assay values progressed.
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PMID:Steroid hormone receptors in the prostate. 11 Sep 48

The usefulness of prophylactic diuretic therapy with furosemide was investigated in 6 patients with stages III and IV prostatic cancer who were undergoing diethylstilbestrol therapy. A significant increase was noted in sodium and water excretion, whereas outputs of chloride and potassium, and serum electrolyte concentrations, blood volume, blood pressure and body weight remained unchanged. The results demonstrate the value of diuretics in preventing fluid retention whenever large doses of estrogen are to be used in the treatment of prostatic cancer.
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PMID:Prevention of body fluid retention by furosemide during estrogen therapy of prostatic cancer. 115 21

Estramustine phosphate (EMP), a complex between estradiol-17 beta and nor-nitrogen mustard, commonly used in treatment of prostatic cancer, also exerts marked antiproliferative effects on cultured human malignant glioma cells. The mechanism of action is unknown but has previously been considered to be mediated through non-DNA targets, specifically via the mitotic spindle, and related to the intact estramustine complex. EMP cytotoxicity was studied on the malignant glioma cell line U-251 MG. A dose-dependent increase in DNA strand breaks was demonstrated at EMP-concentrations ranging 10-40 mg/l. The uptake of 86Rb, used as a tracer for potassium to study ion transport and membrane permeability, was reduced after incubation with EMP. The mean decline in 86Rb accumulation by U-251 MG cells was 12, 20 and 32% at EMP concentrations 10, 20 and 40 mg/l respectively. Scanning electron microscopy gave further evidence for cell membrane damage. In conclusion, EMP seems to affect malignant glioma cells on several vital functions and the results indicate the the cytotoxic potential may at least partially be related to effects on DNA and cell membrane.
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PMID:Effects of estramustine on DNA and cell membrane in malignant glioma cells. 195 92

Estramustine (EM), a complex between estradiol-17 beta and nornitrogen mustard, is commonly used in the treatment of prostatic cancer. The exact mechanism of action is unknown but has previously been considered to be mediated through non-DNA targets, specifically with the mitotic spindle, and to be related to the intact EM complex. In the present study, using different cell-systems (monocyte phagocytosis transformed fibroblasts, colon cancer cells), the EM cytotoxicity was also found to involve direct interaxtion with DNA and cell membranes. The interaction with DNA was shown by a DNA precipitation assay using 3H- and 14C- thymidine, and the cell membrane damage by using 86Rb- accumulation as a sensitive marker for active potassium uptake. EM effects in the fibroblasts were inhibited by various metal chelators and radical scavengers. Involvement of free oxygen radicals was further indicated in a cell-free system with an oxygen electrode. The EM inhibition of monocyte phagocytosis was related to the engulfment, and was not at all influenced by radical scavengers. In contrast to EM, neither of its components alone, or together, affected monocyte engulfment. Finally, it was shown that the colon cancer cell-line HT-29 was resistant to both of the two suggested and separate mechanisms for EM toxicity: an interaction with the microtubuli system by the intact EM complex and a more unspecific action mediated by free-oxygen radicals.
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PMID:The effect of estramustine on microtubuli is different from the direct action via oxygen radicals on DNA and cell membrane. 234 5

One hundred patients with prostate cancer and two different control series [100 benign prostatic hyperplasia (BPH) patients and 100 general hospital patients] were matched to each other upon hospital admittance, age (+/- 3 years) and date of admission (+/- 3 months), and directly interviewed during admission from 1981 to 1984 in Kyoto, Japan. Major dietary findings derived from a quantitative food frequency technique for estimating usual diet are as follows. (a) The smaller the dietary intake of beta-carotene and vitamin A as well, the higher the risk, with a highly significant linear trend. From the beta-carotene analyses, the relative risk (95% confidence interval) for the lowest intake quartile relative to the highest was 2.10 (0.98-4.47) for the uncorrected intake, 2.35 (1.08-5.12) for the intake per kg, and 2.94 (1.34-6.44) for the intake per kcal in the comparison with BPH patients; 2.88 (1.31-6.32), 2.56 (1.14-5.76), and 3.50 (1.52-8.06), respectively, in the comparison with hospital controls. The corresponding relative risk obtained from the vitamin A analyses was 2.82 (1.30-6.14), 2.64 (1.24-5.60), and 3.29 (1.47-7.35) in due order in the comparison with BPH patients; 2.69 (1.22-5.94), 4.78 (1.98-11.52), and 3.50 (1.52-8.06) in the comparison with hospital controls. (b) beta-Carotene as well as vitamin A contained in green/yellow vegetables were significantly protective, and those in seaweeds and kelp suggestively protective. But those in fruits appeared to enhance the risk. (c) The risk reduction by dietary beta-carotene and vitamin A was significant in the older men (70-79 years), but not in the younger men (50-69 years). (d) Total energy intake and the dietary intake of fat, protein, carbohydrate, water, fiber, ash, such vitamins as retinol, B1, B2, C, and niacin, and such minerals as calcium, potassium, sodium, phosphorus, and iron were not linked with prostate cancer risk. (e) A protective effect of dietary beta-carotene and vitamin A against prostate cancer could be related to the low overall fat intake in Japan.
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PMID:Dietary beta-carotene and cancer of the prostate: a case-control study in Kyoto, Japan. 244 78

The leukocyte migration inhibition (LMI) assay was used to determine the cell-mediated immune reactivity of prostate cancer patients to putative tumor antigens present in potassium chloride extracts of surgically removed prostate tumor tissue. Using an extract prepared from prostate tumor tissue, inhibition of leukocyte migration was found more frequently in prostate tumor patients (61%) than in patients with benign prostate hyperplasia (37%), patients with nonprostate cancers (26%), or normal donors (10%). Control extracts prepared from normal prostate tissue, benign prostate hyperplasia tissue, and unrelated tumor tissue were statistically less reactive in the LMI assay than the prostate tumor extract when reacted against leukocytes from prostate tumor patients. These results suggest that the LMI assay might be potentially useful for measuring the tumor-directed, cell-mediated immune responses in patients with prostate cancer.
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PMID:Leukocyte migration inhibition assay in patients with prostate adenocarcinoma. 617 Sep 63

Gossypol, a polyphenolic aldehyde naturally present in cottonseed, has long been recognized as a male contraceptive and recently as a potential anticancer agent. Our study used a rodent model to evaluate gossypol's potential for the treatment of human prostatic carcinoma. Two-month-old Copenhagen male rats received subcutaneous implants of a subpassage of MAT-LyLu prostatic cancer line, a highly metastatic, androgen-independent Dunning prostate tumor subline that specifically metastasizes to lymph nodes and lungs of recipients. After 2 weeks of gossypol treatment (0 or 12.5 mg/kg B.W./day S.C.) initiated immediately after transplantation, the rats were sacrificed and evaluated for prostate tumor growth and metastasis. Testosterone and gossypol levels in tumor tissue and various reproductive organs and serum potassium level were measured by radioimmunoassay (RIA), high pressure liquid chromatography (HPLC) and atomic emission spectroscopy (AES), respectively. Gossypol-treated rats exhibited weight reductions in developed MAT-LyLu prostate tumor mass and prostate of 24% (p < 0.05) and 31% (p < 0.05), respectively; whereas testicular and epididymal weights were not significantly affected. Few metastases (20%) were observed in either lymph nodes or lungs of gossypol-treated recipients. The control rats, however, had a much higher rate of lung (60%) and lymph node metastasis (40%). Testicular testosterone levels, as measured by RIA, were significantly lower in gossypol-treated rats than in controls (p < 0.05), but serum testosterone levels were not different. Extractable gossypol content in the prostate tumor, as measured by HPLC, reached 19.67 ng/gm and was 1.28 times higher than in liver, 1.98 times higher than in testes, but was 3.3% of that in prostate. Moreover, serum had the highest gossypol content (10.7 micrograms/ml). Serum potassium levels, as measured by AES, were significantly higher in gossypol-treated individuals than controls (p < 0.05). Our results indicate for the first time that gossypol has antiproliferative and antimetastatic effects on MAT-LyLu prostate cancer cells and can be explored as a potential therapeutic agent for androgen-independent human prostatic carcinoma.
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PMID:Antiproliferative and antimetastatic effects of gossypol on Dunning prostate cell-bearing Copenhagen rats. 848 76

We interviewed 328 men diagnosed with prostate cancer before the age of 75 years and 328 age-matched population controls. The principal hypotheses were that risk would increase with a high intake of total or saturated fat and would decrease with a high intake of carotene (beta-carotene equivalents) or lycopene. We also examined the associations of other nutrients and foods with risk. There was no evidence for an association between fat intake and risk, although the average fat intake was high and the range of fat intakes was narrow (medians of lower and upper thirds of percentage of energy from fat among controls were 34.3% and 42.9% respectively). Risk was lower in subjects with higher carotene intake: odds ratios 0.65 (95% CI 0.45-0.94) and 0.76 (0.53-1.10) in the middle and upper thirds of carotene intake respectively (P for trend = 0.150). Lycopene was not associated with risk. Among 13 other nutrients examined, the odds ratios in the top third of intake were below 0.8 for: potassium, 0.74 (0.51-1.09; P for trend = 0.054); zinc, 0.73 (0.49-1.08; P for trend = 0.126); iodine, 0.75 (0.51-1.11; P for trend = 0.077); vitamin B6 food only, 0.77 (0.53-1.12; P for trend = 0.077); and vitamin B6 including supplements, 0.70 (0.48-1.03; P for trend = 0.029). Among 18 foods examined, statistically significant associations were observed for: garlic as food, > or = 2/week vs never, 0.56 (0.33-0.93); garlic including supplements, > or = 2/week vs never, 0.60 (0.37-0.96); baked beans, > or = 2/week vs < 1/month, 0.57 (0.34-0.95); and garden peas, > or = 5/week vs < or = 3/month, 0.35 (0.13-0.91). This study does not support the hypothesis that fat increases risk and is equivocal in relation to carotene. The possible relationships of vitamin B6, garlic, beans and peas with risk for prostate cancer should be further investigated.
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PMID:A case-control study of diet and prostate cancer. 930 71

We present a patient with prostate cancer who developed symptomatic hypocalcemia while taking oral clodronate for painful bony metastases. He had a past history of a bowel resection for Crohn's disease, and, although he was normocalcemic prior to taking clodronate, it is likely that the surgery had caused mild hyperparathyroidism. The addition of clodronate prevented the chronic osteolysis of bony metastases, which would have helped maintain normocalcemia. The case was complicated by hypomagnesemia and hypokalemia resulting from diarrhea. Hypomagnesemia is a cause of refractory hypocalcemia and hypokalemia. This case illustrates two important points. First, care must be taken with bisphosphonates in patients with a previous bowel resection. Second, magnesium plays a key role in the metabolism of both calcium and potassium, and must be considered in the evaluation of the hypocalcemic patient.
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PMID:Symptomatic hypocalcemia with oral clodronate. 949 15

Although prostate cancer is the number one diagnosed cancer in men, the importance of emphasizing and preventing other common diseases after diagnosis is essential. For example, heart disease still remains the number one cause of mortality in men, accounting for 50% of the deaths in Western countries. Therefore, promoting overall healthy behaviors also seems essential, especially in light of past and recent evidence that an individual can maintain proper health by following some simple guidelines. The increased consumption of healthy foods, greater intakes of B-vitamins and minerals such as potassium can significantly reduce the risk of heart disease, stroke, and possibly cancer in a patient with a prior or current malignancy. Overall dietary change as observed from the Mediterranean diet, light exercise, and improved mental health should also be stressed to the patient because of recent studies.
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PMID:Emphasizing and promoting overall health and nontraditional treatments after a prostate cancer diagnosis. 1033 26


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