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)

Bone marrow acid phosphatase has been reported to be a sensitive indicator of early bony metastasis from adenocarcinoma of the prostate. In order to evaluate this hypothesis, we measured bone marrow acid and alkaline phosphatase, lactic dehydrogenase, and calcium levels in a group of 84 patients with a variety of problems, including 18 with cancer of the prostate. We found that the bone marrow acid and alkaline phosphatase and lactic dehydrogenase were elevated and calcium was depressed in most patients. Among patients with prostate cancer, bone marrow acid phosphatase was not significantly different between those with or without bone metastases. In addition, the patients with prostatic cancer did not have higher levels of bone marrow acid phosphatase than subjects with other malignant and nonmalignant conditions. The level of acid and alkaline phosphatase, lactic dehydrogenase and calcium varied predictably with the aspiration technique used and was independent of sex, disease state or method of chemical determination. Due to this variation, we believe that bone marrow enzyme and calcium levels are of no value in the detection of metastases in patients with prostate cancer.
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PMID:Lack of usefulness of bone marrow enzymes and calcium in staging patients with prostatic cancer. 63 3

Major developments in birth control vaccines are on the horizon. The human chorionic gonadotropin (hCG) vaccine has entered phase II clinical trials after successful completion of phase I studies at 5 centers in India and 4 centers abroad. It is the most advanced vaccine of its type in the world. The trials are being conducted on women of proven fertility who are sexually active. The available results indicate the efficiency of the vaccine to prevent pregnancy in women at or above titres of 50 ng/ml. A vaccine inducing antibodies against gonadotropin releasing hormone (GnRH) has been approved in India for trials in postpartum women, to determine whether immunization can help prolong lactational amenorrhea. The GnRH vaccine is also in clinical trial in prostate cancer patients at 2 centers in India and in Austria and the Dominican Republic. The follicle stimulating hormone (FSH) vaccine is about to enter phase I clinical trial after completing experimental and toxicological studies. A vaccine against FSH has been developed for human males employing ovine FSH (oFSH) as an immunogen. oFSH adsorbed on alum induces antibodies reactive with human FSH in bonnet monkeys. Immunization leads to oligospermia with resultant impairment of fertilization potential. No reduction in testosterone levels has been reported. Research is in progress to identify antigens on spermatozoa, which could serve as vaccine candidates. PH-20, a protein located on the inner acrosomal membrane of capacitated sperms, has been reported to have 100% contraceptive efficacy in both sexes of guinea pigs in active immunization studies. cDNA probes of PH-20 cross-react with genomic DNAs of mouse, rat, hamster, and human. The sperm antigen, lactate dehydrogenase C4 (LDH-C4), is a glycolytic enzyme. Active immunization with LDH-C4 suppressed fertility in mice, rabbits, and baboons. SP-10, which is a testis-specific human sperm protein, is also a promising candidate.
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PMID:Vaccines for control of fertility. 129 38

Of 91 patients with prostatic cancer treated at our Department of Urology, from January 1976 through December 1987, 42 cases of stage D2 cancer treated with endocrine therapy were evaluated retrospectively with regard to clinical parameters and prognoses. The patients with marked increase in the level of the prostatic acid phosphatase (PACP), and the lactate dehydrogenase (LDH) in serum, and marked decrease in volume of hemoglobin (Hb) had a poor prognosis. The patients who took a long time to obtain a favorable response to the therapy had a poor prognosis. The response grade in NPCP criteria at 3 months after the initiation of therapy reflected the prognosis, and showed good correlation to the grade of favorable response.
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PMID:[Retrospective clinical evaluation of prognosis factors in stage D2 prostatic cancer treated with endocrine therapy]. 171 Aug 71

Serum creatine kinase (CK) and lactate dehydrogenase (LD) isoenzymes were determined electrophoretically, along with various other biochemical markers of malignancy, in 19 patients with metastatic carcinoma of the prostate. Mitochondrial CK appeared in 15 patients, the CK-BB isoenzyme in 6. As a result, CK activity not inhibited by anti-M-subunit antibodies, CK non-M, was above the reference value in altogether 17 patients. There was a cathodic shift among the LD isoenzymes, significantly more prominent with increasing total LD, and a positive correlation between elevations of CK non-M and LD-5, suggesting a relation to tumour burden for both. An LD 'flip' (LD-1 greater than LD-2) was present in 10/15 patients. The frequency of CK non-M elevations was similar to--but not quantitatively correlated with--elevations of prostatic acid phosphatase and alkaline phosphatase. Thus, changes in CK and LD patterns are frequent in patients with prostatic cancer and must be taken into consideration when acute cardiac symptoms are evaluated in such patients.
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PMID:Creatine kinase and lactate dehydrogenase isoenzymes in stage D prostatic carcinoma. 242 86

Human lactate dehydrogenase (1,1,1,27-LDH) isoenzymes were determined in human prostatic carcinoma cell lines. The isoenzymes LDH-4/LDH-5 were identified and quantified in the serum of athymic mice bearing the human prostatic carcinoma cell lines PC-3, PC-3/M and DU 145 subcutaneously. The amounts of the slowly migrating isoenzymes released by the solid tumors correlated with increasing tumor volume and tumor weight. These correlations indicate that the human LDH-4/LDH-5 isoenzymes are useful parameters for monitoring the presence and growth of prostatic cancer in the athymic animal model.
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PMID:Human lactic dehydrogenase as a marker for monitoring the growth of prostatic carcinoma in nude mice. 395 38

Ketoconazole (KT) and fluconazole (FLU) are azole antifungal agents with a broad spectrum of activity against both superficial and systemic mycoses. KT is also an anticancer agent in the treatment of advanced prostate cancer. In many clinical and retrospective studies, KT has been reported to cause liver damage, i.e. chemical hepatitis. Histologic analysis of KT induced hepatotoxicity shows massive centrilobular necrosis in which the hepatotoxicity was not thought to be mediated through an immunoallergic mechanism. According to the medical literature, the pattern of hepatic injury appears to be primarily of the hepatocellular type. Because of the documented reports of KT and FLU hepatotoxicity, a cytotoxicity comparison of KT and FLU was implemented. The objective of this comparison was to evaluate the cytotoxicity of these azoles such that future mechanistic investigations of hepatotoxicity could be performed. The relative hepatotoxicity of KT and FLU was evaluated using primary cultures of postnatal rat hepatocytes. Cytotoxicity was evaluated by measuring the leakage of the cytosolic enzyme, lactate dehydrogenase (LDH), into the medium; by assessing mitochondrial reduction of 3-(4,5-dimethythiazol-2yl)-2,5-diphenyl tetrazolium bromide (MTT); by assessing lysosomal uptake of neutral red (NR); and by gross morphology (phase contrast microscopy). The cultures were exposed to various concentrations of KT (56-188 microM) for 0.5-4 h and to various concentrations of FLU (50 microM to 1.0 mM) for 0.5-6 h. There was a significant increase (P < 0.05) in LDH leakage and a large decrease in MTT reduction and lysosomal uptake of NR at 4 h for KT. One millimolar FLU had minimal effects on the LDH leakage and MTT reduction. These results demonstrate that KT is a more potent cytotoxicant than FLU; and its toxicity was expressed in a dose- and time-dependent manner.
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PMID:Comparison of ketoconazole- and fluconazole-induced hepatotoxicity in a primary culture system of rat hepatocytes. 788 87

Cytotoxicity indicated by increased release of prelabeled 51chromium (51Cr) and lactate dehydrogenase (LDH) was studied in human prostate cancer and melanoma cells in cell culture following irradiation or exposure to several injurious substances. These changes were compared to those observed in bovine aortic endothelial cells (BAEC) subjected to identical treatments. Further, the effect of irradiation on plasminogen activator (PA) secretion from prostate cancer cells, and the effect of glycine on radiation-induced cytotoxicity in BAEC were also investigated. Radiation, lipopolysaccharide and xanthine/xanthine oxidase stimulated no release of 51Cr or LDH from tumor cells, while these treatments induced a dose- and time-related loss of those cytotoxic indicators from BAEC. Protease, elastase and Triton X-100 incited loss of 51Cr and LDH from all three cell types. Radiation, lipopolysaccharide and xanthine/xanthine oxidase have been shown to cause cell injury via a common pathogenic pathway of oxidant generation. Tumor cells appear quite resistant to oxidant stress. Cell damage precipitated by protease, elastase and Triton probably involves hydrolysis of proteins and phospholipids in the cell membrane, leading to an increased leakage of intracellular proteins such as LDH and those bound with 51Cr. Radiation caused a dose- and time-related reduction in the secretion of PA from prostate cancer cells. PA is alleged to play a role in tumor metastasis; the reduced secretion could be another beneficial effect of radiation, in addition to interruption of cell proliferation, in the impediment of tumor growth and spread. Glycine diminished cytotoxic injury of BAEC inflicted by radiation. This amino acid may prove useful in offering a degree of protection of normal tissue against radiation associated side-effects.
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PMID:Injury-specific cytotoxic response of tumor cells and endothelial cells. 868 34

Carcinoma of the prostate gland is one of the most common malignancies in males. This study was undertaken to determine which factors predict the course and outcome of patients treated with first line hormonal manipulation. A total of 144 patients with Stage D2 prostate cancer who received androgen deprivation therapy were studied. Pretreatment parameters analyzed were age, performance status, analgesia usage, concurrent disease, histologic differentiation, hemoglobin, leukocyte and platelet count, serum creatinine, alkaline phosphatase, lactate dehydrogenase, prostate specific antigen, total and prostatic acid phosphatase, serum testosterone, follicle stimulating and luteinizing hormone levels, number of metastatic sites and bone scan grade. Only initial serum testosterone (> 10 nmol/l) had a positive impact on response (p = 0.0304), whereas age older than 60 years had a positive impact on time to progression (16 vs. 11 months, p = 0.0414). Both serum testosterone (26 vs. 20 months, p = 0.003), and age (28 vs. 17 months, p = 0.036) had a significant influence on overall survival. Low testosterone, indicating androgen independence, and a younger age, seem to result in a more aggressive disease and a poorer prognosis in advanced prostate cancer.
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PMID:Low serum testosterone and a younger age predict for a poor outcome in metastatic prostate cancer. 939 50

Hormone-refractory prostate cancer (HRPC) patients often have nonmeasurable disease. In such patients, predictive biomarkers other than tumor response may be required to compare therapeutic effects. We examined the predictive value for survival of various clinical and laboratory parameters, including prostate-specific antigen (PSA), in HRPC patients treated with suramin. Data from 103 HRPC patients were analyzed using various survival analyses, the likelihood ratio approach, and logistic regression analyses. When pretreatment factors, percentage decrease in PSA at 4 weeks from start of treatment (deltaPSA), and updated survival data were fit by a multivariate Cox proportional hazards model, acid phosphatase, lactate dehydrogenase, and deltaPSA were significant, with risk ratios close to 1. There was a decrease in likelihood ratio with increasing APSA. A logistic regression model was developed to predict the probability of <1 year of survival from the start of treatment. Hemoglobin and deltaPSA were found to be significant variables. However, in view of the complexities involving the relationship between PSA expression and prostate cancer growth and possible selective effect of treatment on PSA, further prospective testing is necessary. Therefore, deltaPSA cannot necessarily be used as a biomarker for survival response in individual patients during the evaluation of the therapeutic response of HRPC to new antineoplastic drugs.
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PMID:Evaluation of biomarkers of survival response in hormone-refractory prostate cancer patients treated with suramin. 968 33

Epidemiological and experimental studies have suggested a protective role of phytosterols (PS) in the development of some types of cancer such as colon and prostate cancer. No work has been reported on the role of PS in the development of breast cancer, the second leading cancer in woman. The present study was designed to examine the effect of the two most common dietary PS, beta-sitosterol (SIT) and campesterol, as compared to cholesterol, the main sterol in the Western diet, on growth, apoptosis and cytotoxicity of MDA-MB-231 human breast cancer cells in culture. In addition, we investigated the possible role of protein phosphatase 2A (PP2A), an enzyme that has been shown to regulate growth and apoptosis in tumor parameters studied. Breast cancer cell growth was found to be inhibited by 66% after 3 days and 80% after 5 days with 16 microM SIT. Both campesterol and cholesterol sustained tumor growth at levels comparable to that of the vehicle control. None of the sterols tested at this level (16 microM) induced cytotoxicity as measured by lactic dehydrogenase release. SIT supplementation for 3 days at 16 microM resulted in a 6-fold increase in apoptosis in cells when compared to cholesterol treated cells. SIT treatment was found to have no effect on the level and content of tumor cell PP2A. It is concluded that SIT, by a still unknown mechanism, may offer protection from breast cancer by inhibiting growth and stimulating apoptosis.
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PMID:Inhibition of growth and stimulation of apoptosis by beta-sitosterol treatment of MDA-MB-231 human breast cancer cells in culture. 1076 59


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