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)

Acid phosphatase levels were determined using both an enzymatic method (32 cases) and radioimmunoassay (35 cases) in 35 patients with clinically localised prostatic cancer. All patients underwent total prostatectomy and pelvic lymphadenectomy. In cases of intracapsular prostatic cancer the level of prostatic acid phosphatase (PAP) measured by radioimmunoassay was 1.4 +/- 0.8 micrograms/l. In patients with either local extraprostatic disease or pelvic lymph node metastases the mean level of PAP was 3.5 +/- 2.8 micrograms/l. The difference was statistically significant. The specificity, sensitivity and accuracy of an elevated PAP (greater than 3.0 micrograms/l) in revealing extraprostatic extension of clinically localised prostatic cancer were 100, 37 and 66% respectively. When the enzymatic method was used, the level of acid phosphatase was elevated (greater than 13 u/l) in only 1 case. The specificity, sensitivity and accuracy of the enzymatic method were 100, 6 and 47% respectively. Elevation of PAP predicts, with a high degree of probability, either local extension outside the prostate or lymph node metastases. A normal PAP does not exclude extraprostatic extension of prostatic cancer.
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PMID:The value of acid phosphatase measurements in predicting extraprostatic cancer growth before radical prostatectomy. 320 23

Patients with newly diagnosed prostatic cancer should be investigated with regard to the presence or absence of distant metastases by (1) Taking a history especially of weight loss and recent onset backache (2) Examining them, looking especially for hepatic enlargement or peripheral lymph nodes (3) Performance status (4) Hemoglobin, Bilirubin, Liver enzymes, Alkaline and Acid phosphatase (5) Chest Xray. (6) Bone scan with specific Xrays directed at hot spots. (7) Ultrasound scan of liver if liver function tests are abnormal. Ultrasound scan of lymph nodes and kidneys is optional. (8) Any other tests indicated in special circumstances. Follow-up, 3-monthly as a rule, should include (1) The presence of pain and analgesic requirements (2) Weight (3) Performance status (4) Hemoglobin, Alkaline phosphatase, Acid phosphatase (5) Chest Xray, three monthly if abnormal. Annually otherwise. (6) Bone scan with Xray of new hot spots, 6-monthly. If there is doubt about the presence of a new hot spot, repeat the bone scan and Xray at 3 months.
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PMID:The staging of M1 disease: the role of bone scan, Xray and other imaging techniques. 329 62

Thirty-seven patients with hormonally refractory prostatic carcinoma entered a randomized trial comparing doxorubicin and doxorubicin plus cisplatin. All patients had failed prior hormonal treatment. Mean Karnofsky performance status (76% doxorubicin versus 75% combination), percent of patients with prior palliative irradiation (40% doxorubicin versus 35% combination), and hemoglobin levels of less than or equal to 12 g/dl (30% doxorubicin versus 24% combination) were roughly equivalent in the two treatment groups. More patients treated with doxorubicin than the combination treatment had an elevated acid phosphatase level at study entry (90% versus 65%). Measurable bidimensional tumors were present in 13 patients in 16 sites in the doxorubicin arm and in 10 patients in 11 sites in the combination arm. Partial responses were seen in 1 of 13 patients in the doxorubicin arm and 2 (20%) of 10 patients in the combination arm. Improvement in Karnofsky performance status of 20% or greater was rarely observed with either treatment (7% doxorubicin versus 8% combination). Acid phosphatase levels normalized or improved by 50% in 39% of patients who received doxorubicin and 27% of patients who received the combination. The overall response rate by National Prostatic Cancer Project Criteria was 53% for doxorubicin and 59% for doxorubicin plus cisplatin. Myelotoxicity and gastrointestinal toxicity were severe, particularly in the combination arm, and required discontinuation of treatment in some patients who responded to treatment. Moderate renal dysfunction (creatinine value 2.0-3.0 mg/dl) occurred only in the combination arm at an incidence of 23%. Time to progression and survival were similar for the two treatment groups. In this small group of 37 patients, the combination of cisplatin and doxorubicin showed no improvement over doxorubicin alone in response, response duration, or survival, and was difficult to administer in this patient population.
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PMID:A randomized study of doxorubicin versus doxorubicin plus cisplatin in endocrine-unresponsive metastatic prostatic carcinoma. 405 35

Acid phosphatase in serum was measured in 116 patients with prostatic disease, benign in 59 and malignant in 57 cases. Comparisons were made between radioimmunoassay (RIA) and an enzymatic method. The correlation coefficient between the respective values was 0.96 in patients with untreated prostatic cancer, indicating that no significant difference between results with the two methods was to be expected. The correlation coefficient between RIA values and cancer stage was 0.48, and between catalytic activity and cancer stage it was 0.50. The validity of the two methods consequently was equal. RIA, however, was the more sensitive method, giving elevated values in 10 of 11 patients with untreated stage III or stage IV prostatic cancer, as compared with only 4 of the same 11 in the enzymatic assay. This seeming paradox most probably was attributable to differing intrinsic properties of the methods when the upper limits of normal range were established. Neither RIA nor enzymatic analysis discriminated early prostatic cancer (stages I and II) from benign lesions.
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PMID:Perspectives on serum acid phosphatase in prostatic disease. An evaluation of two methods. 664 90

In order to block the influence of androgens from all sources on the growth of prostatic cancer, we have used a new hormonal therapy based on medical castration achieved with the potent LHRH agonist [D-Ser(TBU)6, des-Gly-NH2(10)]LHRH ethylamide (HOE-766) combined with the administration of a pure antiandrogen that neutralizes the action of adrenal androgens as well as those still secreted in low amounts by the testis during LHRH agonist treatment. This study was performed in ten patients with advanced prostatic carcinoma (9 at stage D2 and one at stage C). Bone pain, prostatism and general well-being were 60 to 90% improved within one month after starting treatment in all patients. After 2 months of treatment, minimal bone pain remained only in one patient who was originally bedridden. Bone scanning showed a 70 to 90% decrease in uptake after 3 to 5 months of treatment in the patients studied. Acid phosphatase levels were 60 to 90% reduced after 2 months of treatment in 3 out of the 4 patients who had elevated levels before therapy. Marked objective and subjective improvement was thus rapidly observed in 9 out of 10 patients treated with the combined therapy, while, in the other patient at stage C, subjective improvement could be documented. Although preliminary, this study indicates that a combined hormonal therapy which neutralizes all androgenic influences on peripheral tissues is of potential benefit in prostatic cancer. Moreover, the ease of application as well as the lack of secondary effects of the present approach should make possible its use early in the disease and should thus minimize the development of metastases and androgen-resistant cell clones. Randomized prospective studies on this potentially beneficial therapy are warranted.
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PMID:New hormonal therapy in prostatic carcinoma: combined treatment with an LHRH agonist and an antiandrogen. 681 1

Analysis of urinary hydroxyproline levels offers a marker to monitor osseous involvement in patients with metastatic malignancies. Such a marker is needed in patients with prostatic cancer when bone metastases predominate. Thirty-two men with stage D2 prostatic cancer were monitored by bone scan, acid and alkaline phosphatase values, and urinary hydroxyproline, beginning from 4 to 36 months after initiation of hormonal manipulation and/or systemic chemotherapy. In patients with disease progression determined by bone scan serial urinary hydroxyproline values progressively increased and were significantly elevated compared to urinary values obtained from patients with a stable or improving scan (p less than 0.001). Simultaneous alkaline phosphatase determinations showed less significant differences between patient groups. Acid phosphatase did not reliably indicate osseous response to therapy. These data suggest that urinary hydroxyproline values are predictive as an early objective sign of osseous response in patients receiving therapy for stage D2 prostatic cancer.
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PMID:Serial spot hydroxyproline/creatinine ratios in metastatic prostatic cancer. 683 97

Acid phosphatase (phosphoric monoester hydrolase) was isolated from the Dunning R3327H prostatic adenocarcinoma, a slow-growing and hormone-sensitive rat prostate tumor histologically similar to well-differentiated human prostatic cancer. The enzyme was purified to homogeneity and characterized. In comparison with the acid phosphatase isolated from human malignant prostate, the acid phosphatase from the Dunning rat tumor was similar in molecular weight [100,000 +/- 10% (S.D.)]. However, it possessed a single isoelectric point of 7.6 (human prostatic acid phosphatase showed multiple isoenzymes at 4.4 to 5.3); an electrophoretic mobility of 0.5 in reference to human prostatic acid phosphatase on 7.5% polyacrylamide gel, pH 8.5; an optimal pH of 5.0 with alpha-naphthyl phosphate as the substrate in 0.1 M citrate buffer (human prostatic acid phosphatase, 5.5); and a Km (alpha-naphthyl phosphate) of 6.9 X 10(-4) M (human prostatic acid phosphatase, 4.4 X 10(-5) M). Furthermore, it did not cross-react with antiserum raised against human prostatic acid phosphatase. These results show that the acid phosphatase of the Dunning R3327H prostatic adenocarcinoma is biochemically and immunologically distinct from human prostatic acid phosphatase and may be unique for this animal model of prostatic cancer.
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PMID:Purification and characterization of acid phosphatase from Dunning R3327H prostatic adenocarcinoma. 735 54

The acid phosphatases are a group of enzymes capable of hydrolyzing esters of orthophosphoric acid in an acid medium. Acid phosphatase activity is widely distributed in human tissues and acid phosphatases represent a heterogeneous group of enzymes containing many isoenzymes, each specific for one type of tissue. The human prostate is particularly rich in this enzyme (PAP) and serum enzyme levels have been used as a tumor marker of prostate cancer. While PAP was markedly increased in patients with bone metastases of prostate cancer, it is unable to detect earlier stage tumors reliably. The sensitivity and specificity of serum acid phosphatases and PAP are low in diagnosing, staging and following patients with prostate cancer. Presently, prostate-specific antigen (PSA) is superior to PAP for diagnosis, screening, and monitoring prostate cancer. PAP may have an adjuvant value in the management of prostate cancer because a combination of PSA and PAP testing has revealed a high sensitivity and specificity in detecting prostate cancer.
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PMID:[Acid phosphatase (ACP)]. 760 79

The effects of the nonsteroidal antiandrogen bicalutamide (Casodex(TM)) and the luteinizing hormone releasing hormone agonist leuprolide depot (Procren Depot(TM), Lupron Depot(TM)) on serum prostate-specific antigen (PSA), acid phosphatase (ACP), and prostatic acid phosphatase (PAP) in patients with benign prostatic hyperplasia (BPH) were determined. Thirty patients with BPH were randomised to receive bicalutamide 50 mg orally once daily or a placebo for 24 weeks, followed by 24 weeks of follow-up (bicalutamide study). In another study 55 men were randomised between 3.75 mg leuprolide depot intramuscularly at every 28 days for 24 weeks or placebo injections (leuprolide study). In both studies blood sampling was performed at baseline, at week 12 at week 24 and 24 weeks after the end of therapy. Androgen suppression with bicalutamide 50 mg daily for 24 weeks resulted in a median of 56% reduction of PSA (P<0.001 when compared to placebo). Acid phosphatase and PAP did not change. Leuprolide resulted in a median of 87% reduction of serum PSA (P<0.001) and a 39% reduction of PAP (P=0.023), whereas ACP was unchanged. Both bicalutamide and leuprolide induced a pronounced decline in serum PSA in BPH patients. The studies suggest a stronger androgen suppressive effect of leuprolide than of bicalutamide, but this difference might largely be due to too low a dosage of bicalutamide. ACP and PAP were relatively insensitive to androgen suppression. Our study suggests a different degree of androgen suppression on PSA originating from benign tissue versus cancer tissue, and that the direction of this discrepancy might be different for various androgen suppressive regimens.Prostate Cancer and Prostatic Diseases (2001) 4, 173-177.
Prostate Cancer Prostatic Dis 2001
PMID:Effects of bicalutamide and leuprolide on prostate-specific antigen (PSA), acid phosphatase (ACP) and prostatic acid phosphatase (PAP) in men with benign prostatic hyperplasia (BPH). 1249 37

Acid phosphatase is ubiquitous in distribution in various organisms. Although it catalyzes simple hydrolytic reactions, it is considered as an interesting enzyme in biological systems due to its involvement in different physiological activities. However, earlier reviews on acid phosphatase reveal some fragmentary information and do not give a holistic view on this enzyme. So, the present review summarizes studies on biochemical properties, structure, catalytic mechanism, and applications of acid phosphatase. Recent advancement of acid phosphatase in agricultural and clinical fields is emphasized where it is presented as potent agent for sustainable agricultural practices and diagnostic marker in bone metabolic disorders. Also, its significance in prostate cancer therapies as a therapeutic target has been discussed. At the end, current studies and prospects of immobilized acid phosphatase are included.
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PMID:A molecular description of acid phosphatase. 2268 63


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