Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We developed an ultrasensitive method for measuring prostate-specific antigen (PSA) in serum. The assay includes a capture monoclonal anti-PSA antibody coated to microtiter wells, a biotinylated rabbit polyclonal detection antibody, and alkaline phosphatase (ALP)-labeled streptavidin. The activity of ALP is measured with the substrate diflunisal phosphate; the released diflunisal forms highly fluorescent complexes with Tb(3+)-EDTA that are quantified with microsecond time-resolved fluorometry. The assay is precise and accurate and correlates well with the established Hybritech Tandem-PSA kit. Its distinguishing feature is extreme sensitivity (lowest limit of detection is 0.002 micrograms/L or 2 x 10(6) PSA molecules per assay). This is the most sensitive PSA assay reported thus far; we used it to quantify PSA in patients who had undergone radical prostatectomy. Many patients had < 0.01 micrograms/L PSA in their serum. This method could have important clinical applications in postsurgical early detection of relapse or residual prostate cancer, as recently suggested in the literature (Clin Chem 1992;38:1930-2).
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PMID:Ultrasensitive time-resolved immunofluorometric assay of prostate-specific antigen in serum and preliminary clinical studies. 769 42

This paper describes the new enzyme immunoassays for the measurement of alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA) and prostate-specific antigen (PSA) in serum and heparinised plasma as developed for the fully automated Serono SR1 analyzer. Each assay incorporates two monoclonal antibodies in an immunoenzymetric sandwich format using alkaline phosphatase as the label and magnetic solid phase separation. All processing steps are performed by the SR1. The assays have good analytical performance with respect to detection limits (typically 0.24 microgram/l, 1.0 microgram/l and 0.1 microgram/l respectively for AFP, CEA and PSA), precision (within and between run CVs less than 7 and 12% respectively) and recovery of added analyte (100 +/- 10%). Regression analysis of linearity on dilution gives correlation coefficients (r) of 0.9984-1.0000. Tumour marker concentrations measured with these assays are in good agreement with concentrations determined by established immunoassays (r > 0.96). Values measured in samples of healthy probands and samples of patients with malignant and non-malignant diseases are as would be expected for clinically valid assays. The study demonstrates that the measurement of AFP, CEA and PSA in serum and heparinised plasma on the fully automated SR1 analyzer is suitable for the clinical diagnosis, monitoring and management of certain cancers and, in the case of AFP, for prenatal screening of maternal serum.
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PMID:Measurement of alpha-fetoprotein, carcinoembryonic antigen and prostate-specific antigen in serum and heparinised plasma by enzyme immunoassay on the fully automated serono SR1 analyzer. 769 86

57 patients with advanced prostate cancer and a failure of prior hormonal treatment were selected for a double-blind placebo-controlled trial, in which they were randomly allocated to receive either clodronate (C) or placebo concomitantly with the basic cancer treatment, estramustine phosphate (E) (560 mg daily). The treatment was started intravenously with 300 mg of C or placebo in 5 consecutive days, and thereafter maintained orally with 1600 mg of C or identical placebo daily for 3 months. Bone biopsies were taken at admission and at 3 months. Measurements of serum calcium, phosphate, alkaline phosphatase, prostate-specific antigen and creatinine were made at the time of both bone biopsies and at 1 month. Serum intact parathyroid hormone and vitamin D metabolites were measured at admission and at 3 months. Because of several discontinuations, the study groups at final analysis comprised 20 patients taking E + C and 19 patients taking E and placebo. Bone resorption, as judged by eroded surface and osteoclast number, was markedly increased especially in biopsies taken from tumour-involved bone. Treatments with E + C or E both induced a significant decrease in bone resorption, but were associated with the development of hypocalcaemia, secondary hypoparathyroidism, hypophosphataemia and severe impairment of mineralisation of newly formed bone, i.e. osteomalacia. Since the patients were not vitamin D deficient, we conclude that osteomalacia resulted from a relative deficiency of calcium and phosphate. The transiency of pain relief achieved with anti-resorptive agents in the treatment of bone metastases from prostate cancer may be due to the development of osteomalacia.
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PMID:The effect of clodronate on bone in metastatic prostate cancer. Histomorphometric report of a double-blind randomised placebo-controlled study. 791 32

So far, no curative treatment is available for hormone-refractory prostate carcinoma. Therapy is thus focused on alleviating symptomatic tumor progression with the aim of improving quality of life. Therefore, anthracyclin-derived mitoxantrone was administered to 25 patients with hormone-refractory prostate carcinoma and symptomatic progressive disease. After a median treatment of 13 weeks, a median of 4 cycles and a follow-up of 14 months, 48% of the patients (12/25) reported improvement in tumor-related pain; in 60% (15/25) there was improvement of the self-assessment symptom score and 32% of the patients (8/25) gained weight. Additionally, partial tumor response with regression of lymph-node metastases occurred in 3/25 patients (12%). In 10/25 patients the serum level of prostate-specific antigen (PSA) decreased as well as the alkaline phosphatase (AP) in 7/25 patients. Side effects subsequent to chemotherapy were leucopenia WHO grade III in 25% of the patients and thrombocytopenia WHO grade III in 3/25 and grade V (treatment-related death) in 1/25 patients. Non-hematological toxicity occurred in 2 patients (cardiotoxicity n = 1, nephrotoxicity n = 1, WHO grade II each).
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PMID:[Therapy of hormone refractory prostate carcinoma with mitoxantrone. A clinical phase II study]. 865 Aug 48

A study was undertaken to evaluate the clinical usefulness of measurements of serum concentrations of the carboxyterminal propeptide of type I procollagen (PICP) and the pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP) as parameters of bone metastasis in patients with prostate cancer. Serum PICP, ICTP, prostate-specific antigen (PSA), and alkaline phosphatase (ALP) were evaluated in 82 patients with prostate cancer and 26 patients with benign prostatic hyperplasia (BPH). These markers were measured serially in 16 prostate cancer patients during treatment. The serum levels of PICP, ICTP, ALP, and PSA were significantly higher in prostate cancer patients with bone metastasis than in patients with either BPH or prostate cancer without bone metastasis. Although the rate of detection of bone metastasis with PICP and ICTP was slightly lower than that with PSA determined by the receiver operating characteristic curve, the correlation between both PICP and ICTP and the extent of disease was much higher than that of PSA. PICP and ICTP levels varied with ALP and PSA levels, the patient's clinical course after the start of endocrine therapy and the progression of bone metastasis. The levels of PICP and ICTP did not change substantially in patients who developed local regrowth or lymph node metastasis, and decreased as bone metastases responded to radiotherapy. PICP and ICTP thus reflect the metastatic burden in bone and are useful for monitoring the response of bone metastasis to therapy.
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PMID:Clinical usefulness of serum carboxyterminal propeptide of type I procollagen and pyridinoline cross-linked carboxyterminal telopeptide of type I collagen in patients with prostate cancer. 865 56

Combined androgen blockade (CAB) is becoming standard treatment for patients with newly diagnosed advanced prostate cancer. This statement is based on the outcome and long-term evaluation of patients treated in prospective randomised trials. Particularly, patients with 'good' prognostic signs at the time of diagnosis benefit most from this approach. Patients with metastatic prostate cancer treated with CAB can be stratified on the basis of clinical prognostic parameters such as performance status, the presence or absence of pain, the levels of alkaline phosphatase, and the levels of prostate-specific antigen (PSA) during the first months of CAB: for combined androgen deprivation, if they fall in the good prognostic category (+/- 30-35% of the patients); for surgical castration and palliative treatment or (experimental) cytotoxic therapy if they belong to the poor prognostic category (+/- 20% of the patients), and, for initial CAB during the first 3-6 months of therapy, followed by an evaluation of the regression of PSA under therapy. If PSA normalises (rapidly) during this period, patients could be considered as good prognostic candidates and continue CAB. If PSA does not decrease or normalise sufficiently, patients might be classified as belonging to the poor prognostic category and should be treated with palliative measures and/or experimental cytotoxic therapy after (surgical) castration.
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PMID:Combined androgen blockade is the treatment of choice for patients with advanced prostate cancer: the argument for. 871 60

Semenogelin I and II (Sgl, Sgll) are two separate gene products of chromosome 20 with extensive (80%) identity in primary structure. They are mainly responsible for immediate gel formation of freshly ejaculated semen. Degradation of Sgl and Sgll is due to the proteolytic action of prostate-specific antigen (PSA); it results within 5-15 minutes in liquefaction of semen and release of progressively motile spermatozoa. By means of cDNA cloning and Northern blots, Sgl and Sgll transcripts have previously been shown to be abundant in human seminal vesicles, but Sgll alone is suggested to be expressed at low levels in the epididymis. To characterize the expression and tissue distribution of Sgl and Sgll in greater detail, we produced monoclonal immunoglobulin Gs (lgGs for immunocytochemistry (lCC) and specific [35S]-, digoxigenin-, or alkaline phosphatase-labeled 30-mer antisense probes to Sgl and Sgll for in situ hybridization (lSH). Immunocytochemical staining for both Sgl and Sgll, and lSH detection of both Sgl and Sgll transcripts, were demonstrated in the cytoplasm of seminal vesicle epithelium. lSH showed Sgll alone to be expressed in the epithelium of the epididymal cauda. Neither lCC nor lSH yielded any evidence of Sgl or Sgll expression in caput or corpus epithelium or in any stromal cells of the epididymis. Consistent with our previous findings using polyclonal lgG, monoclonal anti-Sgll Sgll lgGs identified epitopes on the posterior head, midpiece, and tail of ejaculated spermatozoa. Spermatozoa in the epididymal cauda were also immunoreactive, but those in the caput or corpus region of the epididymis as well as those in the testis were negative. As shown by lCC, neither Sgl nor Sgll were expressed in the testis, the prostate, the female genital tract, or other normal human tissue specimens. Although the significance of Sg attachment to epididymal and ejaculated spermatozoa remains to be established, monoclonal anti-Sg lgG might prove useful in establishing the origin of seminal vesicle tissue components in prostate core biopsies or other biopsy specimens.
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PMID:Distribution and tissue expression of semenogelin I and II in man as demonstrated by in situ hybridization and immunocytochemistry. 883 37

Skeletal alkaline phosphatase (sAP) is a tumor marker indicating osseous metastases, e.g. of prostate cancer. Sera of healthy men and patients with benign prostatic hyperplasia (BPH), localized and advanced prostatic cancer (PCa) were analyzed with Tandem-R-Ostase and prostate-specific antigen (PSA). No significant differences were found in sAP levels between healthy men and patients with BPH and localized PCa, but there was a significant difference with the group of patients with advanced PCa. In some cases, the individual follow-up was better and earlier with sAP compared to PSA. It is possible to discriminate between localized and advanced PCa with sAP. The individual follow-up shows in 30% of patients with advanced PCa an earlier increase in sAP, compared to PSA, during progression of disease.
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PMID:Skeletal alkaline phosphatase: a marker for individual follow-up in patients with advanced prostatic cancer. 909 67

Occult dissemination of tumor cells mainly determines the prognosis of patients with primary prostate cancer. The effect of androgen deprivation on micrometastatic tumor cells in these patients is currently unknown. We therefore used an immunocytochemical assay with monoclonal antibodies (MAbs) directed against epithelial cytoskeleton proteins (i.e., cytokeratins) to monitor the concentration of isolated tumor cells in the bone marrow of 36 prostate cancer patients (stage C), who underwent hormonal androgen deprivation with Flutamide and Leuprorelin acetate. Tumor cells in cytologic bone marrow preparations were detected using an assay that employed the MAb CK2 directed against cytokeratin (CK) 18 and the alkaline anti-alkaline phosphatase staining method. Prior to therapy, we detected between 1 and 38 CK-positive cells per sample of 2 x 10(6) nucleated cells in 21 patients, while the remaining 15 patients displayed tumor-free marrow samples. There was no significant correlation between the concentration of CK-positive cells and the volume of hypo-echogenic lesions as an indicator of the primary tumor volume or the serum level of prostate-specific antigen (PSA). After androgen deprivation, 20 of the 21 initially positive patients either became negative (n = 16) or showed at least a reduction in the concentration of CK-positive cells (n = 4). Moreover, only 2 of the 15 patients with negative pre-treatment findings became positive. All of the 7 patients with remaining tumor cells in the bone marrow after therapy showed no detectable amounts of PSA in their serum. Our findings suggest that serum PSA concentration is no indicator of micrometastatic disease in bone marrow. Neoadjuvant androgen deprivation appears to eliminate disseminated CK-positive tumor cells present in bone marrow, a preferred site of overt metastasis in prostate cancer patients.
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PMID:Immunocytochemical monitoring of micrometastatic disease: reduction of prostate cancer cells in bone marrow by androgen deprivation. 917 3

Prostate-specific antigen (PSA), a 33 kD glycoprotein, was initially reported to be a tissue specific protein, detected in the seminal fluid and produced by normal and abnormal epithelial cells of the prostate gland, as well as other tissues in the human body. The expression of PSA has been described to be elevated during benign and neoplastic cell growth in the prostate, and in a number of other human malignancies. The presence and production of PSA in human primary cutaneous malignant melanomas (CMMs) and metastatic malignant melanomas (MMMs) has not been reported prior to the present study. We examined the expression of PSA employing a biotin-streptavidin based, alkaline phosphatase conjugated antigen detection technique in routine, neutral formalin fixed, paraffin-wax embedded, 3-4 microns thick tissue sections of 30 CMMs and 10 MMMs. Human postnatal thymic tissue, among others, was used as a negative tissue control, while normal prostate and prostate carcinomas (PCs) were included in the collection of antigen positive tissues. We observed the presence of PSA in 16/30 CMMs and 6/10 MMMs. The intensity of the staining was moderate (C to B) and localized to between 20% and 30% of the total tumor cell population in both CMMs and MMMs, with cells of similar immunoreactivity being clustered in groups within the tumor microenvironment. This result directly contradicts the previous opinion concerning the prostate epithelium specificity of PSA expression and production. The immunophenotype (IP) heterogeneity of malignant melanoma cells in further substantiated by the pattern of their PSA immunoreactivity. The establishment of the clinical significance of these findings necessitates further in vivo and in vitro research in malignant melanomas. PSA related, novel antineoplastic immunotherapy may also be recommended in the treatment of both CMMs and MMMs.
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PMID:Immunocytochemical detection of prostate specific antigen expression in human primary and metastatic melanomas. 921 12


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