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)

Three new collagen markers deriving from the collagenous matrix, e.g. carboxyterminal propeptide of type I procollagen (PICP), carboxy-terminal pyridinoline cross-linked telopeptide of type I collagen (ICTP), and aminoterminal propeptide of type III procollagen (PIIINP) were used for the diagnose of prostatic bone metastases. Blood samples were obtained prior to biopsy or TURP. Serum PICP, PIIINP and ICTP were measured with commercial available RIAs and PSA by IRMA. Serum PSA was increased in patients with local prostatic cancer compared with patients with hyperplasia (p < 0.05). The level of PIIINP, ICTP, and PICP did not differ between these two groups. In patients with metastatic prostatic cancer all five markers were increased compared to the level measured in patients with localized cancer (p < 0.0001). All variables showed a significant positive relationship with alkaline phosphatase. The sensitivity ranged from 0.53 to 0.62 and specificity from 0.91 to 0.95. The sensitivity for alkaline phosphatase and PSA was 0.69 and 0.66 and specificity 0.91 and 0.68, respectively.
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PMID:Collagen derived serum markers in carcinoma of the prostate. 857 75

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

To evaluate prognostic factors in stage D2 prostate cancer, 235 patients who had been treated with endocrine therapy were investigated. With univariate analysis, performance status, hemoglobin concentration, serum alkaline phosphatase, LDH, histological grade, extent of disease (EOD), and response of tumor markers at 3 months were shown to be significant prognostic factors. To compare these 7 factors, multivariate analyses was performed in 196 cases. Cox proportional hazard model demonstrated that LDH, followed by response of tumor markers at 3 months, histological grade, and EOD were significant for predicting prognosis. We concluded that the patients whose serum LDH was above the normal range and/or whose tumor markers were not or had not been normalized 3 months after the onset of endocrine therapy were in the high risk group, and should be given more aggressive treatment.
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PMID:[Prognostic factors in stage D2 prostate cancer: results of univariate and multivariate analyses]. 869 58

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

Bone metastasis is a common event and a major cause of morbidity in prostate cancer patients. After colonization of bone, prostate cells induce an osteoblastic reaction which is not associated with marrow fibrosis (i.e., osteoblast but not fibroblast proliferation). In the present study we test the hypothesis that the tumoral prostatic cell line (PC-3) secretes factors that block the osteoblast differentiation process, resulting in an increase of the relative size of the proliferative cell pool. Our results, using fetal rat calvaria cells in culture, show that conditioned medium from PC-3 cells (PC-3 CM) stimulates osteoblast proliferation and inhibits both alkaline phosphatase (AP) activity (an early differentiation marker) and the mineralization process, measured as calcium accumulation (late differentiation marker). The inhibition of the expression of AP and mineralization depends on the presence of PC-3 CM during the proliferative phase of culture and suggests that both processes occur in a nonsimultaneous fashion. The inhibitory effect of PC-3 CM was not reverted by dexamethasone, which would indicate that prostatic-derived factors and the glucocorticoid do not share a common site of action. Measurement of the proliferative capacity of subcultures from control and treated cells demonstrates that PC-3 CM treatment induces the maintenance of the proliferative potential that characterizes undifferentiated precursor cells.
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PMID:Prostate-derived soluble factors block osteoblast differentiation in culture. 872 51

The pretreatment bone scintigrams of 58 patients with prostate cancer with bone metastasis were reviewed and the prognostic value of the initial extent of bone involvement was compared with that of other pretreatment characteristics. The extent of bone metastasis revealed by the scan was related to survival. The serum level of alkaline phosphatase at pretreatment and pathological grade also had some predictive value. Although the pathological grade of primary tumours was related to prognosis, the survival of patients with the same histological grade differed according to the initial extent of disease; patients with extensive disease along with raised serum alkaline phosphatase (twice or more as high as the cut-off value) had poorer prognosis than did those with lower alkaline phosphatase or smaller extent of disease. The extent of bone involvement in combination with serum alkaline phosphatase level therefore apparently has higher prognostic value than does disease extent alone.
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PMID:Clinical study on prognosis of metastatic prostate cancer based on extent of disease on pretreatment bone scintigraphy. 877 41

It is of clinical importance to control pain in the management of patients with endocrine-therapy-refractory prostate cancer. To evaluate factors influencing the manifestation of pain and the relationship between characteristics of pain and prognosis, patients with pain from bone metastasis were analyzed. A total of 48 patients with endocrine-therapy-refractory prostate cancer, who showed progression of bone metastasis and were followed-up until death, comprised the present study. The patients were divided into three groups according to the grade of pain: no need for analgesics, a need for non-opioid analgesics, and a need for opioid analgesics. The time interval between the diagnosis of the endocrine-therapy-refractory state and the requirement for analgesics was estimated. Survivals from the endocrine-therapy-refractory state were calculated according to the grade of pain or the time interval to requirement for analgesics. In addition, the extent of disease, the doubling time of tumor markers at the refractory state, any change of alkaline phosphatase, and other prognostic factors were examined in relation to pain. All 22 endocrine-therapy-resistant cases at initial treatment and 18 of 26 (69%) relapsed cases required analgesics during the clinical course until death. No difference in survival was observed between the grades of pain. The patients who needed analgesics within 1 year after becoming refractory to endocrine therapy showed significantly shorter survival than those without or with analgesics more than 1 year later. Although the time elapsing before analgesics were needed was not related to the extent of disease, the patients who showed a shorter doubling time for tumor markers and/or an exponential increase in alkaline phosphatase tended to require analgesics within 1 year. In endocrine-therapy-refractory prostate cancer, the early requirement for analgesics suggests poor prognosis, and the onset of pain may be attributable not to the extent of the disease but rather to the rapid expansion of bone metastasis.
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PMID:Pain caused by bone metastasis in endocrine-therapy-refractory prostate cancer. 887 62

Urinary concentration of pyridinoline and deoxypyridinoline, novel markers of bone resorption, was measured serially in patients with prostate cancer as markers of metastatic bone tumor. In 11 patients, five without bone metastasis and six with bone metastasis, pyridinoline and deoxypyridinoline were serially monitored for between 6 and 24 months. All patients received some hormonal therapy with or without radical prostatectomy. Pyridinoline and deoxypyridinoline were measured by ion-paired high-performance liquid chromatography and were adjusted according to urinary creatinine concentration. The sequential changes of pyridinoline and deoxypyridinoline were compared with those of prostatic specific antigen and alkaline phosphatase as well as with the findings of bone scintigrams. During the observation periods, no metastatic bone lesion developed and no significant changes in pyridinoline and deoxypyridinoline occurred in the five patients without bone metastasis. In the six patients with bone metastasis, the levels of prostatic-specific antigen showed relatively rapid decreases after starting therapy. In contrast, the levels of pyridinoline, deoxypyridinoline and alkaline phosphatase showed transient increases followed by gradual decreases in most cases. Correlations were observed between the changes of pyridinoline and deoxypyridinoline and the findings of bone scintigrams. The data suggest that serial monitoring of pyridinoline and deoxypyridinoline could be clinically useful as markers of metastatic bone tumors and may allow less frequent bone scintigrams during patient followup.
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PMID:Sequential changes of urinary pyridinoline and deoxypyridinoline as markers of metastatic bone tumor in patients with prostate cancer: a preliminary study. 907 Mar 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


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