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)

Eleven patients with cancer of the prostate and 10 patients with benign prostatic hypertrophy (BPH) had thirteen parameters of coagulation evaluated before and after transurethral resection (TUR). Changes in fibrinogen and fibrin split products in both groups suggested potential incipient disseminated intravascular coagulation (DIC). It is concluded that prostatic cancer patients are no more susceptible to DIC than patients with BPH.
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PMID:Effect of transurethral resection on coagulation in carcinoma of prostate. 8 26

Fibrinogen and plasminogen were measured in plasma samples from prostatic cancer patients before and after 3 months of treatment with either Premarin, Provera, Provera and diethylstilbestrol, one of three doses of diethylstilbestrol, or placebo. Plasminogen levels generally were increased significantly with the estrogens but were unchanged following placebo or Provera treatment. Pretreatment plasminogen levels in Study 3 were significantly lower (p less than .001) than in Study 2. Plasminogen pretreatment levels were significantly correlated with age, hemoglobin, body weight, and blood pressure. Fibrinogen pretreatment levels were significantly elevated above normal. They were not significantly with age, hemoglobin, body weight, or blood pressure. Fibrinogen levels generally were significantly decreased by the estrogens. Comparisons of means of pretreatment fibrinogen and plasminogen levels from patients dying during the first year of the study with the mean pretreatment levels of the patient group alive after 1 year on study yielded no significant differences. Death rates were calculated by pretreatment plasminogen or fibrinogen for all treatments of all Stage III and Stage IV patients combined for Study 2 and Study 3 separately. Such rates were calculated for all causes combined and for deaths from prostatic cancer or cardiovascular disease separately. The levels of plasminogen were significnatly negatively correlated with death rate from all causes combined and with cardiovascular disease considered separately, but not with death from prostatic cancer. The levels of fibrinogen were signigicantly positively correlated with death rates from all cuses and nearly significantly with prostatic cancer, but not cardiovascular disease. Elvated pretreatment fibrinogen levels were associated with an increased proportion of deaths at 1 year from all causes and from cancer of the prostate.
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PMID:Response of plasma fibrinogen and plasminogen to hormone treatment and the relation of pretreatment values to mortality in patients with prostatic cancer. 18 48

Although the possible occurrence of systemic fibrinogenolysis has been suggested in patients with metastasising prostatic cancer (MPC), direct evidence is lacking. We report on a patient with MPC whose laboratory data were consistent with hyperfibrinolysis: marked decrease of alpha 2-antiplasmin (AP) level (less than 50% of normal), increase of plasmin-alpha 2-antiplasmin complex, D-fragment of fibrin and fibrinogen degradation products [FDP(D)] and cross-linked fibrin degradation products (XDP). The patient neither showed laboratory nor clinical evidence for consumption coagulopathy except for a slight increase in thrombin-antithrombin III complex level. Immunoblotting of the patient's serum using an anti-fibrinogen antibody revealed the presence of a 250 kDa protein in addition to DD fragments. Following reduction of this protein by 2-mercaptoethanol after extraction from SDS-PAGE gel, gamma-chain of fibrinogen (47 kDa) was found by immunoblotting using a monoclonal antibody recognising a 86-302 residue of the gamma-remnant of fibrinogen. Moreover, the 250 kDa protein did not bind to Sepharose 4B to which a monoclonal antibody recognising the N-terminus of fragment D was conjugated. These findings indicated that this protein was not fragment DY, but rather fibrinogen fragment X. With the retraction of the prostatic tumour by an effective therapy, the patient's AP level increased gradually. When the plasma AP level rose to 60% of normal, the fragment X was no longer detectable. These findings suggested that systemic fibrinogenolysis occurred in the patient with MPC only when AP levels were markedly decreased.
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PMID:Direct evidence for systemic fibrinogenolysis in a patient with metastatic prostatic cancer. 151 30

To explore mechanisms of coagulation activation in adenocarcinoma of the prostate, the occurrence and distribution of components of coagulation and fibrinolysis pathways in situ were studied by means of immunohistochemical techniques applied to frozen sections of fresh malignant and benign hyperplastic prostatic tissue obtained at transurethral resection. Fibrinogen was distributed throughout the perivascular and tumor connective tissue in both malignant and benign disease but was not present in adjacent areas of normal prostate. Antibodies specific for fibrin and D-dimer crosslink sites stained vascular endothelium focally in both malignant and benign tissues. Both neoplastic cells and benign hyperplastic glandular epithelial cells stained weakly and in a patchy distribution for tissue factor and focally for low-molecular-weight urokinase-type plasminogen activator. Focal staining of vascular endothelium was also observed for tissue plasminogen activator and plasmin-antiplasmin complex neoantigen. By contrast, no tissue staining was observed for factor VII, factor X, factor XIII "a" subunit, high-molecular-weight urokinase-type plasminogen activator, plasminogen activator inhibitors 1 to 3, protein C, and protein S. Thus, the similarity in findings between benign hyperplastic and neoplastic prostate tissue, the lack of either an intact tumor cell-associated coagulation pathway or fibrin formation, and the presence of fibrin on vascular endothelium are consistent with the concept that coagulation activation in prostatic cancer may not be due to a direct effect of the tumor cells on the clotting mechanism. Rather, such activation may be induced by a soluble tumor product that activates procoagulant activity on certain host (for example, vascular endothelial) cells. These findings, together with the lack of effect of warfarin anticoagulation on the clinical course of patients with prostatic cancer, contrast with findings in certain other tumor types and suggest that coagulation activation may not contribute to progression of adenocarcinoma of the prostate.
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PMID:Fibrin formation on vessel walls in hyperplastic and malignant prostate tissue. 170 19

The isolation and partial characterization of a novel anticoagulant from the plasma of a patient with metastatic prostate cancer is described. The patient had a prolonged activated partial thromboplastic time, prothrombin time and thrombin time which did not correct by mixing with normal plasma. The reptilase time was normal and the prolonged thrombin time was corrected with protamine sulfate suggesting a heparin-like anticoagulant. A glycosaminoglycan anticoagulant (GAC) was isolated from the patient's plasma. The inhibitory activity of the GAC was destroyed by treatment with chondroitinase ABC. The GAC migrated on agarose gel electrophoresis between keratin sulfate and heparan sulfate. Purified GAC possessed only 2% (W/W) of the antithrombin III cofactor activity of porcine heparin. In assays using purified fibrinogen, the GAC was shown to directly inhibit fibrinogen proteolysis by thrombin. It is concluded that this glycosaminoglycan anticoagulant directly inhibits thrombin clotting of fibrinogen and is a new mechanism for abnormal hemostatic assays in cancer.
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PMID:A glycosaminoglycan inhibitor of thrombin: a new mechanism for abnormal hemostatic assays in cancer. 189 11

Blood loss measurement in transurethral prostatic surgery (TUR) has been studied with the following objectives: (1) to measure the total lost volume (during surgery and 48 hours postoperatively); (2) to compare surgical bleeding and coagulogram alterations in benign prostatic hypertrophy (BPH) and prostatic carcinoma (CaP); (3) to establish the relationship between blood loss, duration of the procedure, and amount of resected tissue. The method of Jansen was used to measure blood loss, and the "coagulogram" included the following parameters: hematrocrit; prothrombin, recalcification, thrombin, and partial thromboplastin times; fibrinogen; platelets and fibrin split products. The study is based on TUR performed on 75 patients from whom a mean weight of 25.68 grams was resected resulting in a mean total bleeding volume of 305 ml. Blood loss over 400 ml was associated with surgical durations of 60 minutes or with resection of over 40 grams of tissue. There was a slight tendency for fibrinolysis in prostatic cancer, which could explain the relatively higher amount of blood loss observed in these cases.
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PMID:Blood loss during and following transurethral resection. 241 33

Clinical and laboratory studies have confirmed the efficacy of alpha-fetoprotein (AFP) and human chorionic gonadotropin (hCH) as tumor markers in the diagnosis, monitoring and assessment of prognosis in cases of testicular tumor. Serum AFP level is positive in 75% of yolk sac tumors, 70% of embryonal carcinomas and 62% of teratomas. All cases of choriocarcinoma show elevated serum hCG. In the treatment of prostatic cancer, prostatic acid phosphatase (PAP), prostatic-specific antigen (PA) and gamma-seminoprotein (gamma-Sm) are important serum markers, and the RIA method has improved their specificity and sensitivity. These markers are also correlated well with therapeutic efficacy. Especially, improvement of the serum PAP level in patients with stage C and D cancer indicates prolongation of survival time. Over 90% of the metastatic lesions of prostatic cancer are encountered in the skeletal system. Thus, serum alkaline phosphatase and urinary hydroxyproline are considered to be useful markers for indicating bone involvement. In other urological malignancies, there are no specific tumor markers. As non-specific markers for renal cell carcinoma, ESR, LDH, CEA, alpha 2-globulin, haptoglobin, fibrinogen and various hormones have been investigated. In the treatment of bladder cancer, it is important to distinguish the malignant potential of the tumor. From this viewpoint, various immunohistochemical investigations and flow cytometric analysis are now in progress. It is expected that some of the findings of the studies could prove to be of clinical use in the near future.
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PMID:[Significance of tumor markers in the treatment of urological malignancies]. 244 94

Twenty patients with prostatic carcinoma were randomized to therapy with either oestrogens (n = 10) or orchidectomy (n = 10). Activators and inhibitors of coagulation were studied before treatment, 1.5 months and 6 months after the start of treatment. We found that the patients in the oestrogen group had already increased their factor VII level after 1.5 months (P less than 0.001) and this increased level persisted after 6 months. Factor X tended to increase after 1.5 months and this increase reached significance after 6 months (P less than 0.01). In the orchidectomy groups there was a significant increase in factor X at 6 months (P less than 0.01) and, in addition, antithrombin III (AT III) was increased at this time. Furthermore, there was a parallelism between the increase in factor VII and electrocardiographic evidence of increased coronary insufficiency (r = 0.60; P less than 0.025; n = 15). We found a significant increase of thromboxane as evidenced by the major urinary metabolite 2,3-dinorthromboxane B2 in the oestrogen group as compared to the orchidectomy group. In summary, patients with prostatic cancer during long-term oestrogen treatment were found to have increased levels of factor VII, factor VIII:C and fibrinogen. In addition these patients showed increased formation of thromboxane. The changes imply a hypercoaguable state and platelet activation. No such signs were found after orchidectomy. The findings in the oestrogen group might explain the continuously increased risk of cardiovascular complications during long-term oestrogen therapy.
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PMID:Effects of oestrogen therapy and orchidectomy on coagulation and prostanoid synthesis in patients with prostatic cancer. 251 99

An analysis of haemostatic variables was done in 31 prostate cancer patients treated with oestrogens (13 pts), estramustine phosphate (7 pts) or orchidectomy (11 pts) before, at about 7 weeks and 6 months of treatment. Six patients treated with either of the drugs developed venous thromboembolism or ischemic vascular disease. Already before treatment there were changes indicating some activation of blood coagulation, fibrinolysis and kallikrein systems. The drug treated group showed significant changes in several variables: i.e. increase in factor VII, plasminogen and prekallikrein but also a decrease in antithrombin and in inhibitors to the fibrinolytic and kallikrein system. Significant difference between the drug treated groups was found in circulating platelet aggregates and in kallikrein inhibiting activity. Tissue plasminogen activator capacity was significantly lower in the drug treated patients with complications than in those without. The study also showed that in addition to the assay of the tissue plasminogen activator capacity during the first weeks of therapy it might be helpful in predicting cardiovascular complications to investigate platelet aggregates, prothrombin complex, factor X, von Willebrand factor antigen, fibrinogen, antithrombin, fibrino-peptide A, and the inhibitors of fibrinolysis as well as C1-esterase inhibitor.
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PMID:Changes in blood coagulation and fibrinolysis in patients on different treatment regimens for prostatic cancer. Predictors for cardiovascular complications? 312 58

Hemostatic abnormalities are common in patients with metastatic malignancy and are attributed, in part, to materials secreted by tumor cells. Tumor stimulation might therefore cause further perturbation of hemostasis. This article reports observations on the effects of androgen stimulation on multiple hemostatic parameters in patients with metastatic prostate cancer. Testosterone was given before chemotherapy in an experimental protocol designed to increase tumor sensitivity to cytotoxic agents. The following parameters were measured on day 0 (before) and days 2 and 4 of fluoxymesterone administration: PT, APTT, platelet count, plasma betathromboglobulin (BTG), platelet factor 4 (PF4), fibrinogen, fibrin(ogen) split products (FSP), factor VIII coagulant activity (VIII C), von Willebrand factor antigen (vWF Ag), fibrinopeptide A (FPA), antithrombin III (AT III), and protein C antigen (PC). Ten patients were studied during 17 cycles of hormonal stimulation. Baseline levels of BTG, PF4, fibrinogen, FSP, factor VIII C, vWF Ag, and FPA were significantly elevated compared with normal control. Although androgen stimulation resulted in elevation of BTG, FPA, and FSP levels by day 4 in many patients, the changes for the entire group were not statistically significant. Other parameters remained unchanged or were only slightly elevated. Two patients developed laboratory evidence of disseminated intravascular coagulation (DIC) but were clinically unaffected. Our data suggest that most patients with metastatic prostate cancer show evidence of ongoing activation of platelets, coagulation, and fibrinolysis. In a few individual patients, androgen stimulation of this hormonally dependent tumor may cause further activation of platelets, coagulation, and fibrinolysis.
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PMID:Hemostatic effects of hormonal stimulation in patients with metastatic prostate cancer. 340 35


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