Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1519176 (PSA)
 5,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhibitors of factor VIII are a rare condition in non-hemophiliacs, but they are frequently responsible for life threatening hemorrhage. Acquired factor VIII:C inhibitors represent the spontaneous development of autoantibodies that partially or completely neutralize the plasma coagulant activity of the clotting factor. The autoantibodies can arise in diverse clinical settings, in older adults they are frequently associated with immunologic disorders or malignancies. We report of a 75-year-old man with acquired factor VIII:C inhibitor associated with adenocarcinoma of the prostate and a successful treatment of a severe bleeding complication with porcine factor VIII. A 75-year-old man was admitted because of a hematoma of his right cheek and an isolated prolonged aPTT. Acquired factor VIII:C inhibitor was identified as the cause and immuno-suppressive therapy was begun. In the clinical course severe hemorrhaging occurred and was successfully treated with porcine factor VIII (Hyate:C). The initially high inhibitor titer of 32 Bethesda Units (BU) disappeared. As the cause of acquired factor VIII:C inhibitor a newly diagnosed adenocarcinoma of the prostate is likely. After complete remission of acquired factor VIII:C inhibitor radiation therapy was begun. Six months after severe hemorrhaging the patient was clinically stable and PSA levels were normal. This case demonstrates the necessity of a precise diagnosis and therapy regimen of this coagulopathy based on clinical and laboratory data. In the absence of hemorrhage immuno-suppressive therapy with corticosteroids is indicated, in a patient with severe bleeding and high inhibitor titer (> or = 5 BU) porcine factor VIII should be administered.
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PMID:[Prostate carcinoma associated spontaneous factor VIII:C inhibitor hemophilia. Successful therapy of severe hemorrhagic complication with porcine factor VIII in a 75-year-old patient]. 922 9

LNCaP tumors were treated by either administration of paclitaxel, thalidomide or by orchiectomy in order to determine their relationship with markers pertaining to the process of tumor growth, apoptosis or angiogenesis. Forty rats bearing LNCaP tumors were divided into 4 groups of 10 and treated by either paclitaxel (20 mg/kg x 5 days); thalidomide (200 mg/kg x 5 days/week x 5 weeks); or orchiectomy. After 6 weeks serum samples were removed for PSA determination and the animals sacrificed for evaluation of: A) tumor volume; B) tissue bcl-2, cyclin D, PSA and factor VIII immunohistochemically graded (0-5 scale) for marker expression; and C) serum PSA. Comparisons were made to untreated LNCaP tumors. Statistically significant differences were determined using the nonparametric Mann-Whitney test. Paclitaxel produced significant differences in volume (p < 0.001), expression of bcl-2 (p < 0.043), cyclin D (p < 0.023), tissue PSA (p < 0.001) and serum PSA (p < 0.019) levels. Thalidomide altered expression of bcl-2 (p < 0.011) and tissue PSA (p < 0.002). Orchiectomy altered volume (p < 0.002) and bcl-2 expression (p < 0.001). All three therapies have been suggested for prostate cancer and each produced alterations in accepted markers for treatment response (either reduced volume or serum PSA). Paclitaxel significantly influenced the most markers. Of interest was that all treatments, especially thalidomide, a known antiangiogenesis agent, reduced factor VIII, although not significantly. Evidently each treatment evokes different pathways of activity.
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PMID:Paclitaxel is more effective than thalidomide in inhibiting LNCaP tumor growth in a prostate cancer model. 1002 26

Diagnostic and prognostic markers for prostatic cancer (PCa) include conventional protein markers (e.g., PAP, PSA, PSMA, PIP, OA-519, Ki-67, PCNA, TF, collagenase, and TIMP 1), angiogenesis indicator (e.g., factor VIII), neuroendocrine differentiation status, adhesion molecules (E-cadherin, integrin), bone matrix degrading products (e.g., ICPT), as well as molecular markers (e.g., PSA, PSMA, p53, 12-LOX, and MSI). Currently, only PSA is used clinically for early diagnosis and monitoring of PCa. The histological differential diagnosis of prostatic adenocarcinoma includes normal tissues such as Cowper's gland, paraganglion tissue and seminal vesicle or ejaculatory duct as well as pathological conditions such as atypical adenomatous hyperplasia, atrophy, basal cell hyperplasia and sclerosing adenosis. A common PCa is characterized by a remarkable heterogeneity in terms of its differentiation, microscopic growth patterns and biological aggressiveness. Most PCa are multifocal with signi ficant variations in tumor grade between anatomically separated tumor foci. The Gleason grading system which recognizes five major grades defined by patterns of neoplastic growth has gained almost uniform acceptance. In predicting the biologic behavior of PCa clinical and pathological stages are used as the major prognostic indicators. Among the cell proliferation and death regulators androgens are critical survival factors for normal prostate epithelial cells as well as for the androgen-dependent human prostatic cancer cells. The androgen ablation has been shown to increase the apoptotic index in prostatic cancer patients and castration also promotes apoptotic death of human prostate carcinoma grown in mice. The progression of PCa, similarly to other malignancies, is a multistep process, accompanied by genetic and epigenetic changes, involving phenomenons as adhesion, invasion and angiogenesis (without prostate specific features).
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PMID:Prostate Cancer - Old Problems and New Approaches. (Part II. Diagnostic and Prognostic Markers, Pathology and Biological Aspects). 1117 6

Microvessel density (MVD) has been associated with progression of prostate cancer. Although basic fibroblast growth factor (bFGF) is a known endothelial mitogen, the prognostic role of bFGF and its receptor FGFR-1 in prostate cancer has been controversial. The aim of our study was to examine the tissue distribution and prognostic significance of bFGF, FGFR-1, and microvascular proliferation. Sections from 104 radical prostatectomy specimens were examined by factor VIII/Ki-67 staining for proliferating capillary index (PCI) and MVD, and tissue microarray sections were immunostained for bFGF and FGFR-1. Increased PCI (median 0.49%) was related to strong stromal expression of bFGF (P=0.003) but was without prognostic impact. Strong bFGF staining was associated with well-differentiated tumors, no capsular penetration, low serum-prostate-specific antigen (s-PSA), low tumor cell proliferation, and increased time to biochemical failure (P=0.007), and was of independent prognostic importance in multivariate survival analysis. bFGF expression in vessels was associated with low MVD (P=0.0003). In contrast, strong tumor cell FGFR-1 expression was related to high preoperative s-PSA. Thus, increased stromal and vessel bFGF was associated with less aggressive tumors. Our findings indicate a complex relationship between bFGF/FGFR-1 expression and prognosis of prostate cancer. Vascular proliferation revealed no prognostic impact in this study.
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PMID:Expression of bFGF/FGFR-1 and vascular proliferation related to clinicopathologic features and tumor progress in localized prostate cancer. 1622 Feb 97

We report the case of a 86-year-old man admitted in a local hospital with spontaneous haematoma, an isolated prolonged activated partial prothrombin time (114/32 seconds; ratio = 3.6), an anemia and a normal platelet count. Two diagnosis were suspected: a coagulation factor defect, or the presence of a lupus anticoagulant or of anti-factor antibodies. An acquired haemophilia A was confirmed with a factor VIII activity level < 1 U/dL associated with the presence of an anti-factor VIII inhibitor. The factor VIII inhibitor titer reached 195 Bethesda U/mL. A prostatic adenocarcinoma was suspected: a 5 cm prostatic tumour was found and the PSA level was 113 ng/mL. The patient was treated with recombinant factor VIIa: Novoseven (90 microg/kg). None immunosuppressive agents were prescribed in this elderly patient. The patient's disease was identified as a spontaneously acquired haemophilia A associated with prostatic adenocarcinoma.
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PMID:[Spontaneously acquired haemophilia: report of a patient with prostatic adenoma]. 1682 79