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)

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

Retroperitoneal fibrosis (Ormond's disease) is rare chronic inflammatory process, that can occur at any age. It is characterised by development of periaortic fibrous mass leading to progressive obstruction of vessels around the abdominal aorta and ureters. In the one third of cases we can find the causes of disease. There are ergotamine abuse, radiation, retroperitoneal surgery or hemorrhage, urine extravasation and response to different cancers. The other cases are idiopathic disease. We report a case of prostate cancer with unique course. The first manifestations of disease were diffuse peritoneal fibrosis and ureteral obstruction leading to bilateral hydronephrosis. Clinical course and histopathology showed idiopathic Ormond's fibrosis. Patient received oral immunosuppressive treatment (prednisolone 1 mg/kg/day + azathioprine 1 mg/kg/day), followed by intravenous methylprednisolone puls (2 g). Treatment also consisted of DJ-stent placement on the left side. On the right side we were unable to overcome the obstruction of ureter. Because of persistent renal failure, thrombocytopenia, DIC and progressive lower back pain we did control MR and CT scan. The CT scans showed multiple osteolytic bone metastases in vertebral column (the sizes of them were between a few millimetres and 1.5 centimetre). Patient died due to renal failure and haemorrhagic diathesis in the course of disseminated cancer of unknown origin. The postmortem examination revealed diffuse peritoneal infiltration surrounding the ureters, intramural ventricular metastases, pulmonary metastases and vertebral metastases. The prostate was only slightly enlarged. Histological and immunohistochemical examinations of prostate showed primary low-differentiated prostate carcinoma (CK/+/, PAP/+/, PSA/+/). Peritoneal, ventricular and bone infiltrations also were metastases from low-differentiated carcinoma of prostate origin (CK/+/, PAP/+/, PSA/-/).
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PMID:[Ormond's fibrosis, bone osteolysis and stomach intramural metastases in the course f low-differentiated prostatic cancer]. 1192 71

Cancer screening guidelines are developed by numerous agencies. These guidelines are often conflicting leaving the primary care physician in a difficult position. He (she) is requested to choose the best test for his or her patients taking into consideration the principles of screening, the test cost and most importantly the patient's emotional and physical well-being. Screening for some cancers, like lung cancer, has been considered of no benefit. Other cancers, like breast, colon, cervix and prostate, have been the subject of numerous recommendations: For breast cancer, clinical examination and mammography are recommended every 1-2 years for women between 50 to 70 years. For cervical cancer, PAP smear is suggested every 1-3 years and for colorectal cancer, a yearly fecal occult blood, sigmoidoscopy or colonoscopy every 5-10 years. Annual serum prostate specific antigen (PSA) and digital rectal examination screening for prostate cancer are still controversial.
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PMID:Cancer screening for the primary care physician. 1224 26

High consumption of soybean products, such as phytoestrogens, has been hypothesized to contribute to a reduced incidence of prostate cancer in Southeast Asian people, although there have been inconsistent results among studies. Human LNCaP cells, extensively used as a model for androgen-dependent prostate tumor, express the androgen receptor (AR) mutant T877A promiscuously transactivated by estrogens and other ligands, which may further facilitate cancer progression. Here, for the first time to our knowledge, we demonstrate that genistein and quercetin, two phytoestrogens abundantly present in soybeans, activate either the AR mutant T877A in LNCaP or in transfected Chinese hamster ovary cells. This observation is supported by their capability to induce AR accumulation in the nuclear compartment of LNCaP together with mRNA down-regulation of the androgen target genes AR and PAP, and PSA up-regulation. Of interest, at concentrations eliciting transcriptional activity, both genistein and quercetin stimulate LNCaP cell growth, whereas at high levels, they become cytotoxic independently of AR expression, as ascertained in steroid receptor-negative Hela cells. The results of our study provide evidence that phytoestrogens may regulate several signaling processes in LNCaP cells; however, further studies are needed to assess their potential capability to restrain prostate tumor progression.
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PMID:The mutant androgen receptor T877A mediates the proliferative but not the cytotoxic dose-dependent effects of genistein and quercetin on human LNCaP prostate cancer cells. 1239 Dec 64

Monoclonal antibodies with high specificity for prostate tissue are of interest for prostate cancer research and treatment. Reactivity and specificity of a new murine monoclonal antibody, 107-1A4, was assessed by immunohistochemistry, ELISA and indirect immunofluorescence (IDIF). 107-1A4 stained all normal and malignant prostate tissue specimens while reactivity to non-prostate tissue was limited to the tubules of the normal kidney and renal cell carcinoma. Twenty two human cell lines were included in the reactivity survey; only the immunogen prostate cancer line LNCaP reacted with 107-1A4. Seminal plasma proteins PSA, PAP, PSMA, and PSP-94 were determined not to be the 107-1A4 antigen.
Prostate Cancer Prostatic Dis 1998 Jun
PMID:A novel monoclonal antibody 107-1A4 with high prostate specificity: generation, characterization of antigen expression, and targeting of human prostate cancer xenografts. 1249 97

Hormonotherapy is the standard treatment for advanced prostate cancer but disease progression ineluctably occurs. Subsequent chemotherapy has a modest symptomatic palliative role even if encouraging results were recently presented with docetaxel and estramustine combination. In this context, there is a great deal of interest in using dendritic cells therapeutically, as they are the most potent professional antigen-presenting cells in the immune system. Based on their unique adjuvant capacity, two vaccinal strategies are therefore tested in clinical trials. First approach includes the administration of cancer cells transduced by a cytokine gene to stimulate the in vivo recruitment and activation of dendritic cells, and the most advanced studies use GM-CSF gene-transduced allogenic cells. The second approach consists in infusions of dendritic cells loaded ex vivo with relevant tumoral antigens. Two prostate antigens have already been used. PSMA evaluated in 130 patients and a fusion protein PAP-GM-CSF (Provenge) in 144 patients. All treatments were well tolerated and frequently generated weak specific responses, but resulted in a limited clinical efficacy. However, engineering of dendritic cells can provide optimised cell vectors able to amplify vaccine response and clinical efficacy.
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PMID:[Cell therapy and prostate cancer]. 1460 63

Activation of immune defense mechanisms against tumor antigens appears to be a promising therapeutic option for advanced prostate cancer (PCa). Specific immunotherapy critically depends on target antigens that are selectively expressed in the tumorous and optional in the normal prostate tissue in sufficient amounts. Although several prostate antigens have been described and some have already been used in clinical trials, a detailed comparative evaluation of their tissue-specificity and expression levels is still lacking. We determined the transcript levels of eight prostate targets (PSA, PAP, PSCA, PSGR, Prostein, PSMA, AIbZIP, trp-p8) in 16 different tissues by quantitative PCR and calculated a tissue-specificity index (TSI) for each molecule. Besides a preferential expression in prostate for all targets, striking differences in the expression levels and TSI were revealed which may be important for the selection of appropriate antigens for immunotherapy of PCa.
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PMID:Tissue-specificity of prostate specific antigens: comparative analysis of transcript levels in prostate and non-prostatic tissues. 1604 56

Conventional treatment of recurrent and metastasized prostate cancer (CaP) remains inadequate; this fact mandates development of alternative therapeutic modalities, such as specific active or passive immunotherapy. Previously, we reported the identification of a novel highly immunogenic HLA-A*0201-restricted Prostatic Acid Phosphatase-derived peptide (PAP-3) by a two-step in vivo screening in an HLA-transgenic (HHD) mouse system. In the present study we aimed at elucidating the efficiency of PAP-3-based vaccine upon active antitumor immunization. To this end we established preventive and therapeutic carcinoma models in HHD mice. The 3LL murine Lewis lung carcinoma clone D122 transduced to express HLA-A*0201 and PAP served as a platform for these models. The HLA-A*0201-PAP-3 complex specific recombinant single chain scFV-PAP-3 antibodies were generated and used to confirm an endogenous PAP processing resulting in PAP-3 presentation by HLA-A*0201. PAP-3 based vaccines significantly decreased tumor incidence in a preventive immunization setting. Therapeutic vaccination of HHD mice with PAP-3 led to rejection of early established tumors and to increase of mouse survival. These results strongly support a therapeutic relevance of the identified CTL epitope upon active antitumor immunization. The newly established carcinoma model presented herein might be a useful tool for cancer vaccine design and optimization.
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PMID:Preventive and therapeutic vaccination with PAP-3, a novel human prostate cancer peptide, inhibits carcinoma development in HLA transgenic mice. 1673 49

Dural metastases have traditionally been considered a rare complication of prostate cancer; various case reports and autopsy series from the past have shown rates between 1 and 9%. Recent data from our advanced prostate cancer autopsy series, however, demonstrate a rate of dural lesions around 25%, suggesting that such complications may be more prevalent than previously reported. A case of prostate cancer, which was diagnosed after the patient presented with visual changes, is reported. Subsequent work-up revealed a lesion in the left tentorium, which was determined to be adenocarcinoma and stained positive for PSA and PAP.
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PMID:Prostate cancer presenting as visual changes. 1673 49

We previously reported that several DNA fragments from human prostate-specific membrane antigen (hPSM), mouse prostatic acid phosphatase (mPAP), and human prostate-specific antigen (hPSA) genes were selected and fused to create a novel hPSM-mPAP-hPSA fusion gene (named 3P gene), and human secondary lymphoid tissue chemokine (SLC), 3P, and human IgG Fc genes were inserted into pcDNA3.1 to construct a DNA vaccine, designated pSLC-3P-Fc. In this report, to establish a more efficient treatment for immunotherapy against prostate cancer, the construct was transfected into B16F10 to generate gene-modified tumor cell vaccine (named B16F10-SLC-3P-Fc). In poorly immunogenic B16F10 mouse melanoma model, the immunization with B16F10-SLC-3P-Fc resulted in a strong antitumor response and 50% of tumor-bearing mice achieved long-term survival (>120 days). In vivo depletion of lymphocytes indicated that CD8(+) T cells were involved in the direct tumor killing, whereas CD4(+) T lymphocytes were required for the induction of CD8(+) CTL response in B16F10-SLC-3P-Fc-immunized mice. Splenocytes from B16F10-SLC-3P-Fc-immunized mice specifically recognized and lysed PSM, PAP, PSA, and 3P expressing tumor cells. The combined therapy of B16F10-SLC-3P-Fc plus anti-B7-H1 MAbs further enhanced the immune response. Rechallenge experiment showed that a persistent memory response was successfully induced by the combined therapy. These observations suggest pSLC-3P-Fc-modified tumor cells could serve as a vaccine against prostate cancer, and the therapy combined with anti-B7-H1 MAbs further enhanced the antitumor immune response.
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PMID:Potent systemic antitumor immunity induced by vaccination with chemotactic-prostate tumor associated antigen gene-modified tumor cell and blockade of B7-H1. 1718 Apr 70


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