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)

A number of biological markers have been recently introduced in clinical use as an aid for diagnosis and monitoring of malignant tumors. Some of them are relatively tumor-specific, i.e. CA 125 for non-mucinous ovarian cancer, CA 15.3 for breast cancer, PSA for prostate cancer, CA 19.9 for colo-rectal and pancreatic cancers. The clinical usefulness, the sensitivity and specificity of these tumor markers and of a few others (CA 50, SCC and TPA) are commented in this review.
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PMID:[Critical study of current tumoral markers]. 245 33

Concurrent measurements of serum TPA and PAP concentrations by double antibody radioimmunoassays were done in 49 patients with prostatic cancer in different clinical stages. The reference group comprised patients suffering from BPH. Positive TPA was found in 32.7% of cancer patients, the lowest percentage in stage A (11.1%) and the highest in stage D (55.6%). The additional value as a diagnostic aid of the TPA test was revealed on the basis of examination of the selected group of patients with not increased PAP. Positive TPA was found in 16.7% of patients: none in stage A, 22.2% in stage B, and 33.3% in stage D. Prostatic cancer remains the most common malignancy of the genitourinary tract. The improvement in the results of treatment involves not only a modernization of treatment modalities but also the introduction of laboratory tests which give the most ample information on the stage of tumour development and improve possibilities to control tumour therapy. Besides the refinement of the determination procedures of specific prostatic markers, prostatic acid phosphatase (PAP), through radio- and enzyme-immunological methods, there is a search for additional markers which might be helpful in diagnosis and follow-up of treatment.
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PMID:Serum tissue polypeptide antigen (TPA) and prostatic acid phosphatase (PAP) in patients with prostatic cancer. 245 95

Tumour markers are often circulating tumour-associated indicators of tumour development. As such they are not suitable for tumour screening and localization, but valuable as adjuncts for medical follow-up care of tumour patients, where their serum level alterations may anticipate the clinical detection of tumour behaviour by a lead time of 1 to 6 months before other methods. The following tumour may be controlled by established markers: endocrine tumours by NSE, calcitonin, parathormone, 5-HIAA, catecholamines/metabolites etc.; head-neck tumours: SCC, CEA; thyroid carcinoma: TG, calcitonin; lung cancer: CEA, NSE, SCC; liver cancer: AFP (PLC), CA 19-9 (cholangiocell.), CEA (secondary): biliary tract and pancreatic cancer: CA 19-9; colorectal carcinoma: CEA, CA 19-9; squamous cell carcinoma (ENT, oesophagus, anal): SCC; breast cancer: CEA and CA 15-3; ovarian cancer: CA 125 (epithelial), CA 19-9 (mucinous); germ cell tumours (ovary including trophoblastic tumours/testes): AFP and HCG; prostatic cancer: PAP and PSA; bladder cancer: TPA.
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PMID:[Clinical relevance of tumor markers]. 267 6

We measured the serum and urinary TPA in 64 patients with urological cancer, 55 patients with benign urological disease and 37 healthy volunteers. The serum TPA levels in patients with pre-treated cancer were significantly higher than those of healthy volunteers, but showed no significant difference compared to those in patients with a benign urological disease. The urinary TPA levels in patients with pre-treated cancer were significantly higher than those with a benign urological disease, but in some patients with urinary tract infection, very high urinary TPA concentrations were observed. Therefore, the determination of serum and urinary TPA may be useful in detecting urological cancer, but they were not specific tests. On the other hand, as lower serum and urinary TPA levels were observed after treatment of bladder and prostatic cancer, their determinations were considered to be useful in following up patients with these cancers.
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PMID:[Serum and urinary tissue polypeptide antigen (TPA) in patients with urological cancer]. 383 15

We measured the serum TPA level in 260 patients with benign urogenital diseases, 189 patients with urogenital cancer and 72 healthy blood donors by using a radio-immunoassay kit in order to evaluate its usefulness as an indicator for the presence of cancer. TPA value (mean +/- 2SD) in healthy blood donors was in the range of 36.8-110.8 units per liter, so that values higher than 110 U/L were considered to be abnormal. Significantly higher serum TPA levels were observed in patients with non-treated cancers, compared to healthy blood donors. But elevated serum TPA levels were also observed in the patients with benign diseases, especially in cases of benign prostatic hyperplasia with urinary tract infection. Consequently, it is considered that the serum TPA test is very useful for detecting urogenital diseases, but not for screening urogenital cancer. In cases of urogenital cancer, serum TPA levels elevated significantly by recurrence or recrudescence of the disease. Therefore, a good correlation was established between serum TPA and the efficiency of a given therapy in patients with prostatic cancer and bladder cancer.
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PMID:[Serum tissue polypeptide antigen (TPA) in patients with urogenital cancer]. 650 5

The level of serum TPA was determined by radio-immunoassay in 19 healthy subjects and 90 patients with urogenital cancer. The normal level of serum TPA was 86 +/- 24 U/l, and the level of more than 134 U/l was determined positive. The positive rate of TPA was 38.9% in 90 patients, while that of CEA was 25.6%. In 19 patients with bladder tumor and 7 with testicular tumor, the positive rates of TPA were 52.6% and 71.4%, respectively, and the level of serum TPA was high in these positive patients. Considering the low positive rate of CEA, TPA may be a more useful marker than CEA in patients with bladder tumor and testicular tumor. Serial determinations of serum TPA and CEA showed the considerable variation of serum TPA compared with serum CEA and a temporary elevation of serum TPA following radical nephrectomy and retroperitoneal lymphadenectomy. However, the level of serum TPA fell significantly after the successful treatment in 8 patients (2 with renal cell cancer, 3 with bladder tumor, 1 with prostate cancer, 2 with testicular tumor) and rose sharply with recurrent or metastatic disease in 4 patients (2 with bladder tumor, 2 with testicular tumor). Although there was no correlation between the levels of serum TPA and serum PAP, the level of serum TPA tended to change in parallel with the level of serum AFP or HCG in 3 patients with testicular tumor.
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PMID:[Evaluation of serum tissue polypeptide antigen (TPA) in patients with urogenital cancer]. 672 13

Blood tissue polypeptide specific antigen (TPS) concentration was serially measured by IRMA radioimmunodetective procedure in hormonally treated prostate cancer patients with Stage Do-D1 tumor (20 subjects free of bone lesions) and Stage D2 disease (20 subjects with bone metastases). Monoclonal antibody against the principle M3-TPA epitope was used in this TPS assay. Serum TPS values were compared with respective blood prostate specific antigen (PSA), prostatic acid phosphatase (PAP), carcinoembryonic antigen (CEA) and testosterone levels in a retrospective manner. A control group included healthy men, patients with benign prostatic hypertrophy (BPH), subjects with inflammation of the prostate, and men with diabetes. PSA is reported to be a quantitative calibration for prostate cancer load in untreated patients, especially during early stages of the disease. In hormonally treated, advanced, and dedifferentiated prostatic carcinoma this serotest fails to reflect properly both tumor status and response to treatment. In Stage Do-D1 patients TPS concentrations remain normal or become slightly elevated even during local tumor progression. This finding is in accord with the slow proliferation of nonaggressive primary tumors. Circulating TPS concentrations are elevated in progressive metastatic patients, in the majority of Stage D2 subjects with stable disease and even in some of these patients during partial tumor remission. This latter result may be attributed not only to the heterogeneity of the advanced prostatic cancer but also to the actual tumor response to treatment, since serum PSA level fails to reflect properly the outcome of hormonal treatment. There is some evidence that an abrupt elevation in serum TPA level in such patients is a consequence of NK cell-mediated lysis of circulating tumor cells, thus giving rise to a simultaneous and rapid delivery of intracellular TPS into the bloodstream. Prostatic inflammation elevates TPS concentrations only slightly, while diabetes, even during a proper treatment, raises TPS concentration more intensely. In patients with BPH normal or slightly increased TPS values were measured. The results ot these preliminary investigations seem to open the way for further prospective studies.
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PMID:Serial measurements of tissue polypeptide specific antigen (TPS), PSA, PAP and CEA serotest values in treated patients with primary and metastatic prostate cancer. 768 62

12-O-tetradecanoyl phorbol ester (TPA) has profound cytotoxic effects on a human prostate cancer cell line, LNCaP. The TPA effect may be mediated via a protein kinase C (PKC) pathway, since staurosporine, a potent PKC inhibitor, could reverse the cell-killing effect. Our studies, based on cellular fragmentation, chromatin condensation, and nuclear fragmentation, suggest that the cell-killing effect is due to apoptosis. Moreover, we also examined expression of early growth response genes and androgen-induced genes in association with TPA-induced apoptosis. Northern blot analysis demonstrated that androgen induction of human glandular kallikrein-1 (hKLK2) mRNA was repressed by TPA in a concentration-dependent manner. A time course study showed that both hKLK2 and c-myc mRNAs were repressed by TPA as early as four hours. In contrast, the steady state mRNA levels for c-fos, c-jun, nerve growth factor induced gene A, and the orphan steroid receptor nur77 were rapidly induced within the first two hours of the treatment. Furthermore, transient co-transfection experiments demonstrated that c-fos and c-jun could repress androgen receptor-mediated gene induction. The above studies suggest that (1) the repression of androgen induction of gene expression by TPA-activated PKC is at least in part due to overexpression of c-jun and c-fos and (2) PKC may be a negative growth regulator in prostate cells.
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PMID:Tumor-promoting phorbol ester-induced cell death and gene expression in a human prostate adenocarcinoma cell line. 784 43

The proliferation of the human prostatic cancer JCA-1 cells showed a complex response to different concentrations of TPA. Whereas cells exposed for 24 h had growth reduction which was proportional to the concentration of TPA added to the culture media, they showed resistance to low (0.016 and 0.16 nM) but not high (> or = 1.6 nM) doses of TPA after 72 h. Growth-inhibited, treated cells also displayed a distinct cell morphology compared with the controls. Since c-myc expression has previously been shown to be correlated with cellular proliferation, we determined changes in its steady-state level in control and treated cells by Northern analysis. Following a 24h, 48h, and 72h treatment, with 16 nM TPA, c-myc mRNA was suppressed by 91%, 83%, and 78%, respectively, in good agreement with the extent of growth reduction observed. At the low dose of TPA (0.16 nM), however, the c-myc mRNA expression remained inhibited by 85% even though cell growth was only reduced by 10-14%. No difference in the total amount of c-myc protein could be detected between control and treated cells by Western analysis.
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PMID:Regulation of cell growth and the c-myc proto-oncogene expression by phorbol ester 12-0-tetradecanoyl phorbol-13-acetate (TPA) in the androgen-independent human prostatic JCA-1 cells. 784 24

The effects of various reagents on the induction of differentiation of the human prostatic cancer cell line, TSU-Pr1, were examined. Among these agents, the phorbol ester, TPA, almost completely suppressed cell proliferation at the concentration of 10(-8) M, and induced remarkable morphologic changes yielding cells with the microglial feature of an ameboid and/or ramified shape. More than 90% of the cells underwent the induction of morphologic changes by day 7 after treatment with 10(-8) M TPA. The expression of reliable microglial markers, alpha-naphthyl acetate esterase activity and CD11b, was observed in the differentiated cells. The data presented here suggest that TPA induces differentiation of a human prostate cancer cell line into cells with the characteristics of microglia.
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PMID:Phorbol ester induces differentiation of a human prostatic cancer cell line TSU-Pr1 into cells with characteristics of microglia. 956 64


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