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)

We used heterogeneous parental cultures of AXC/SSh rat prostate cancer cells to isolate clonally derived prostate cancer cell lines. Light and electron microscopic analyses established that parental and clonally isolated cells possess features characteristic of secretory epithelium. Biochemical analyses showed that these cells contained androgen receptors and acid phosphatase and 5 alpha-reductase activity; phenotypic markers characteristic of differentiated prostate epithelium. Content of these prostate epithelial cell markers was variable and cell line specific. We used selected cell lines to examine androgen modulation of AXC/SSh rat prostate cancer cell proliferation in vitro. We found that proliferation of C-family or D-family cells, those respectively maintained on medium without additions or medium containing 10(-7) M 5 alpha-dihydrotestosterone, was not affected by changes in medium testosterone concentration through the range 10(-6)-10(-9) M. In contrast, testosterone modified proliferation of T-family cells, those maintained on medium containing 10(-7) M testosterone, and effects were antagonized by the anti-androgen RU 23908. Preliminary studies established that AXC/SSh rat prostate cancer cells elaborate polypeptide components which stimulate in vitro cell proliferation. Both the ability to elaborate these components and their effects on in vitro cell proliferation appeared to be cell line specific.
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PMID:Proliferation of AXC/SSh rat prostate cancer cells in vitro is androgen modulated. 332 May 41

Eight monoclonal antibodies (MAbs) raised against human prostate cancer cell lines are described. One MAb was derived from the fusion of mouse myeloma P3x63Ag8-653 cells with spleen cells of mice immunized with DU145 prostate cancer cells. The other seven were from the fusion of myeloma lines P3x63Ag8-653 or SP2/0 with spleen cells of mice immunized with PC3, DU145 and 1013L prostate cancer cells. All of the antibodies also reacted with cell lines of other human cancer types, especially carcinomas. Immunoperoxidase staining on fixed tissue revealed strong reactivity only with antibody PrN10. Seven other antibodies seemed to bind to cell surface-associated (glyco)proteins. Antibodies PrL22 and PrO11 showed similar reactivity in radioimmunoassay, and immunoprecipitated a 160 kD molecular weight polypeptide from [125I]lactoperoxidase-labeled cells. Antibodies PrHk an PrQ12 bound to molecules with apparent MW of 115 kD and 100 kD, respectively; antibodies PrM24 and PrP14 revealed a more complex picture in immunoprecipitation of surface-labeled cells.
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PMID:Shared antigens of human prostate cancer cell lines as defined by monoclonal antibodies. 388 36

Tumor marker for tumors in urology has been widely used to testicular and prostatic tumors. A part of testicular tumor produces alpha-fetoprotein (AFP) and HCG, thus these markers can not be used for early detection of disease. However, they are very useful in typing testicular tumor, and in monitoring a course of disease which produces them. beta-HCG seems to be more specific than HCG. In case of prostatic cancer, prostatic acid phosphatase (PAP) assayed immunochemically is sensitive and specific marker. Prostate antigen seems to be another excellent marker for this tumor, and this is well correlated with PAP. In reactivated case, tissue polypeptide antigen was elevated, suggesting use of this marker.
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PMID:[Tumor marker in urology]. 619 69

Serial serum prostate tumor markers (acid phosphatase, prostate-specific antigen-Yang, prostate-specific antigen-Hybritech, lipid-associated sialic acid in plasma, and tissue polypeptide antigen) were obtained every four hours during a twenty-four-hour interval from men with Stage D adenocarcinoma of the prostate. No therapeutic or diagnostic manipulations occurred during sample procurement, so that the amount of fluctuation in these serum prostate cancer markers could be determined. The average co-efficient of variation for acid phosphatase 28.8, prostate-specific antigen-Yang 8.85, prostate-specific antigen-Hybritech 7.2, lipid-associated sialic acid in plasma (LASA-P) 6.19, and tissue polypeptide antigen (TPA) 14.75 indicate that prostate-specific antigen determined by either method fluctuates minimally, indicating stability and, because it is prostate-cancer specific, is the most useful tumor marker tested.
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PMID:Comparative analysis of fluctuation of serum tumor markers in advanced cancer of prostate. 750 49

Bone scans, serum tissue-specific polypeptide antigen (TPS), prostate specific antigen (PSA), and neuron-specific enolase (NSE) were assessed in a total of 80 hormonally treated prostate cancer patients. Thirty-nine patients were free of osseous lesions; in 8 subjects, 3 or fewer scintigraphic hot spots were found; in 29 patients, more than 3 bone lesions were recorded. In 3 patients, a partial contribution of endocrine cell cancer structures was found, while in one patient, a homogeneous small cell carcinoma was detected at autopsy. Measurement of the serum PSA test showed a clear-cut rise from stage D0 subjects to stage D2 patients, with a small number of bone lesions (> or = 3). However, a relative decrease in the mean PSA level was measured with further progression in a number of hot spots in bone (> 3). Androgen threshold that is critical for the induction of the PSA (and PAP) expression seems to differ markedly in various cell subpopulations that arise during adenocarcinoma dedifferentiation. This fact explains not only the rise in serum PSA in the majority of progressive and previously castrated subjects after an initial period of hormonal responsiveness, but also a relative decline of androgen-dependent PSA expression with further tumor progression. Localized disease was accompanied with normal or just slightly elevated TPS concentration. In metastatic tumors, serum TPS values revealed a steady increase with the progression in bone. These data seem to reflect not only an increase in tumor proliferation rate with progressively transformed genome, but also the rise in the number of proliferating cells. The presence of nonepithelial transformed tumor structures, such as small cell cancer within a bulk of adenocarcinoma, reduces or normalizes numerical serotests values of both TPS and PSA even during tumor progression. The extent of such decline depends upon the bulk of the endocrine component. The assessment of the above parameters, especially when associated with elevated plasma NSE concentrations, may help in distinguishing an advanced adenocarcinoma with and without elements of malignant neuroendocrine structures. The proposed approach, modified by applying corresponding organ-specific markers, may be checked for its possible general use in staging protocols of various heterogeneous tumors.
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PMID:A more objective staging of advanced prostate cancer--routine recognition of malignant endocrine structures: the assessment of serum TPS, PSA, and NSE values. 750 85

We have recently cloned a 2.65-kilobase complementary DNA (cDNA) encoding the prostate-specific membrane antigen (PSM) recognized by the 7E11-C5.3 anti-prostate monoclonal antibody. Immunohistochemical analysis of the LNCaP, DU-145, and PC-3 prostate cancer cell lines for PSM expression using the 7E11-C5.3 antibody reveals intense staining in the LNCaP cells with no detectable expression in both the DU-145 and PC-3 cells. Coupled in vitro transcription/translation of the 2.65-kilobase full-length PSM cDNA yields an M(r) 84,000 protein corresponding to the predicted polypeptide molecular weight of PSM. Posttranslational modification of this protein with pancreatic canine microsomes yields the expected M(r) 100,000 PSM antigen. Following transfection of PC-3 cells with the full-length PSM cDNA in a eukaryotic expression vector, we detect expression of the PSM glycoprotein by Western analysis using the 7E11-C5.3 monoclonal antibody. Ribonuclease protection analysis demonstrates that the expression of PSM mRNA is almost entirely prostate specific in human tissues. PSM expression appears to be highest in hormone-deprived states and is hormonally modulated by steroids, with 5-alpha-dihydrotestosterone down-regulating PSM expression in the human prostate cancer cell line LNCaP by 8-10-fold, testosterone down-regulating PSM by 3-4-fold, and corticosteroids showing no significant effect. Normal and malignant prostatic tissues consistently show high PSM expression, whereas we have noted heterogeneous, and at times absent, expression of PSM in benign prostatic hyperplasia. LNCaP tumors implanted and grown both orthotopically and s.c. in nude mice abundantly express PSM, providing an excellent in vivo model system to study the regulation and modulation of PSM expression.
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PMID:Expression of the prostate-specific membrane antigen. 751 Oct 53

Serum tissue polypeptide-specific antigen (TPS), prostate-specific antigen (PSA), and prostatic acid phosphatase (PAP) concentrations were serially measured in 31 prostate cancer patients with bone metastases who had relapsed following hormonal therapy. Of these subjects 7 had well-differentiated cancer (G1), 13 patients were assessed to have moderately differentiated tumor (G2) while in 11 subjects poorly differentiated tumor (C13) was found. With increasing tumor grade (G1 to G3), a proportional increase in mean TPS value was found while the increase in respective PAP serotest values was not linear. Simultaneously measured mean PSA values showed a curved effect. Both PSA and PAP serotest concentrations depend on the respective hormone-dependent gene expressions that gradually decrease with tumor dedifferentiation. Therefore, in progressive hormonally treated stage D2 prostate cancer patients an androgen-independent TPS serotest seems to be a useful clinical addition for monitoring protocols. The combined use of TPS, PSA, and PAP seems to give a better reflection of tumor status. According to the bone scan data metastatic tumor mass in G3 carcinomas was virtually equal to cancer burden in G2 tumors. Hence, the marked elevation of TPS serotest values in G3 adenocarcinomas could not be attributed to greater tumor mass but was most likely due to an increase in proliferation rate. Some authors have recently proposed cytokeratins 8, 18, and 19 to be the origin of TPS serum findings. However, cytokeratin content has been proven to be lower in G3 tumors than in better-differentiated neoplasms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum TPS, PSA, and PAP values in relapsing stage D2 adenocarcinoma of the prostate. 753 45

The serum concentration of the cell proliferation marker TPS (tissue polypeptide-specific antigen) was compared with the tumour marker PSA (prostate specific antigen). PSA was found elevated in 50% of the benign prostatic hypertrophy (BPH) patients, in 88% of the patients with active prostate cancer and in 40% of the patients who were in an inactive phase. For TPS these values were 6, 34 and 0%, respectively. The metastatic progression was biochemically mirrored by pronounced elevations of PSA and TPS. These data suggest that TPS might be a valuable adjunct in the diagnosis and follow-up of patients with prostate cancer, especially in differentiating benign from malignant deterioration of the disease.
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PMID:Tissue polypeptide-specific antigen: a discriminative parameter between prostate cancer and benign prostatic hypertrophy. 767 80

Tissue polypeptide specific antigen (TPS) is a new tumor proliferation serotest marker. The respective radioimmunodetective procedure is based on the application of monoclonal antibodies raised against one the principle epitopes of tissue polypeptide antigen (TPA). TPS is useful tool for the identification of proliferative epithelial cells and is negative in all non-epithelial tissues such as lymph nodes, bone marrow, carcino-sarcomic and neuroendocrine prostatic tumors. In previous studies we have shown the clinical usefulness of this serotest in serial measurements during prostate cancer monitoring. In this study serum prostatic specific antigen (PSA) concentrations and natural killer (NK) cell activity data were compared with serum TPS values in a wide spectrum of prostate cancer condition (99 patients), benign prostatic hypertrophy (BPH, 40 patients), atypical prostate (12 subjects) and in 8 healthy men. Measured parameters reflect different aspects of the disease. Blood PSA concentrations and TPS serotest values were found to denote the status of disseminated prostate cancer with nearly equal significance, while PSA appears to be a more appropriate tumor marker in early stages of the disease. In atypical prostate a nonsignificant elevation of both PSA and TPA values were recorded when compared with BPH. In parallel, a pronounced and sharp drop in NK activity data was assessed resembling closely respective data in progressive Stage D2 patients. TPS serotest clearly detects cancer progression in treated and untreated patients (P < 0.01) while being less efficient in distinguishing between tumor stabilization and partial remission (p > 0.05). In this respect NK activity data serve as a sensitive probe for the presence of epithelial tumor cells in the circulation even during stabilization of the disease. According to the reported results we advocate the application of the TPS serotest as a useful addition in monitoring progressive patients with advanced prostatic carcinoma.
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PMID:Correlation of cell proliferation marker (TPS), natural killer (NK) activity and tumor load serotest (PSA) in untreated and treated prostatic tumors. 768

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


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