Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The xenograft line, UCRU-PR-2, has been characterized further. Established from a primary human undifferentiated small cell carcinoma of the prostate, it has been maintained as a stable xenograft line in nude mice and is currently in passage 9. The tumor has maintained the features of small cell undifferentiated carcinoma but shows epithelial as well as neuroendocrine characteristics. In this paper, we describe synthesis and secretion of peptide hormones, ACTH, beta-endorphin and somatostatin in vivo and ACTH and beta-endorphin in vitro by the tumor, UCRU-PR-2. This suggests that the gene for proopiomelanocortin is expressed and that processing of the molecule occurs. This line may yield insights into the histogenesis of the subtypes of prostate cancer, and also aid studies of regulation of ectopic hormone production.
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PMID:Ectopic hormone production by a prostatic small cell carcinoma xenograft line. 283 15

The aim of the present study was to examine the correlation between the immunohistochemical findings and the serum markers for neuroendocrine (NE) cells in patients with carcinoma of the prostate. Preoperative serum values of chromogranin A (CgA), chromogranin B (CgB), pancreastatin (Pst), neuron-specific enolase (NSE), and prostatic specific antigen (PSA) were determined in 22 patients. The tissue specimens were obtained by a palliative transurethral resection of the prostate (TURP) because of urinary outflow obstruction. Immunohistochemistry was performed by using antibodies against CgA, CgB, NSE,.serotonin, thyroid-stimulating hormone (TSH), and somatostatin. Tumor cells with NE differentiation were found in 91% of the cases. No patient had elevated serum values of NSE, despite the presence of NSE-positive tumor cells in 77% of the tumors. Neither did CgB in serum correlate with the immunohistochemical findings. Elevated serum values of CgA were found in 59% of patients. A positive correlation between the number of CgA-staining cells and the serum values of CgA was found, as seven out of eight patients with groups of CgA-positive tumor cells had elevated serum values of CgA. We conclude that CgA, in contrast to NSE, CgB, and Pst, seems to be a useful serum marker in predicting the extent of NE differentiation in prostatic tumors.
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PMID:Neuroendocrine differentiation in carcinomas of the prostate: do neuroendocrine serum markers reflect immunohistochemical findings? 901 29

mRNA differential display-PCR analysis was used to perform a systematic screening of Somatostatin (SS)-regulated genes in the human prostatic carcinoma cell line LNCaP (Lymph Node Carcinoma of the Prostate). A 170 bp fragment was shown to be up-regulated by SS. Sequence analysis of this fragment revealed its homology with the human Topoisomerase II Alpha gene. Up-regulation of Topoisomerase II Alpha was confirmed by Northern blot hybridisation and was induced by the same dose of SS (1 nM) earlier demonstrated to inhibit LNCaP cell growth. Furthermore, SS possible effects on timing, as well as concentration of Topoisomerase II Alpha along the different phases of the cell cycle were investigated. To this purpose changes in the enzyme protein concentration in response to SS were assessed in synchronised LNCaP cells. The hormone was shown to exert a perturbing effect on both parameters considered, possibly related to its inhibitory action on LNCaP cell replication.
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PMID:Somatostatin up-regulates topoisomerase II alpha expression and affects LNCaP cell cycle. 1136 49

Chromogranin A-like immunoreactivity (CgA-LI) has been, and remains, the most widely used diagnostic and prognostic marker for endocrine tumors. The availability of assay kits combined with moderately high sensitivity and specificity has meant that there has been no great incentive to develop alternative markers. However, circulating concentrations of CgA-LI are elevated in several non-neoplastic diseases and in patients receiving acid-suppression therapy which may lead to false positive diagnosis. Additionally, certain endocrine tumors, such as rectal carcinoids, do not express the CgA gene so that there is a need for additional markers to complement CgA measurements. Plasma concentrations of the CgA-derived peptide, pancreastatin, measured with antisera of defined regional specificity, have a prognostic value in patients with metastatic midgut carcinoid tumors receiving somatostatin analog therapy or hepatic artery chemoembolization. Other CgA-derived peptides with potential as tumor markers are vasostatin-1, WE-14, catestatin, GE-25, and EL-35 but their value has yet to be fully assessed. Circulating concentrations of chromogranin B-like immunoreactivity (CgB-LI) are not elevated in non-neoplastic diseases and measurements of CCB, the COOH-terminal fragment of CgB, may be useful as a biochemical marker for neuroendocrine differentiation in lung tumors. Antisera to the secretogranin II-derived peptide, secretoneurin detects carcinoid tumors of the appendix with greater frequency than antisera to CgA and are of value in identifying therapy-resistant carcinoma of the prostate (clinical stage D3). Measurement of concentrations of a second secretogranin II-derived peptide, EM-66 in tumor tissue has been used to differentiate between benign and malignant pheochromocytoma. These examples point to a limited although potentially valuable role for granin-derived peptides as tumor markers.
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PMID:Granin-derived peptides as diagnostic and prognostic markers for endocrine tumors. 1993 74

Certain components of the somatostatin-system play relevant roles in Prostate Cancer (PCa), whose most aggressive phenotype (Castration-Resistant-PCa (CRPC)) remains lethal nowadays. However, neuronostatin and the G protein-coupled receptor 107 (GPR107), two novel members of the somatostatin-system, have not been explored yet in PCa. Consequently, we investigated the pathophysiological role of NST/GPR107-system in PCa. GPR107 expression was analyzed in well-characterized PCa patient's cohorts, and functional/mechanistic assays were performed in response to GPR107-silencing and NST-treatment in PCa cells (androgen-dependent (AD: LNCaP) and androgen-independent (AI: 22Rv1/PC-3), which are cell models of hormone-sensitive and CRPC, respectively), and normal prostate cells (RWPE-1 cell-line). GPR107 was overexpressed in PCa and associated with key clinical parameters (e.g., advance stage of PCa, presence of vascular invasion and metastasis). Furthermore, GPR107-silencing inhibited proliferation/migration rates in AI-PCa-cells and altered key genes and oncogenic signaling-pathways involved in PCa aggressiveness (i.e., KI67/CDKN2D/MMP9/PRPF40A, SST5TMD4/AR-v7/In1-ghrelin/EZH2 splicing-variants and AKT-signaling). Interestingly, NST treatment inhibited proliferation/migration only in AI-PCa cells and evoked an identical molecular response than GPR107-silencing. Finally, NST decreased GPR107 expression exclusively in AI-PCa-cells, suggesting that part of the specific antitumor effects of NST could be mediated through a GPR107-downregulation. Altogether, NST/GPR107-system could represent a valuable diagnostic and prognostic tool and a promising novel therapeutic target for PCa and CRPC.
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PMID:Unleashing the Diagnostic, Prognostic and Therapeutic Potential of the Neuronostatin/GPR107 System in Prostate Cancer. 3249 36