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1. Petit T, Davidson KK, Lawrence RA, von Hoff DD, Izbicka E: Neuropeptide receptor status in human tumor cell lines. Anticancer Drugs; 2001 Feb;12(2):133-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tumor types expressing a neuroendocrine phenotype secrete neuropeptides with paracrine or autocrine growth factor activity.
  • Once specific receptors are identified, specific neuropeptide antagonists disrupting paracrine and autocrine loops could be potential treatments in neuropeptide-secreting tumors.
  • In the present study, 11 human tumor cell lines representing astrocytoma, lymphoma, and pancreatic, prostate, lung and colon carcinomas were examined for expression of five different neuropeptide receptors (cholecystokinin, neurotensin, vasopressin, tachykinine substance P and cannabinoid) using RT-PCR and radioligand binding.
  • The presence of various neuropeptide receptors in different human cancer cell lines supports development of new antitumor treatments based on disruption of neuropeptide autocrine growth pathways.
  • [MeSH-minor] Cell Division / drug effects. DNA Primers / chemistry. Humans. RNA, Messenger / metabolism. RNA, Neoplasm / metabolism. Radioligand Assay. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 11261886.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Neuropeptide
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2. Jennbacken K, Tesan T, Wang W, Gustavsson H, Damber JE, Welén K: N-cadherin increases after androgen deprivation and is associated with metastasis in prostate cancer. Endocr Relat Cancer; 2010 Jun;17(2):469-79
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  • [Title] N-cadherin increases after androgen deprivation and is associated with metastasis in prostate cancer.
  • Androgen-deprivation therapy (ADT) is the standard treatment for metastatic prostate cancer.
  • In this study, we investigated if the expression of N-cadherin was influenced by androgen deprivation and was associated with metastasis in prostate cancer.
  • The effect of androgen deprivation on N-cadherin expression was initially studied in androgen-dependent (AD) LNCaP and androgen-independent (AI) LNCaP-19 and PC-3 prostate cancer cell lines.
  • No clear associations between N-cadherin and factors related with epithelial-mesenchymal transition or neuroendocrine differentiation could be established.
  • In addition, N-cadherin was evaluated by immunohistochemistry in human prostate tumors.
  • Expression of N-cadherin was more frequently found in tumors from patients treated with ADT than in tumors from patients with no prior hormonal treatment.
  • Furthermore, increased N-cadherin was detected in prostate cancer biopsies already 3 months after initiation of ADT when tumors were in a regressed state.
  • In summary the results indicate that androgen deprivation induces N-cadherin in prostate tumors.
  • [MeSH-minor] Animals. Cell Line, Tumor. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Metastasis. Receptors, Androgen / metabolism. Receptors, Androgen / physiology. Transplantation, Heterologous. Treatment Failure. Up-Regulation / drug effects. Up-Regulation / genetics

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  • (PMID = 20233707.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Antigens, CD; 0 / CDH2 protein, human; 0 / Cadherins; 0 / Receptors, Androgen
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3. Berruti A, Mosca A, Tucci M, Terrone C, Torta M, Tarabuzzi R, Russo L, Cracco C, Bollito E, Scarpa RM, Angeli A, Dogliotti L: Independent prognostic role of circulating chromogranin A in prostate cancer patients with hormone-refractory disease. Endocr Relat Cancer; 2005 Mar;12(1):109-17
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  • [Title] Independent prognostic role of circulating chromogranin A in prostate cancer patients with hormone-refractory disease.
  • The presence of neuroendocrine (NE) differentiation in the context of predominantly exocrine prostate cancer may play a key role in androgen-independent tumor growth.
  • The prognostic significance of plasma chromogranin A (CgA) was assessed in a series of consecutive prostate cancer patients with hormone-refractory disease.
  • One hundred and eight patients with newly diagnosed hormone-refractory prostate cancer entered the study.
  • Plasma CgA levels and other biochemical parameters, such as serum prostate specific antigen, serum alkaline phosphatase, serum lactate dehydrogenase, serum albumin and hemoglobin concentration, were measured at baseline (i.e. when hormone refractoriness occurred) and their prognostic role was evaluated together with patient performance status, Gleason score (at diagnosis of prostate cancer) and the presence of visceral metastases.
  • Furthermore, plasma CgA was prospectively evaluated in 50 patients undergoing chemotherapy.
  • In the patient subset undergoing chemotherapy, median CgA (range) values were 13.3 (3.0-141.0) U/l at baseline, 19.1 (3.0-486.0) U/l after 3 months, 20.8 (3.0-702.0) U/l after 6 months and 39.4 (3.0-414.0) U/l after 9 months (P<0.01).
  • Elevated plasma CgA levels are frequently observed in prostate cancer patients with hormone-refractory disease and correlate with poor prognosis.
  • NE differentiation in hormone-refractory patients is a time-dependent phenomenon and is not influenced by conventional antineoplastic treatments.
  • [MeSH-minor] Aged. Aged, 80 and over. Albumins / metabolism. Alkaline Phosphatase / blood. Bone Neoplasms / blood. Bone Neoplasms / secondary. Cell Differentiation. Chromogranin A. Hemoglobins / metabolism. Humans. L-Lactate Dehydrogenase / blood. Liver Neoplasms / blood. Liver Neoplasms / secondary. Lung Neoplasms / blood. Lung Neoplasms / secondary. Male. Middle Aged. Neoplasm Staging. Prognosis. Prospective Studies. Prostate-Specific Antigen / blood. Survival Rate

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  • (PMID = 15788643.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Albumins; 0 / Biomarkers, Tumor; 0 / CHGA protein, human; 0 / Chromogranin A; 0 / Chromogranins; 0 / Hemoglobins; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 3.1.3.1 / Alkaline Phosphatase; EC 3.4.21.77 / Prostate-Specific Antigen
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4. Sugi M, Yanishi M, Shimada O, Kawakita S, Murota T, Shikata N: [Neuroendocrine differentiation and metastasized to brain stem, intraorbit and base of tongue in prostate cancer during hormonal treatment: a case report]. Hinyokika Kiyo; 2008 May;54(5):373-6
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  • [Title] [Neuroendocrine differentiation and metastasized to brain stem, intraorbit and base of tongue in prostate cancer during hormonal treatment: a case report].
  • Prostatic neuroendocrine (NE) carcinoma is a rare disease and the NE differentiation in prostate cancer is characterized by poor prognosis, rapidly progressing tumor and an androgen-independent state, for which there is currently no successful therapy.
  • This is the first Japanese report of prostate cancer metastasis to the brain stem and base of the tongue.
  • [MeSH-major] Adenocarcinoma / pathology. Brain Stem Neoplasms / secondary. Carcinoma, Neuroendocrine / pathology. Cell Differentiation. Orbital Neoplasms / secondary. Prostatic Neoplasms / pathology. Tongue Neoplasms / secondary
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Drug Resistance, Neoplasm. Humans. Male. Middle Aged


5. Fixemer T, Remberger K, Bonkhoff H: Apoptosis resistance of neuroendocrine phenotypes in prostatic adenocarcinoma. Prostate; 2002 Oct 1;53(2):118-23
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  • [Title] Apoptosis resistance of neuroendocrine phenotypes in prostatic adenocarcinoma.
  • BACKGROUND: Neuroendocrine (NE) differentiation has been implicated in prostate cancer progression and hormone therapy failure.
  • It has been shown that prostate cancer cells with NE features lack proliferation activity in vitro and in vivo.
  • The current study reports on the apoptotic status of NE phenotypes in human prostate cancer.
  • CONCLUSION: The present data suggest that the vast majority of prostate cancer cells with NE features escapes programmed cell death.
  • This escape may contribute significantly to their drug resistance and their malignant potential.
  • [MeSH-minor] Cell Differentiation / physiology. Chromogranin A. Chromogranins / metabolism. DNA Fragmentation. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Male. Neoplasm Staging. Neurosecretory Systems / pathology

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12242726.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins
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6. Tang Y, Wang L, Goloubeva O, Khan MA, Lee D, Hussain A: The relationship of neuroendocrine carcinomas to anti-tumor therapies in TRAMP mice. Prostate; 2009 Dec 01;69(16):1763-73
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  • [Title] The relationship of neuroendocrine carcinomas to anti-tumor therapies in TRAMP mice.
  • BACKGROUND: Neuroendocrine differentiation and neuroendocrine carcinoma (NEC) have been linked to androgen deprivation in prostate cancers.
  • No previous study has directly connected neuroendocrine phenotypes to chemotherapy.
  • METHODS: Using the transgenic adenocarcinoma of mouse prostate (TRAMP) model, we studied tumor progression after hormone ablation (castration) and/or chemotherapy (docetaxel), and analyzed the incidence of NEC as a function of the anti-tumor therapies.
  • Protein expressions in tumor tissues were analyzed by Western blots and immunohistochemistry.
  • RESULTS: Although all animals developed prostate cancer, no NEC was found in control mice.
  • However, over 30% of the mice that received an anti-tumor therapy developed NEC.
  • A similar incidence of NEC was found in the castration-only and docetaxel-only treatment groups, while a higher incidence was observed in the combined treatment (castration and docetaxel) group.
  • However, NEC tumors had a higher proliferative index and greater potential for metastasis and drug-resistance, as evidenced by significantly higher expression levels of PCNA, S100A4, and Pgp, but lower levels of E-cadherin.
  • CONCLUSIONS: Stress induced by anti-cancer treatments may play a role in NEC development.
  • Although NEC and ADC differ in their expressions of many proteins, a high level of SV40 T-antigen in both tumor types suggest a common progenitor..
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / adverse effects. Antineoplastic Agents / adverse effects. Carcinoma, Neuroendocrine / chemically induced. Prostatic Neoplasms / drug therapy. Taxoids / adverse effects
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette Transporters / metabolism. ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Animals. Cell Proliferation. Drug Therapy, Combination. Incidence. Male. Mice. Mice, Transgenic. Neoplasm Proteins / metabolism. Survival Analysis

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 19691128.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Androgen Antagonists; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Taxoids; 15H5577CQD / docetaxel
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7. Shimizu T, Ohta Y, Ozawa H, Matsushima H, Takeda K: Papaverine combined with prostaglandin E2 synergistically induces neuron-like morphological changes and decrease of malignancy in human prostatic cancer LNCaP cells. Anticancer Res; 2000 Mar-Apr;20(2A):761-7
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  • We are interested in the possibility of new prostate cancer therapy that would control tumor malignancy via the induction of terminal cell differentiation.
  • Here, we investigated the combined effect of various cAMP reagents on LNCaP human prostate carcinoma cells.
  • Electron microscope study suggested that cells treated with both reagents become like neuroendocrine cells.
  • [MeSH-major] Cell Differentiation / drug effects. Dinoprostone / pharmacology. Neurons / cytology. Papaverine / pharmacology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Actins / genetics. Cell Division / drug effects. Drug Synergism. Gene Expression Regulation, Neoplastic / drug effects. Genes, myc. Humans. Kinetics. Male. Neoplasm Invasiveness. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-myc / genetics. Tumor Cells, Cultured

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  • (PMID = 10810351.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] GREECE
  • [Chemical-registry-number] 0 / Actins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; DAA13NKG2Q / Papaverine; K7Q1JQR04M / Dinoprostone
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8. Lara PN Jr, Longmate J, Evans CP, Quinn DI, Twardowski P, Chatta G, Posadas E, Stadler W, Gandara DR: A phase II trial of the Src-kinase inhibitor AZD0530 in patients with advanced castration-resistant prostate cancer: a California Cancer Consortium study. Anticancer Drugs; 2009 Mar;20(3):179-84
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  • [Title] A phase II trial of the Src-kinase inhibitor AZD0530 in patients with advanced castration-resistant prostate cancer: a California Cancer Consortium study.
  • Prostate cancer cells undergo neuroendocrine differentiation during androgen deprivation and secrete neuropeptides, hence activating androgen receptor-regulated genes.
  • Src-family protein kinases are involved in neuropeptide-induced prostate cancer growth and migration.
  • A phase II trial of AZD0530, an oral Src-family kinase inhibitor, in patients with advanced castration resistant prostate cancer was conducted.
  • The primary endpoint was prostate cancer-specific antigen (PSA) response rate, defined as a 30% or greater decrease.
  • Eligibility criteria included documentation of castration resistance (including antiandrogen withdrawal), adequate end-organ function, and performance status, and not more than one prior taxane-based chemotherapy regimen.
  • Nine patients (32%) had prior docetaxel-based chemotherapy.
  • Median progression-free survival time was 8 weeks.
  • Treatment was generally well tolerated.
  • Strong preclinical evidence warrants further investigation of AZD0530 in earlier-stage prostate cancer or as combination therapy.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / therapeutic use. Benzodioxoles / therapeutic use. Prostatic Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. src-Family Kinases / antagonists & inhibitors
  • [MeSH-minor] Aged. Aged, 80 and over. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Chemical and Drug Induced Liver Injury / etiology. Combined Modality Therapy. Disease-Free Survival. Drug Resistance, Neoplasm. Gastrointestinal Diseases / chemically induced. Humans. Lymphopenia / chemically induced. Male. Middle Aged. Orchiectomy. Prostate-Specific Antigen / blood

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  • (PMID = 19396016.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CM / N01 CM062209; United States / NCI NIH HHS / CA / N01CM62209; United States / NCI NIH HHS / CM / N01-CM62209; United States / NCI NIH HHS / CM / N0I-CM17102
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Benzodioxoles; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 9KD24QGH76 / saracatinib; EC 2.7.10.2 / src-Family Kinases; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Other-IDs] NLM/ NIHMS330482; NLM/ PMC3225398
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9. Assikis VJ, Do KA, Wen S, Wang X, Cho-Vega JH, Brisbay S, Lopez R, Logothetis CJ, Troncoso P, Papandreou CN, McDonnell TJ: Clinical and biomarker correlates of androgen-independent, locally aggressive prostate cancer with limited metastatic potential. Clin Cancer Res; 2004 Oct 15;10(20):6770-8
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  • [Title] Clinical and biomarker correlates of androgen-independent, locally aggressive prostate cancer with limited metastatic potential.
  • PURPOSE: We have identified a subset of patients exhibiting extended survival with metastases from androgenindependent prostate cancer of which the principal site of progression was the tumor primary.
  • The purpose of this study was to evaluate the expression of selected biomarkers to characterize this subset of prostate cancer patients.
  • EXPERIMENTAL DESIGN: A 105 core tissue microarray was constructed from primary tumor samples from 16 patients, with matched lymph node metastases in 5 cases.
  • Immunohistochemistry was used to evaluate selected biomarkers associated with prostate cancer progression.
  • Standard statistical methodologies were used to compute the distribution of time to progression and overall survival associations between pairs of biomarkers.
  • The profile of biomarker expression was notable for virtual absence of neuroendocrine features, high CD10, low matrix metalloproteinase (MMP)-9, high E-cadherin expression, and high membranous beta-catenin.
  • CONCLUSIONS: The cohort of prostate cancer patients, characterized by locally aggressive disease rather than lethal metastatic progression, was associated with a distinctive biomarker signature.
  • The biomarker profile was, in general, more consistent with low-grade prostate cancer exhibiting local growth rather than metastatic progression.


10. Zufferey L, Roques B, Fléchon A, Droz JP: [Study of the hormone-refractory prostate cancer clinical practice in an anti-cancer center]. Bull Cancer; 2001 Dec;88(12):1213-21
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  • [Title] [Study of the hormone-refractory prostate cancer clinical practice in an anti-cancer center].
  • [Transliterated title] La pratique clinique du cancer de la prostate horomonorésistant dans un centre de lutte contre le cancer.
  • We have examined 82 patients with hormonoresistant prostate cancer in a retrospective study.
  • Objective and palliative effect of chemotherapy is marked for weekly doxorubicin, prednisone with mitoxantrone and etoposide associated with platin-salts for prostatic carcinoma with neuroendocrine differentiation.
  • This study suggests the presence of different subpopulations of patients with specific evolutive patterns, thus further specific therapy should be evaluated.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / blood. Bone Neoplasms / secondary. Brain Neoplasms / secondary. Drug Resistance, Neoplasm. Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Phosphopyruvate Hydratase / blood. Prospective Studies. Prostate-Specific Antigen / blood


11. Uysal-Onganer P, Kawano Y, Caro M, Walker MM, Diez S, Darrington RS, Waxman J, Kypta RM: Wnt-11 promotes neuroendocrine-like differentiation, survival and migration of prostate cancer cells. Mol Cancer; 2010 Mar 10;9:55
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  • [Title] Wnt-11 promotes neuroendocrine-like differentiation, survival and migration of prostate cancer cells.
  • We previously reported that Wnt-11 expression is elevated in hormone-independent prostate cancer and that the progression of prostate cancer from androgen-dependent to androgen-independent proliferation correlates with a loss of mutual inhibition between Wnt-11- and androgen receptor-dependent signals.
  • However, the prevalence of increased expression of Wnt-11 in patient tumours and the functions of Wnt-11 in prostate cancer cells were not known.
  • RESULTS: Wnt-11 protein levels in prostate tumours were determined by immunohistochemical analysis of prostate tumour tissue arrays.
  • Androgen-depleted LNCaP prostate cancer cells form neurites and express genes associated with neuroendocrine-like differentiation (NED), a feature of prostate tumours that have a poor prognosis.
  • In contrast, Wnt-11 did not induce NSE expression in RWPE-1 cells, which are derived from benign prostate, suggesting that the role of Wnt-11 in NED is specific to prostate cancer.
  • CONCLUSIONS: These observations suggest that the increased level of Wnt-11 found in prostate cancer contributes to tumour progression by promoting NED, tumour cell survival and cell migration/invasion, and may provide an opportunity for novel therapy in prostate cancer.


12. D'Antonio JM, Ma C, Monzon FA, Pflug BR: Longitudinal analysis of androgen deprivation of prostate cancer cells identifies pathways to androgen independence. Prostate; 2008 May 15;68(7):698-714
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  • [Title] Longitudinal analysis of androgen deprivation of prostate cancer cells identifies pathways to androgen independence.
  • BACKGROUND: Following androgen ablation therapy, the majority of prostate cancer patients develop treatment resistance with a median time of 18-24 months to disease progression.
  • METHODS: To identify molecular targets that promote prostate cancer cell survival and contribute to androgen independence, we evaluated changes in LNCaP cell gene expression during 12 months of androgen deprivation.
  • At time points reflecting critical growth and phenotypic changes, we performed Affymetrix expression array analysis to examine the effects of androgen deprivation during the acute response, during the period of apparent quiescence, and following the emergence of a highly proliferative, androgen-independent prostate cancer cell phenotype (LNCaP-AI).
  • RESULTS: We discovered alterations in gene expression for molecules associated with promoting prostate cancer cell growth and survival, and regulating cell cycle progression and apoptosis.
  • Additionally, expression of AR co-regulators, adrenal androgen metabolizing enzymes, and markers of neuroendocrine disease were significantly altered.
  • CONCLUSIONS: These findings contribute greatly to our understanding of androgen-independent prostate cancer.
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / genetics. Cell Cycle / drug effects. Cell Cycle / genetics. Cell Line, Tumor. Cell Survival / drug effects. Drug Resistance, Neoplasm / drug effects. Endothelin-1 / genetics. Endothelin-1 / metabolism. Gene Expression Profiling. Humans. Male. Receptor, Endothelin A / genetics. Receptor, Endothelin A / metabolism. Receptors, Androgen / genetics. Receptors, Androgen / metabolism

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18302219.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P30CA047904-18; United States / NCI NIH HHS / CA / R01CA095239
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Endothelin-1; 0 / Receptor, Endothelin A; 0 / Receptors, Androgen
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13. Huang J, Yao JL, di Sant'Agnese PA, Yang Q, Bourne PA, Na Y: Immunohistochemical characterization of neuroendocrine cells in prostate cancer. Prostate; 2006 Sep 15;66(13):1399-406
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical characterization of neuroendocrine cells in prostate cancer.
  • BACKGROUND: Neuroendocrine (NE) cells increase in high grade/stage prostate cancer (PC) and may contribute to androgen-independent cancer.
  • METHODS: PC tissue was stained immunohistochemically for luminal secretory cell-associated cytokeratin, basal cell markers, ki-67, androgen receptor (AR), PSA, prostate acid phosphatase (PAP), and alpha-methylacyl coenzyme A racemase (AMACR).
  • They do not express AR, consistent with their resistance to hormonal therapy.
  • [MeSH-major] Neuroendocrine Tumors / metabolism. Neuroendocrine Tumors / pathology. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology
  • [MeSH-minor] Acid Phosphatase / genetics. Acid Phosphatase / metabolism. Androgen Antagonists / pharmacology. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Keratins / genetics. Keratins / metabolism. Ki-67 Antigen / genetics. Ki-67 Antigen / metabolism. Male. Phenotype. Prostate-Specific Antigen / genetics. Prostate-Specific Antigen / metabolism. Racemases and Epimerases / genetics. Racemases and Epimerases / metabolism. Receptors, Androgen / genetics. Receptors, Androgen / metabolism

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  • (PMID = 16865726.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Ki-67 Antigen; 0 / Receptors, Androgen; 68238-35-7 / Keratins; EC 3.1.3.2 / Acid Phosphatase; EC 3.4.21.77 / Prostate-Specific Antigen; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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14. Alapont Alacreu JM, Montaner Ramírez MJ, Pontones Moreno JL, Valls Blasco F, Vera-Sempere FJ, Jiménez-Cruz JF: [Small cell carcinoma of the prostate]. Actas Urol Esp; 2002 Sep;26(8):585-8
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  • [Title] [Small cell carcinoma of the prostate].
  • Pure small cell carcinoma of the prostate is rare (less than 1% of all prostatic neoplasm).
  • Small cell carcinomas of the prostate are a heterogeneous group of tumors, a number of them have neuroendocrine differentiation and are highly aggressive, commonly with visceral metastases at time of diagnosis.
  • Complete temporary remission has been reported with chemotherapy but this tumor has a poor prognosis.
  • The median overall survival from the time of diagnosis is between 5-17.5 months.
  • We report 2 new cases of small cell carcinoma of the prostate and a review of the literature.

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  • (PMID = 12448178.001).
  • [ISSN] 0210-4806
  • [Journal-full-title] Actas urologicas espanolas
  • [ISO-abbreviation] Actas Urol Esp
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 12
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15. Sella A, Konichezky M, Flex D, Sulkes A, Baniel J: Low PSA metastatic androgen- independent prostate cancer. Eur Urol; 2000 Sep;38(3):250-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low PSA metastatic androgen- independent prostate cancer.
  • OBJECTIVES: To describe the clinical parameters of low PSA, progressive metastatic androgen-independent prostate cancer.
  • METHODS: From April 1995 to May 1999, we selected 18 patients with clinically progressive androgen-independent prostate cancer and low PSA (</=10 ng/ml).
  • Patients received cisplatin-based therapy.
  • Specimens from the primary tumor were reviewed and neuroendocrine differentiation was determined with chromogranin-A and neuron-specific enolase immunocytochemical staining.
  • Of the 12 patients who consented to chemotherapy, 8 (66.6%) achieved an objective response (95% CI, 34.
  • Hematoxylin and eosin evaluation revealed two major groups: neuroendocrine tumors, either pure small cell cancer in 6 patients (37.5%) or combined small cell cancer and adenocarcinoma in 8 (50%), and predominant poorly differentiated prostate cancer in 2 (12.5%).
  • Neuroendocrine immunoreactivity was detected in all the specimens.
  • CONCLUSIONS: Progressive androgen-independent prostate cancer with low serum PSA is characterized by visceral metastases, high proportion of lytic bone disease, sensitivity to cisplatin-based chemotherapy, and histological features of small cell or poorly differentiated prostate cancer.
  • In this subgroup of patients, selection of the therapeutic approach can be based on clinical parameters.
  • [MeSH-major] Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology
  • [MeSH-minor] Androgens. Humans. Male. Neoplasm Metastasis. Neoplasm Staging. Prospective Studies


16. Lissoni P, Vigano P, Vaghi M, Frontini L, Giuberti C, Manganini V, Casu M, Brivio F, Niespolo R, Strada G: A phase II study of tamoxifen in hormone-resistant metastatic prostate cancer: possible relation with prolactin secretion. Anticancer Res; 2005 Sep-Oct;25(5):3597-9
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  • [Title] A phase II study of tamoxifen in hormone-resistant metastatic prostate cancer: possible relation with prolactin secretion.
  • Recent experimental observations, showing the potential role of prolactin (PRL) as a tumor growth factor for prostate cancer and the unfavourable prognostic significance of enhanced chromogranin-A-secreting neuroendocrine cell proliferation, could contribute to a better understanding of the mechanisms responsible for the occurrence of hormone-resistance in the prostate cancer.
  • Moreover, it has been shown that tamoxifen, which consistently exerts estrogenic activity in males, may inhibit prostate cancer cell proliferation in experimental studies.
  • This preliminary phase II study was planned in an attempt to evaluate the therapeutic efficacy of tamoxifen in hormone-refractory metastatic prostate cancer.
  • The study included 14 consecutive metastatic prostate cancer patients, who had progressed under the classical endocrine therapy with LHRH-analogs and/or anti-androgens.
  • Patients received the same treatment plus tamoxifen at 20 mg/day orally.
  • A decline greater than 50% in prostate-specific antigen (PSA) levels occurred in 4/14 (29%) patients within the first 2 months of therapy, with a median duration of 5 months.
  • Mean pre-treatment levels of PRL were significantly higher in responder patients than in those who progressed.
  • Moreover, abnormally high pre-treatment levels of PRL were found in 5/14 (36%) patients.
  • The percent of clinical responses observed in patients with pre-treatment hyperprolactinemia was significantly higher than that found in patients with normal pre-treatment PRL concentrations.
  • Finally, a significant decline in mean PRL levels upon tamoxifen therapy occurred only in the responder patients.
  • This preliminary study seems to justify further clinical research to confirm the potential efficacy of tamoxifen in the treatment of hormone-refractory prostate cancer and to identify possible parameters, which may predict the response to treatment.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Prolactin / secretion. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / secretion. Tamoxifen / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Androgen Antagonists / therapeutic use. Drug Resistance, Neoplasm. Gonadotropin-Releasing Hormone / analogs & derivatives. Humans. Male. Middle Aged. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / secretion


17. Stein ME, Bernstein Z, Abacioglu U, Sengoz M, Miller RC, Meirovitz A, Zouhair A, Freixa SV, Poortmans PH, Ash R, Kuten A: Small cell (neuroendocrine) carcinoma of the prostate: etiology, diagnosis, prognosis, and therapeutic implications--a retrospective study of 30 patients from the rare cancer network. Am J Med Sci; 2008 Dec;336(6):478-88
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  • [Title] Small cell (neuroendocrine) carcinoma of the prostate: etiology, diagnosis, prognosis, and therapeutic implications--a retrospective study of 30 patients from the rare cancer network.
  • Within the framework of the Rare Cancer Network Study, we examined 30 patients suffering from small cell neuroendocrine prostate cancer, either in an early/localized or an advanced/metastatic stage.
  • Patients were treated with cisplatin-based chemotherapy, with or without pelvic radiotherapy.
  • Small cell neuroendocrine prostate carcinoma is a very aggressive disease with a poor prognosis, even in its localized form.
  • Despite initial response, the common cisplatin-based chemotherapy plus radiotherapy failed to improve outcome markedly.
  • Improvement will come from understanding the biology of the disease and integrating new targeted therapies into the treatment of this rare and aggressive tumor.
  • [MeSH-major] Carcinoma, Small Cell / etiology. Carcinoma, Small Cell / therapy. Diagnosis, Differential. Prostatic Neoplasms / etiology. Prostatic Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Humans. Male. Middle Aged. Neoplasm Metastasis. Prognosis. Retrospective Studies


18. Hogan BA, Thornton FJ, Brannigan M, Browne TJ, Pender S, O'Kelly P, Lyon SM, Lee MJ: Hepatic metastases from an unknown primary neoplasm (UPN): survival, prognostic indicators and value of extensive investigations. Clin Radiol; 2002 Dec;57(12):1073-7
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  • [Title] Hepatic metastases from an unknown primary neoplasm (UPN): survival, prognostic indicators and value of extensive investigations.
  • AIM: The objectives of this study were to identify prognostic features for patients with hepatic metastases and unknown primary neoplasms (UPN), determine the common primary tumours, assess the value of diagnostic tests in finding these tumours, and evaluate the impact of therapy and knowledge of the primary tumour on patient survival.
  • Histopathology, diagnostic investigations and success at identifying the primary neoplasm were recorded.
  • In addition, in 70 patients with adenocarcinoma histology (M:F, 48:22; age range 27-91 years, median 65 years), treatment and survival data from the date of biopsy were recorded.
  • RESULTS: The histological spectrum included adenocarcinoma in 70, neuroendocrine in four, squamous cell carcinoma in four, small cell carcinoma in four, carcinoid in two, hepatoma in one and three others.
  • Extensive investigation identified a primary neoplasm in 16/88 patients (18%) including colorectal in six, gastric in two, lung in four, oesophageal in two, prostate in one and carcinoid in one.
  • Sixteen of 62 patients received active treatment with either surgery, chemotherapy, radiotherapy or a combination protocol.
  • Patients <65 years were more likely to receive active treatment than those >65 years (P=0.006).
  • Age with a hazard ratio (HR) of 1.01 (P=0.178), active treatment (HR=0.65;P=0.194), knowledge of the primary neoplasm (HR=0.60;P=0.213) and male gender (HR=0.88;P=0.642) had no significant effect on survival.

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  • (PMID = 12475531.001).
  • [ISSN] 0009-9260
  • [Journal-full-title] Clinical radiology
  • [ISO-abbreviation] Clin Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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19. Yashi M, Nukui A, Kurokawa S, Ochi M, Ishikawa S, Goto K, Kobayashi Y, Muraishi O, Tokue A: Elevated serum progastrin-releasing peptide (31-98) level is a predictor of short response duration after hormonal therapy in metastatic prostate cancer. Prostate; 2003 Sep 1;56(4):305-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevated serum progastrin-releasing peptide (31-98) level is a predictor of short response duration after hormonal therapy in metastatic prostate cancer.
  • BACKGROUND: The neuroendocrine (NE) pathway has been attracting attention as a mechanism for the androgen-independent progression because the neuropeptide provokes tumor growth and inhibits apoptosis under androgen-deprived milieu in prostate cancer cells.
  • Seventy patients with metastatic prostate cancer including four patients (5.7%) with NE carcinoma who underwent hormonal therapy were enrolled in the prognostic analyses by Cox proportional hazards model.
  • RESULTS: The serum status steadily shifted toward predominant expression of ProGRP with the progression of prostate cancer into metastatic and androgen-independent stages.
  • Univariate analysis revealed that the deteriorated performance status (PS) and extent of bony disease (EOD), and high serum alkaline phosphatase (ALP), serum ProGRP, and nadir prostate-specific antigen (PSA) levels were associated with a lower progression-free survival (PFS) rate (P < 0.005).
  • Serum ProGRP was the most significant predictor among pre-treatment factors in this model (P = 0.0094).
  • CONCLUSIONS: The neuropeptide precursor ProGRP is a distinct serum marker that is useful to know the NE milieu and provides prognostic information in patients with advanced prostate cancer.
  • Standard therapy for metastatic prostate cancer may make progress when further studies will clarify the causative link between serum ProGRP level and androgen-independent disease progression.
  • [MeSH-major] Biomarkers, Tumor / analysis. Gastrointestinal Hormones / analysis. Neoplasm Metastasis. Neoplasm Staging / methods. Peptide Fragments / analysis. Peptides / analysis. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Recombinant Proteins / analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Androgens / pharmacology. Antineoplastic Agents, Hormonal / pharmacology. Drug Resistance, Neoplasm. Enzyme-Linked Immunosorbent Assay. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis. Prostate-Specific Antigen / analysis. Treatment Outcome

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12858359.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Gastrointestinal Hormones; 0 / Peptide Fragments; 0 / Peptides; 0 / Recombinant Proteins; 0 / pro-gastrin-releasing peptide (31-98); EC 3.4.21.77 / Prostate-Specific Antigen
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20. Medvedev VL: [Hormone-resistant epithelial cancer of the prostate]. Urologiia; 2001 Jul-Aug;(4):29-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Hormone-resistant epithelial cancer of the prostate].
  • Hormone-resistance is typical for tumors from urothelial, basal and neuroendocrine PC cells, glandular epithelium cells which lost androgen receptors (AR) and tumors consisting of cells which retain AR but simultaneously express Bcl-2 and/or p53 genes.
  • The development of hormone-resistant cancer 2.5-3 years after hormonal therapy is associated with changes in immunophenotype of tumor cells.
  • Thus, immunophenotype of tumor cells may serve a prognostic marker of hormonal resistance of the tumor and dictate the treatment policy.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma, Basal Cell / drug therapy. Carcinoma, Transitional Cell / drug therapy. Drug Resistance, Neoplasm. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis. Humans. Immunophenotyping. Male. Middle Aged. Mutation. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / immunology. Prognosis. Receptors, Androgen / genetics. Time Factors

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  • (PMID = 11569231.001).
  • [ISSN] 1728-2985
  • [Journal-full-title] Urologii︠a︡ (Moscow, Russia : 1999)
  • [ISO-abbreviation] Urologiia
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Androgen
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21. Casini Raggi C, Pinzani P, Gelmini S, Tricarico C, Orlando C, Calabrò A, Renzi D, Cianchi F, Valanzano R, Distante V, Cortesini C, Tonelli F, Cataliotti L, Cameron Smith M, Messerini L, Bianchi S, Pazzagli M, Serio M, Maggi M: [Somatostatin receptors in non-endocrine tumours]. Minerva Endocrinol; 2001 Sep;26(3):149-58
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The study of the antiproliferative action of somatostatin (ss) is important not only to understand the regulation of neuroendocrine tumours that express receptors (sst), but also non-endocrine tumours which express these receptors.
  • Although hypotheses have been put forward that treatment with ss or its analogs may be beneficial in oncological patients, this does not appear to be the case in neuroblastoma; patients with high sst2 levels (who are therefore sensitive to ss treatment) have per se a relatively positive outcome.
  • Therefore, adjuvant treatment with ss is not necessary.
  • Viceversa, patients with a poor prognosis are essentially characterized by a low expression of sst2 (and therefore are insensitive to a therapy with ss).
  • In these patients adjuvant treatment with ss might be indicated, but would have little chance of success.
  • Although the majority of neuroendocrine tumours expresses sst2, pancreas and prostate cancer express sst1 but not sst2, and are therefore insensitive to octreotide treatment which binds preferentially to sst2.
  • However, the concentration of sst2 in colorectal cancer is similar, if not lower than that in the surrounding normal tissue.
  • Therefore, the probability of successful adjuvant therapy with ss is relatively low.
  • [MeSH-major] Neoplasm Proteins / physiology. Neoplasms / metabolism. Receptors, Somatostatin / physiology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Antineoplastic Agents, Hormonal / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism. Female. Humans. Male. Neuroblastoma / genetics. Neuroblastoma / metabolism. Octreotide / therapeutic use. Somatostatin / physiology. Somatostatin / therapeutic use

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  • (PMID = 11753238.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Neoplasm Proteins; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 77
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22. Alberti C: Neuroendocrine differentiation in prostate carcinoma: focusing on its pathophysiologic mechanisms and pathological features. G Chir; 2010 Nov-Dec;31(11-12):568-74
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  • [Title] Neuroendocrine differentiation in prostate carcinoma: focusing on its pathophysiologic mechanisms and pathological features.
  • Neuroendocrine differentiation in prostate carcinoma: focusing on its pathophysiologic mechanisms and pathological features. C.
  • Alberti Prostate carcinoma, even at advanced stages, responds in most patients to androgen deprivation therapies, that are able to exploit the androgen-sensitivity of prostate cancer cells.
  • However, more than half of such tumors, within one to three years, escape these treatments, thus progressing to the hormone-refractory condition.
  • Intriguing links between the development of hormone-insensitivity and neuroendocrine (NE) differentiation in prostate carcinoma have been hypothesized.
  • While, some time ago, NE cells have been considered as derived from progenitor neural crest cells, currently are thought to arise, as well as both basal and secretory cells of prostate gland, from common pluripotent stem cells.
  • The propensity of prostate cancer cells to undergo a transdifferentiation pathway towards NE phenotype is due to several microenvironmental conditions such as androgen depletion (induced by LH-RH analogs or antagonists, antiandrogens, 5-α-reductase inhibitors), ionizing-radiation therapy, adrenergic factors, increase in interleukin-6 signaling cascade.
  • NE differentiation in prostate malignancy arises in three different forms: carcinoid, oat cell carcinoma, focally NE-differentiated conventional tumor.
  • Selective expression of stem cell-associated markers, such as CD44/Oct4A gene, in NE cancerous cells explain their therapy escape together with tumor recurrence and metastasis.
  • Serum levels of CgA reflect NE differentiation in prostate carcinoma more suitably than those of NSE.
  • Intriguingly, intermittent androgen deprivation therapy, by preventing NE differentiation, significantly reduces the risk of a rise in serum CgA levels meanwhile delaying the time of cancer progression due to hormone-independence.
  • Although valuable insights into the nature of NE differentiation in prostate carcinoma have been achieved in the last decades, additional understanding is needed about its pathogenetic mechanisms in order to devise novel therapy strategies to target them.
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Androgens / metabolism. Antineoplastic Agents, Hormonal / therapeutic use. Apoptosis / drug effects. Biomarkers / metabolism. Cell Transformation, Neoplastic / drug effects. Chromogranins / metabolism. Humans. Male. Neoplasm Invasiveness. Phosphopyruvate Hydratase / metabolism. Pluripotent Stem Cells / metabolism. Prognosis. Prostate-Specific Antigen / metabolism. Receptors, Androgen / metabolism. Treatment Failure


23. Cabrespine A, Guy L, Chollet P, Debiton E, Bay JO: [Molecular mechanisms involved in hormone resistance of prostate cancer]. Bull Cancer; 2004 Oct;91(10):747-57
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  • [Title] [Molecular mechanisms involved in hormone resistance of prostate cancer].
  • [Transliterated title] Mécanismes moléculaires impliqués dans l'hormonorésistance du cancer de la prostate.
  • Prostate cancer has an androgen-dependent growth mediated by the androgen receptor (AR).
  • Androgen pathway blockage is the standard therapy for the treatment of prostate cancers at an advanced stage.
  • In spite of an initial sensitivity, prostate cancers become more or less quickly towards androgen-independent.
  • In condition of androgenic deprivation, AR remains actively involved in the growth of the cancerous cells prostate.
  • Nevertheless, there are others partial AR-independent pathways as neuroendocrine differentiation.
  • The comprehension of these various mechanisms is the key of the development of more effective therapies on hormono-refractory prostate cancers.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Neoplasms, Hormone-Dependent / genetics. Prostatic Neoplasms / genetics. Receptors, Androgen / genetics
  • [MeSH-minor] 3-Oxo-5-alpha-Steroid 4-Dehydrogenase / metabolism. Androgen Antagonists / therapeutic use. Androgens / physiology. Apoptosis / genetics. Cell Proliferation. Growth Substances / metabolism. Humans. Interleukins / metabolism. Male. Mutation. Neurosecretory Systems / pathology. Orchiectomy. Phenotype. Receptor, Epidermal Growth Factor / metabolism. Receptor, ErbB-4. Receptors, Growth Factor / metabolism. Sex Hormone-Binding Globulin / metabolism. Testosterone / metabolism. Transplantation, Heterologous

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  • (PMID = 15556875.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / Growth Substances; 0 / Interleukins; 0 / Receptors, Androgen; 0 / Receptors, Growth Factor; 0 / Sex Hormone-Binding Globulin; 3XMK78S47O / Testosterone; EC 1.3.99.5 / 3-Oxo-5-alpha-Steroid 4-Dehydrogenase; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-4
  • [Number-of-references] 67
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24. Margiotti K, Wafa LA, Cheng H, Novelli G, Nelson CC, Rennie PS: Androgen-regulated genes differentially modulated by the androgen receptor coactivator L-dopa decarboxylase in human prostate cancer cells. Mol Cancer; 2007;6:38
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  • [Title] Androgen-regulated genes differentially modulated by the androgen receptor coactivator L-dopa decarboxylase in human prostate cancer cells.
  • BACKGROUND: The androgen receptor is a ligand-induced transcriptional factor, which plays an important role in normal development of the prostate as well as in the progression of prostate cancer to a hormone refractory state.
  • We have also shown that DDC is a neuroendocrine (NE) marker of prostate cancer and that its expression is increased after hormone-ablation therapy and progression to androgen independence.
  • In the present study, we generated tetracycline-inducible LNCaP-DDC prostate cancer stable cells to identify DDC downstream target genes by oligonucleotide microarray analysis.
  • Changes in cellular gene transcription detected by microarray analysis were confirmed for selected genes by quantitative real-time RT-PCR.
  • CONCLUSION: Taken together, our results provide evidence for linking DDC action with AR signaling, which may be important for orchestrating molecular changes responsible for prostate cancer progression.
  • [MeSH-major] Adenocarcinoma / enzymology. Androgens. Dopa Decarboxylase / physiology. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / physiology. Neoplasms, Hormone-Dependent / enzymology. Prostatic Neoplasms / enzymology. Receptors, Androgen / physiology
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor / metabolism. Enzyme Induction / drug effects. Gene Expression Profiling. Genetic Vectors / pharmacology. Humans. Male. Oligonucleotide Array Sequence Analysis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / physiology. Reverse Transcriptase Polymerase Chain Reaction. Tetracycline / pharmacology. Transfection

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  • (PMID = 17553164.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Androgen; 0 / Recombinant Fusion Proteins; EC 4.1.1.- / Dopa Decarboxylase; F8VB5M810T / Tetracycline
  • [Other-IDs] NLM/ PMC1904238
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25. Buxhofer V, Ruckser R, Kier P, Habertheuer KH, Zelenka P, Tatzreiter G, Dorner S, Vedovelli H, Sebesta C, Hinterberger W: [High dosage therapy with stem cell transplantation in neuroendocrine carcinoma]. Acta Med Austriaca Suppl; 2000;52:37-9
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  • [Title] [High dosage therapy with stem cell transplantation in neuroendocrine carcinoma].
  • [Transliterated title] Hochdosistherapie mit Stammzelltransplantation beim neuroendokrinen Karzinom.
  • Neuroendocrine carcinoma and small-cell lung cancer (SCLC) are highly responsive to chemo- and radiotherapy.
  • At the 2nd department of medicine in the Donauspital, 4 pts. with neuroendocrine carcinomas of different primary sites underwent high-dose chemotherapy with autologous stem-cell transplantation (ASTx). Pt.
  • 1 suffered from neuroendocrine lung cancer, pt.
  • 4 presented with neuroendocrine carcinoma of the prostate.
  • After 4-6 cycles induction chemotherapy pts. were consolidated with 1 cycle of HDCht and ASTx.
  • 1, 2 and 4 died from relapse 10, 16 and 5 month after ASTx and 16, 22 and 9 month after diagnosis. Pts. with neuroendocrine carcinomas might be suitable candidates for HDCht and ASTx.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Small Cell / drug therapy. Hematopoietic Stem Cell Transplantation. Lung Neoplasms / drug therapy. Neuroendocrine Tumors / drug therapy
  • [MeSH-minor] Adult. Dose-Response Relationship, Drug. Humans. Male. Middle Aged. Neoplasm Staging. Survival Rate

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  • (PMID = 11261277.001).
  • [ISSN] 0303-8181
  • [Journal-full-title] Acta medica Austriaca. Supplement
  • [ISO-abbreviation] Acta Med Austriaca Suppl
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Austria
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26. Tsao KC, Wu JT: Development of an ELISA for the detection of serum chromogranin A (CgA) in prostate and non-neuroendocrine carcinomas. Clin Chim Acta; 2001 Nov;313(1-2):21-9
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  • [Title] Development of an ELISA for the detection of serum chromogranin A (CgA) in prostate and non-neuroendocrine carcinomas.
  • INTRODUCTION: Chromogranin A (CgA) is a glycoprotein found in neuroendocrine cells and may be useful as a tumor marker for neuroendocrine tumors.
  • METHODS: We developed an enzyme-linked immunosorbent assay (ELISA) for serum CgA on a microtiter plate.
  • For patients with prostate cancer, serum CgA was increased much earlier than serum PSA in approximately one-third of prostate cancer patients developing resistance to hormonal therapy.
  • CONCLUSIONS: The early rise of serum CgA provides an early signal for prostate cancer patients who developed resistance to hormonal therapy: this advance signal could create a critical window for therapy changes to be made before diseases progress to a fatal stage.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma, Neuroendocrine / blood. Carcinoma, Neuroendocrine / urine. Chromogranin A. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. Reference Values. Sensitivity and Specificity

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  • (PMID = 11694235.001).
  • [ISSN] 0009-8981
  • [Journal-full-title] Clinica chimica acta; international journal of clinical chemistry
  • [ISO-abbreviation] Clin. Chim. Acta
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / CHGA protein, human; 0 / Chromogranin A; 0 / Chromogranins
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27. Ferrero-Poüs M, Hersant AM, Pecking A, Brésard-Leroy M, Pichon MF: Serum chromogranin-A in advanced prostate cancer. BJU Int; 2001 Nov;88(7):790-6
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  • [Title] Serum chromogranin-A in advanced prostate cancer.
  • OBJECTIVE: To determine the value of serum chromogranin A (CgA), a marker of neuroendocrine differentiation, for monitoring prostate cancer: CgA levels were related to three other tumour markers, i.e. total prostate-specific antigen (tPSA), prostatic acid phosphatase (PAP), neurone-specific enolase (NSE), and to testosterone, to assess the importance of hormone withdrawal.
  • PATIENTS AND METHODS: Serum samples (218) were obtained from 118 patients with prostate cancer, including 111 patients with advanced prostate cancer: 103 presented to our centre for systemic radionuclide therapy of painful skeletal metastases.
  • Testosterone was also measured with an IRMA assay; tPSA, PAP and NSE were assayed using the time-resolved amplified cryptate emission.
  • Patients resistant to endocrine treatments and with elevated tPSA (i.e. hormone-independent) showed increased CgA and NSE in 62% and 29%, respectively.
  • Patients with hormone-dependent prostate cancer (i.e. with a normal tPSA level) had elevated CgA in 59% but no abnormal NSE.
  • For 30 patients, blood samples were drawn and markers measured before and after systemic radionuclide therapy.
  • There was a significant increase in the CgA and tPSA concentrations after treatment (P=0.0146 and 0.0025, respectively).
  • CONCLUSIONS: In association with tPSA, serum CgA appears to be a promising marker for monitoring patients with prostate cancer.
  • [MeSH-minor] Acid Phosphatase. Antineoplastic Agents, Hormonal / therapeutic use. Chromogranin A. Drug Resistance, Neoplasm. Humans. Male. Phosphopyruvate Hydratase / blood. Prostate-Specific Antigen / blood. Protein Tyrosine Phosphatases / blood. ROC Curve. Sensitivity and Specificity. Testosterone / blood

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  • (PMID = 11890255.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / CHGA protein, human; 0 / Chromogranin A; 0 / Chromogranins; 3XMK78S47O / Testosterone; EC 3.1.3.2 / Acid Phosphatase; EC 3.1.3.2 / prostatic acid phosphatase; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.4.21.77 / Prostate-Specific Antigen; EC 4.2.1.11 / Phosphopyruvate Hydratase
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28. Uphoff J, Woziwodzki J, Schattka SO, Kollias A: [Loss of differentiation of a prostate adenocarcinoma after hormone therapy: the example of a metastasis in the spongy body of the penis]. Aktuelle Urol; 2008 Sep;39(5):373-7
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  • [Title] [Loss of differentiation of a prostate adenocarcinoma after hormone therapy: the example of a metastasis in the spongy body of the penis].
  • [Transliterated title] Differenzierungsverlust eines Adenokarzinoms der Prostata nach Hormontherapie: am Beispiel einer Schwellkörpermetastase des Penis.
  • Prostate cancer as the most frequent malignoma of the male is the main primary lesion.
  • Changes in the morphology of the prostate carcinoma are specially known for the occurrence of small-cell neuroendocrine and undifferentiated carcinomas.
  • Often prior to the transformation an anti-androgen therapy has been undertaken.
  • At this state of the disease, there is only the possibility of a palliative therapy with a poor prognosis.
  • The increasing histological dedifferentiation of the tumour tissue can make it difficult or even impossible to identify the primary lesion.
  • [MeSH-major] Adenocarcinoma / secondary. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma, Basal Cell / secondary. Carcinoma, Transitional Cell / secondary. Cell Transformation, Neoplastic / pathology. Diphosphonates / therapeutic use. Gonadotropin-Releasing Hormone / antagonists & inhibitors. Neoplasms, Multiple Primary / drug therapy. Penile Neoplasms / secondary. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biopsy. Bone Neoplasms / drug therapy. Bone Neoplasms / pathology. Bone Neoplasms / secondary. Bone Neoplasms / surgery. Combined Modality Therapy. Cystectomy. Diagnosis, Differential. Disease Progression. Humans. Lymphatic Metastasis. Male. Neoplasm Staging. Penis / pathology. Penis / surgery. Prostate / pathology. Prostate / surgery. Prostatectomy

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  • (PMID = 18798127.001).
  • [ISSN] 0001-7868
  • [Journal-full-title] Aktuelle Urologie
  • [ISO-abbreviation] Aktuelle Urol
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Diphosphonates; 33515-09-2 / Gonadotropin-Releasing Hormone
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29. Gilbert JA, Frederick LM, Ames MM: The aromatic-L-amino acid decarboxylase inhibitor carbidopa is selectively cytotoxic to human pulmonary carcinoid and small cell lung carcinoma cells. Clin Cancer Res; 2000 Nov;6(11):4365-72
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  • The carcinoid tumor is an uncommon neuroendocrine neoplasm the hallmark of which is excessive serotonin production.
  • Here, we report Western and Northern analyses detecting large quantities of AAAD polypeptide and mRNA in human carcinoid primary as well as metastatic tumors compared with normal surrounding tissues.
  • To assess the feasibility of targeting these high AAAD levels for chemotherapy, AAAD inhibitors carbidopa (alpha-methyl-dopahydrazine), alpha-monofluoromethyldopa (MFMD), and 3-hydroxybenzylhydrazine (NSD-1015) were incubated (72 h) with NCI-H727 human lung carcinoid cells.
  • Carbidopa (100 microM) decreased growth of (but did not kill) SK-N-SH neuroblastoma and A204 rhabdomyosarcoma cells and did not affect proliferation of DU 145 prostate, MCF7 breast, or NCI-H460 large cell lung carcinoma lines.
  • [MeSH-major] Aromatic Amino Acid Decarboxylase Inhibitors. Carbidopa / pharmacology. Carcinoid Tumor / drug therapy. Carcinoma, Small Cell / drug therapy. Enzyme Inhibitors / pharmacology. Lung Neoplasms / drug therapy
  • [MeSH-minor] Cell Division / drug effects. Humans. Ileum / enzymology. Liver / enzymology. Microscopy, Electron. Tumor Cells, Cultured

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  • (PMID = 11106255.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 58450
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Aromatic Amino Acid Decarboxylase Inhibitors; 0 / Enzyme Inhibitors; MNX7R8C5VO / Carbidopa
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30. Volante M, Marci V, Andrejevic-Blant S, Tavaglione V, Sculli MC, Tampellini M, Papotti M: Increased neuroendocrine cells in resected metastases compared to primary colorectal adenocarcinomas. Virchows Arch; 2010 Nov;457(5):521-7
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  • [Title] Increased neuroendocrine cells in resected metastases compared to primary colorectal adenocarcinomas.
  • Neuroendocrine differentiation has been described in rectal adenocarcinomas receiving neoadjuvant therapy prior to radical surgery, but its clinical relevance is controversial and no data are currently available in colorectal carcinoma metastases as compared to primary tumors.
  • In 47 patients, tumor metastases were resected 1 month to 12 years after chemotherapy and/or radiotherapy, while in the remaining seven patients no additional therapy after primary surgery was performed.
  • In primary tumors, neuroendocrine differentiation was found in 12/54 cases (22.2%) as compared to 25/54 metastatic lesions (46.3%; p = 0.01).
  • The presence of neuroendocrine phenotype was not correlated with any clinical pathological parameter nor with a different proliferation index.
  • However, patients having neuroendocrine cells in the primary tumor had a significantly shorter survival from the time of metastatic spread than those having not (33.3 vs. 55.5 months; p = 0.04).
  • In summary, our data show that colorectal carcinoma metastases contain a higher percentage of neuroendocrine differentiated cells as compared to their corresponding primaries, a finding possibly related to the influence of chemotherapy in neuroendocrine differentiation during colorectal carcinoma progression.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / secondary. Colorectal Neoplasms / pathology. Neoplasm Metastasis / pathology. Neuroendocrine Cells / pathology
  • [MeSH-minor] Adult. Aged. Cell Differentiation. Chromogranin A / biosynthesis. Female. Humans. Immunohistochemistry. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Lymphatic Metastasis / pathology. Male. Middle Aged. Neoplasm Staging. Ovarian Neoplasms / metabolism. Ovarian Neoplasms / secondary. Peritoneal Neoplasms / metabolism. Peritoneal Neoplasms / secondary

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  • (PMID = 20812018.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chromogranin A
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31. Petraki C, Vaslamatzis M, Petraki K, Revelos K, Alevizopoulos N, Papanastasiou P, Gregorakis A: Prostate cancer with small-cell morphology: an immunophenotypic subdivision. Scand J Urol Nephrol; 2005;39(6):455-63
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  • [Title] Prostate cancer with small-cell morphology: an immunophenotypic subdivision.
  • The streptavidin-biotin complex immunohistochemical method was used on paraffin-embedded tissue sections to test positivity for prostate-specific antigen, prostate-specific acid phosphatase, CD57, androgen receptors, CK8-18, epithelial membrane antigen, carcinoembryonic antigen, CD56, neuron-specific enolase, chromogranin, synaptophysin, serotonin, various hormones, thyroid transcriptional factor-1 and Ki-67/MIB1.
  • The final diagnosis was U-PC (Gleason score 10) in Group 1 (n=9) and pure or mixed neuroendocrine small-cell carcinoma in Group 2 (n=7).
  • He was then treated with cisplatin + etoposide and showed a PR for 3 months and survived for 5 months after the initiation of the second-line chemotherapy (CTH) treatment.
  • CONCLUSION: U-PC-SCM with a neuroendocrine immunophenotype is a histogenetically distinct entity with different clinical and laboratory manifestations which responds well to a cisplatin + etoposide CTH regimen.
  • [MeSH-minor] Acid Phosphatase. Aged. Aged, 80 and over. Antigens, CD57 / immunology. Antigens, CD57 / metabolism. Biopsy. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Prostate-Specific Antigen / immunology. Prostate-Specific Antigen / metabolism. Protein Tyrosine Phosphatases / immunology. Protein Tyrosine Phosphatases / metabolism. Retrospective Studies

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  • (PMID = 16303720.001).
  • [ISSN] 0036-5599
  • [Journal-full-title] Scandinavian journal of urology and nephrology
  • [ISO-abbreviation] Scand. J. Urol. Nephrol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antigens, CD57; 0 / Biomarkers, Tumor; EC 3.1.3.2 / Acid Phosphatase; EC 3.1.3.2 / prostatic acid phosphatase; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.4.21.77 / Prostate-Specific Antigen
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32. Yashi M, Terauchi F, Nukui A, Ochi M, Yuzawa M, Hara Y, Morita T: Small-cell neuroendocrine carcinoma as a variant form of prostate cancer recurrence: a case report and short literature review. Urol Oncol; 2006 Jul-Aug;24(4):313-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small-cell neuroendocrine carcinoma as a variant form of prostate cancer recurrence: a case report and short literature review.
  • BACKGROUND: Small-cell neuroendocrine carcinoma has been recognized as a rare histologic variant occurring in only 0.5% to 2% of prostatic primary tumors.
  • CASE PRESENTATION: A case of conventional adenocarcinoma before androgen-ablation therapy but showing progression to small-cell neuroendocrine carcinoma at the recurrence.
  • The immunohistochemistry of the tumor showed strong positive staining for progastrin-releasing peptide (ProGRP), a carboxy terminal region common to 3 precursors for gastrin-releasing peptide, but almost negative staining for chromogranin-A and prostate-specific antigen.
  • Combination chemotherapy based on cisplatin and etoposide was effective for controlling the tumor progression for 7 months, and the serum ProGRP level correlated well to the clinical course.
  • Neither objective nor subjective responses were observed to somatostatin analogue therapy performed in the late stage of disease.
  • CONCLUSIONS: The present case reminds the urologist that small-cell neuroendocrine carcinoma may be a variant form of disease recurrence during androgen ablation in advanced prostate cancer.
  • A strategic approach for this phenotype evaluating serum neuroendocrine markers, such as ProGRP, should be taken when serum prostate-specific antigen does not reflect the disease state.
  • This approach would allow one to choose alternative therapies targeting neuroendocrine cells other than androgen ablation.
  • [MeSH-major] Carcinoma, Small Cell / pathology. Neoplasm Recurrence, Local / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Chromogranin A. Chromogranins / blood. Humans. Immunohistochemistry. Male. Peptides / blood. Phosphopyruvate Hydratase / blood. Prostate-Specific Antigen / blood. Protein Precursors / blood

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  • (PMID = 16818183.001).
  • [ISSN] 1078-1439
  • [Journal-full-title] Urologic oncology
  • [ISO-abbreviation] Urol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Peptides; 0 / Protein Precursors; 0 / gastrin-releasing peptide precursor; EC 3.4.21.77 / Prostate-Specific Antigen; EC 4.2.1.11 / Phosphopyruvate Hydratase
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33. Kitamoto K, Hayashi T, Tamada S, Ezaki K, Kawashima H, Sugimura K, Nakatani T: [Neuroendocrine differentiation in adenocarcinoma of prostate during combined androgen blockade therapy: a case report]. Hinyokika Kiyo; 2005 Jan;51(1):33-5
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  • [Title] [Neuroendocrine differentiation in adenocarcinoma of prostate during combined androgen blockade therapy: a case report].
  • Prostatic neuroendocrine (NE) carcinoma is a rare disease with a poor prognosis because of its rapid progression and the androgen-independent characteristic, for which no successful therapy is available presently.
  • We report a case of NE differentiated prostate cancer, which was diagnosed as adenocarcinoma initially and progressed with NE differentiation during the combined androgen blockade therapy.
  • [MeSH-major] Adenocarcinoma / pathology. Androgen Antagonists / therapeutic use. Carcinoma, Neuroendocrine / pathology. Cell Transformation, Neoplastic / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Drug Resistance, Neoplasm. Humans. Magnetic Resonance Imaging. Male. Neoplasm Staging

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  • (PMID = 15732339.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Androgen Antagonists
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