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3. Mencobonii M, Tredici S, Rebella L, Bergaglio M, Galbusera V, Manzara A, Claudiani F, Malcangi B, Varaldo M: Effect of chemotherapy on somatostatin receptor detection with octreotide scintigraphy in hormone-refractory prostate cancer patients. Anticancer Res; 2006 May-Jun;26(3B):2233-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of chemotherapy on somatostatin receptor detection with octreotide scintigraphy in hormone-refractory prostate cancer patients.
  • BACKGROUND: Neuroendocrine cells have been found in all stages of prostate cancer.
  • Neuroendocrine differentiation of prostate adenocarcinoma is a possible target for therapeutic strategies, such as administration of GH analogs (e.g., somatostatin), especially in patients with hormone-refractory prostate cancer (HRPC).
  • The presence of receptors for these drugs in tumor cells and tissues is essential and is assessed with 111In-octreotide scintigraphy (Octreoscan).
  • The relationship between these receptors and chemotherapy, the new standard therapy for HRPC, is unknown.
  • Chemotherapy with a single agent was also administered to all patients.
  • Several metastases were positive in 37% of patients only, compared to 94% previously described in a chemotherapy-naive population.
  • CONCLUSION: Chemotherapy seemed to reduce the cellular receptors for somatostatin analogs.
  • [MeSH-major] Indium Radioisotopes. Octreotide / analogs & derivatives. Pentetic Acid / analogs & derivatives. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / radionuclide imaging. Receptors, Somatostatin / metabolism
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents, Phytogenic / therapeutic use. Bone Neoplasms / radionuclide imaging. Bone Neoplasms / secondary. Humans. Male. Middle Aged. Positron-Emission Tomography. Radiopharmaceuticals / metabolism. Taxoids / therapeutic use. Vinblastine / analogs & derivatives. Vinblastine / therapeutic use

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  • (PMID = 16821593.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Indium Radioisotopes; 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 0 / Taxoids; 142694-57-3 / SDZ 215-811; 15H5577CQD / docetaxel; 5V9KLZ54CY / Vinblastine; 7A314HQM0I / Pentetic Acid; Q6C979R91Y / vinorelbine; RWM8CCW8GP / Octreotide
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4. 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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5. Tokunaga M, Yasuda M, Osamura RY, Itoh J, Mukai M, Shima M, Usui Y, Masuda A, Miyakita H, Terachi T: Association of neuroendocrine differentiation with neoadjuvant hormone therapy effects in prostatic cancer. Oncol Rep; 2005 Jun;13(6):1081-7
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  • [Title] Association of neuroendocrine differentiation with neoadjuvant hormone therapy effects in prostatic cancer.
  • Histological therapeutic effects of neoadjuvant hormone therapy (NHT) in prostatic cancer were examined, focusing on the association with neuroendocrine differentiation (NED), using 69 radical prostatectomy cases.
  • According to the therapeutic effects, the cases are divided as follows: good response in 26 patients, intermediate in 20, poor in 23.
  • The histological therapeutic effects were significantly weaker in the CgA-positive group than the CgA-negative group (p=0.02).
  • In the biopsy specimens before NHT, CgA was positive in 46% (32/69) and there was no significant difference in histological therapeutic effects between the positive and negative groups.
  • However, the therapeutic effects were significantly weaker in 22 CgA-positive cases for both biopsy and prostatectomy specimens than in 18 CgA-negative cases for both specimens (p=0.001).
  • In conclusion, although it seems difficult to predict the therapeutic effects of NHT using the biopsy specimens of prostatic cancer, we believe that NED is negatively associated with histological response of prostatic cancer to NHT.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Cell Differentiation. Neoadjuvant Therapy. Prostatic Neoplasms / drug therapy

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  • (PMID = 15870925.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Chromogranins
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6. Peehl DM: Primary cell cultures as models of prostate cancer development. Endocr Relat Cancer; 2005 Mar;12(1):19-47
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  • [Title] Primary cell cultures as models of prostate cancer development.
  • This review focuses on primary cultures of human prostatic epithelial cells and their applications as models of normal and malignant biological behavior.
  • Current abilities to culture cells from normal tissues, from premalignant dysplastic lesions (prostatic intraepithelial neoplasia), from primary adenocarcinomas, and from metastases are described.
  • Evidence for representation of the interrelated cells of the normal prostatic epithelium--stem cells, basal epithelial cells, secretory epithelial cells, transit amplifying cells and neuroendocrine cells--in primary cultures is presented.
  • Comparisons between normal and cancer-derived primary cultures are made regarding biological activities relevant to carcinogenesis, such as proliferation, apoptosis, differentiation, senescence, adhesion, migration, invasion, steroid hormone metabolism, other metabolic pathways and angiogenesis.
  • Analyses of tumor suppressor activity, differential gene expression and cytogenetics in primary cultures have revealed changes relevant to prostate cancer progression.
  • Preclinical studies with primary cultures have provided information useful for designing new strategies for chemoprevention, chemotherapy, cytotoxin therapy, radiation therapy, gene therapy and imaging.
  • While the behavior of normal primary cultures is often used as a basis for comparison with established, immortal prostate cancer cell lines, the most informative studies are performed with donor-matched pairs of normal and malignant primary cultures, grown under identical conditions.
  • [MeSH-major] Adenocarcinoma / pathology. Models, Biological. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Epithelial Cells / cytology. Gene Expression Regulation. Humans. Male. Neoplastic Stem Cells / pathology. Prostate / cytology

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  • (PMID = 15788637.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 230
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7. 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.
  • The material included primary prostatic adenocarcinoma (n = 18), lymph node metastases (n = 5), bone metastases (n = 2), and recurrent lesions (n = 10) showing NE differentiation at the immunohistochemical level.
  • RESULTS: Irrespective of grades, stages, and the degree of NE differentiation, DNA fragmentation was restricted to exocrine (ChrA-negative) tumor cells and was undetectable in most of NE tumor cells expressing ChrA.
  • 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-major] Adenocarcinoma / pathology. Apoptosis / physiology. Prostatic Neoplasms / pathology
  • [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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8. Pouessel D, Gallet B, Bibeau F, Avancès C, Iborra F, Sénesse P, Culine S: Liver metastases in prostate carcinoma: clinical characteristics and outcome. BJU Int; 2007 Apr;99(4):807-11
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  • [Title] Liver metastases in prostate carcinoma: clinical characteristics and outcome.
  • OBJECTIVE: To assess the clinical characteristics and outcome of patients with liver metastases in prostate carcinoma.
  • PATIENTS AND METHODS: From January 1995 to December 2005, 345 patients with metastatic prostate cancer were prospectively recorded in the database of the Montpellier Cancer Centre, France.
  • The clinical characteristics and outcome of 28 patients who developed liver metastases during the course of the disease were analysed.
  • Serum measurement of neuroendocrine markers showed increased levels of chromogranin A and neurone-specific enolase in 84% and 44% of patients, respectively.
  • Six patients had a pathological analysis; there were two different histological patterns in liver biopsies, i.e. four were adenocarcinomas with a moderate (one patient) or poor (three) differentiation and two were neuroendocrine carcinomas.
  • Three patients had no treatment because of a poor performance status.
  • One patient had hormone therapy for synchronous liver metastases at diagnosis as the first-line treatment; other patients were treated with chemotherapy.
  • They are frequently associated with neuroendocrine characteristics.
  • [MeSH-major] Adenocarcinoma / secondary. Carcinoma, Neuroendocrine / secondary. Liver Neoplasms / secondary. Prostatic Neoplasms / pathology

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  • (PMID = 17155968.001).
  • [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 / Chromogranin A
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9. Sciarra A, Cardi A, Dattilo C, Mariotti G, Di Monaco F, Di Silverio F: New perspective in the management of neuroendocrine differentiation in prostate adenocarcinoma. Int J Clin Pract; 2006 Apr;60(4):462-70
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  • [Title] New perspective in the management of neuroendocrine differentiation in prostate adenocarcinoma.
  • In this review, we will present some of the information that is known about neuroendocrine (NE) cells and differentiation in the prostate.
  • We will then speculate on the potential role that NE differentiation in prostate carcinoma may play and how this differentiation may be clinically analysed and treated.
  • The androgen-independent growth of prostate cancer can be caused by different mechanisms; one of these is receptor-specific paracrine or autocrine growth modulation of human prostatic cancer cells by neuropeptides secreted by NE cells.
  • Our results affirm that different methods of androgen deprivation can influence the serum chromogranin A (CgA) levels to different extents in prostate cancer.
  • In particular, bicalutamide produces a significantly lower increase in serum CgA compared with castration therapy.
  • In the light of other evidence that supports a significant relationship between serum CgA levels, tissue CgA expression and NE activity, we hypothesise that bicalutamide may reduce the risk of NE cell hyperactivation in prostate cancer.
  • It is important to determine whether increases in CgA levels and NE cell activation are associated with progression towards hormone-independent prostate cancer.
  • We recently proposed as therapy of NE activation in hormone-independent prostate cancer, a combination of oestrogens and somatostatin analogues.
  • The combination of ethinyl estradiol and lanreotide had a favourable toxicity profile, offered objective and symptomatic responses in patients with limited treatment options and refractoriness to conventional hormonal therapy strategies and, in particular, offered a median overall survival that was superior to the 10-month median survival in patients with hormone refractory disease.
  • This combination therapy also sustains the novel concept in cancer treatment in which therapies may target not only cancer cells but also its microenvironment in combination, which can confer protection from apoptosis.
  • [MeSH-major] Adenocarcinoma / pathology. Neuroendocrine Tumors / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Antineoplastic Agents / therapeutic use. Cell Transformation, Neoplastic / drug effects. Humans. Immunohistochemistry. Male. Middle Aged. Nitriles. Tosyl Compounds. Treatment Outcome

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  • (PMID = 16620361.001).
  • [ISSN] 1368-5031
  • [Journal-full-title] International journal of clinical practice
  • [ISO-abbreviation] Int. J. Clin. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide
  • [Number-of-references] 44
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10. Cabrespine A, Guy L, Gachon F, Curé H, Chollet P, Bay JO: Circulating chromogranin a and hormone refractory prostate cancer chemotherapy. J Urol; 2006 Apr;175(4):1347-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Circulating chromogranin a and hormone refractory prostate cancer chemotherapy.
  • PURPOSE: Neuroendocrine differentiation is a frequent pattern in prostate adenocarcinoma.
  • CgA seems to be a useful indicator of neuroendocrine differentiation in patients with HRPC.
  • Baseline CgA and its variation during chemotherapy were studied.
  • Previous local radiotherapy and the duration of hormonal therapy were independent factors that influenced CgA.
  • There was no correlation between CgA and prostate specific antigen.
  • The chemotherapy response correlated with a CgA decrease of greater than 25%.
  • CONCLUSIONS: The current study suggests that CgA assessment facilitates patient selection by predicting the chemotherapy response and providing complementary information to follow the chemotherapy response.
  • [MeSH-major] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / blood. Carboplatin / therapeutic use. Chromogranins / blood. Mitoxantrone / therapeutic use. Paclitaxel / therapeutic use. Prostatic Neoplasms / blood. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Androgen Antagonists / therapeutic use. Chromogranin A. Humans. Male. Middle Aged. Treatment Failure

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  • (PMID = 16515996.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / CHGA protein, human; 0 / Chromogranin A; 0 / Chromogranins; BG3F62OND5 / Carboplatin; BZ114NVM5P / Mitoxantrone; P88XT4IS4D / Paclitaxel
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11. Nemoto K, Tomita Y: Neuroendocrine differentiation of localized prostate cancer during endocrine therapy. Scand J Urol Nephrol; 2007;41(6):558-60
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  • [Title] Neuroendocrine differentiation of localized prostate cancer during endocrine therapy.
  • A 74-year-old male was treated with endocrine therapy for localized prostate cancer.
  • After 25 months he complained of a swollen neck, and was diagnosed with prostate cancer with lymph node metastasis of neuroendocrine differentiation.
  • Neuroendocrine differentiation without elevation of conventional tumor markers is rare during the initial recurrent course of localized prostate cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Anilides / therapeutic use. Cell Differentiation / drug effects. Goserelin / therapeutic use. Nitriles / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Tosyl Compounds / therapeutic use
  • [MeSH-minor] Aged. Antineoplastic Agents, Hormonal / pharmacology. Antineoplastic Agents, Hormonal / therapeutic use. Humans. Lymphatic Metastasis. Male. Neoplasm Recurrence, Local / diagnosis. Prostate-Specific Antigen / blood

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  • (PMID = 17853028.001).
  • [ISSN] 0036-5599
  • [Journal-full-title] Scandinavian journal of urology and nephrology
  • [ISO-abbreviation] Scand. J. Urol. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Anilides; 0 / Antineoplastic Agents, Hormonal; 0 / Nitriles; 0 / Tosyl Compounds; 0F65R8P09N / Goserelin; A0Z3NAU9DP / bicalutamide; EC 3.4.21.77 / Prostate-Specific Antigen
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12. Bonkhoff H, Fixemer T: [Neuroendocrine differentiation in prostate cancer. An unrecognized and therapy-resistant phenotype]. Urologe A; 2004 Jul;43(7):836-42
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  • [Title] [Neuroendocrine differentiation in prostate cancer. An unrecognized and therapy-resistant phenotype].
  • Neuroendocrine (NE) differentiation frequently occurs in common prostatic malignancies and has attracted increasing attention in contemporary prostate cancer research.
  • This particular phenotype, however, usually escapes pathological and clinical detection in routine practice.
  • The present review focuses on the biological properties of NE tumor cells that make them resistant to androgen deprivation and radiation therapy.
  • Morphogenetic studies have identified intermediate phenotypes between the three basic cell types of the prostatic epithelium indicating their common origin from stem cells located in the basal cell layer.
  • Virtually all prostatic adenocarcinomas show NE differentiation as defined by the most commonly used endocrine marker chromogranin A.
  • Clinical studies suggest that the extent of NE differentiation increases with tumor progression and the development of androgen insensitivity.
  • NE differentiation exclusively occurs in the G0 phase of the cell cycle in which tumor cells are usually resistant to radiation therapy and cytotoxic drugs.
  • This indicates that the vast majority of NE tumor cells represent an immortal cell population in prostate cancer.
  • They derive through a process of intermediate differentiation from exocrine tumor cells, the most prevalent phenotype in common prostatic adenocarcinoma.
  • Elevated serum levels of chromogranin A in prostate cancer patients correlate with poor prognosis and are scarcely influenced by either androgen deprivation or chemotherapy.
  • Looking for NE differentiation is recommended in the pathological and clinical evaluation of prostate cancer patients for whom radiation and androgen deprivation are therapeutic options.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Neuroendocrine Tumors / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Combined Modality Therapy. Diagnosis, Differential. Humans. Male. Prognosis. Prostate / pathology. Prostatectomy. Radiotherapy, Adjuvant. Treatment Failure

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  • [Cites] BJU Int. 2003 Mar;91(5):438-45 [12603395.001]
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  • (PMID = 15048555.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 30
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13. Sciarra A, Di Silverio F: Effect of nonsteroidal antiandrogen monotherapy versus castration therapy on neuroendocrine differentiation in prostate carcinoma. Urology; 2004 Mar;63(3):523-7
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  • [Title] Effect of nonsteroidal antiandrogen monotherapy versus castration therapy on neuroendocrine differentiation in prostate carcinoma.
  • OBJECTIVES: To determine whether the administration of the nonsteroidal antiandrogen bicalutamide reduces the risk of an increase in chromogranin A (CgA) levels in patients with prostate cancer who experienced biochemical failure after radical retropubic prostatectomy (RRP) compared with pharmacologic castration therapy.
  • It has been hypothesized that continuous androgen suppression for the treatment of prostate cancer results in hyperactivation of neuroendocrine cells and an increase in CgA levels.
  • METHODS: Forty-eight patients with pT3pN0M0 prostate cancer and biochemical (prostate-specific antigen) progression after RRP were randomized to bicalutamide monotherapy or pharmacologic castration.
  • The serum levels of CgA and prostate-specific antigen were measured at 1, 3, 6, 12, 18, and 24 months of therapy.
  • The changes in serum CgA levels were compared for patients who successfully responded to the first 24 months of therapy.
  • RESULTS: In both treatment groups, a statistically significant trend was noted for CgA levels to increase from baseline to 24 months.
  • CONCLUSIONS: The results of this study provide the first evidence to show that in patients with prostate cancer undergoing hormonal therapy, nonsteroidal antiandrogen monotherapy produces a significantly lower increase in serum CgA compared with castration.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgens. Anilides / therapeutic use. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Biomarkers, Tumor / blood. Chromogranins / blood. Neoplasm Proteins / blood. Neoplasms, Hormone-Dependent / drug therapy. Prostatic Neoplasms / drug therapy. Triptorelin Pamoate / therapeutic use
  • [MeSH-minor] Aged. Cell Differentiation. Chromogranin A. Disease Progression. Gonadotropin-Releasing Hormone / agonists. Humans. Lymph Node Excision. Male. Middle Aged. Neurosecretory Systems / pathology. Nitriles. Prostate-Specific Antigen / blood. Prostatectomy / methods. Tosyl Compounds

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  • (PMID = 15028450.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Anilides; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Chromogranins; 0 / Neoplasm Proteins; 0 / Nitriles; 0 / Tosyl Compounds; 33515-09-2 / Gonadotropin-Releasing Hormone; 57773-63-4 / Triptorelin Pamoate; A0Z3NAU9DP / bicalutamide; EC 3.4.21.77 / Prostate-Specific Antigen
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14. 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.
  • The pathogenesis of prostatic NEC has not yet been determined.
  • 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.
  • The NEC-bearing mice had smaller tumors in their prostates and lived longer than mice with adenocarcinoma (ADC-only).
  • 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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15. Culine S, El Demery M, Lamy PJ, Iborra F, Avancès C, Pinguet F: Docetaxel and cisplatin in patients with metastatic androgen independent prostate cancer and circulating neuroendocrine markers. J Urol; 2007 Sep;178(3 Pt 1):844-8; discussion 848
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  • [Title] Docetaxel and cisplatin in patients with metastatic androgen independent prostate cancer and circulating neuroendocrine markers.
  • PURPOSE: A link between neuroendocrine cell differentiation and resistance to androgen deprivation has been observed in prostate cancer, suggesting the possible efficacy of specific treatments.
  • We assessed the efficacy and toxicity of a chemotherapy regimen combining docetaxel and cisplatin in men with androgen independent prostatic adenocarcinoma and circulating neuroendocrine markers.
  • The primary study end point was the neuroendocrine response rate, defined as a decrease in neuron specific enolase and/or chromogranin A to 50% or greater of the supranormal baseline serum value.
  • A neuroendocrine response was observed in 13 patients (33%).
  • The prostate specific antigen response rate was 48%.
  • Five patients had to stop therapy due to toxicity.
  • Further studies are necessary to determine whether patients with circulating neuroendocrine markers require specific therapeutic approaches.
  • [MeSH-major] Adenocarcinoma / secondary. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / blood. Chromogranin A / blood. Phosphopyruvate Hydratase / blood. Prostatic Neoplasms / pathology


16. Inoue S, Oka K, Araki T, Yano A, Tacho T, Fujii M, Kimoto K, Murakami M, Ohshiro Y: [Neuroendocrine carcinoma of the prostate effectively treated by cisplatin and irinotecan--a case report]. Gan To Kagaku Ryoho; 2007 Aug;34(8):1323-5
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  • [Title] [Neuroendocrine carcinoma of the prostate effectively treated by cisplatin and irinotecan--a case report].
  • Because the serum PSA was 2,9 39 ng/mL,we performed transabdominal prostatic needle biopsy.
  • Pathological examination of the prostate revealed conventional adenocarcinoma.
  • He was treated with diethyl stilbestrol diphosphate,followed by maximal androgen blockade therapy,and the serum PSA level decreased favorably.
  • Follow-up CT revealed prostate and lymph node metastasis were reduced, but liver metastases, measuring 45 x 34 mm and 28 x 24 mm, respectively, were newly recognized in February 2006.
  • The NSE level was high at 88.5 ng/mL, so a percutaneous liver biopsy was performed,and pathological examination of the liver revealed metastatic prostate cancer which showed neuroendocrine differentiation.
  • The treatment was changed to chemotherapy comprising cisplatin and irinotecan.
  • After three courses of the chemotherapy,liver metastasis was reduced in CT scans.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymph Nodes / pathology. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Carcinoma, Neuroendocrine / pathology. Cisplatin / administration & dosage. Drug Administration Schedule. Humans. Liver Neoplasms / pathology. Liver Neoplasms / secondary. Lymphatic Metastasis. Male. Prostate-Specific Antigen / blood

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  • (PMID = 17687224.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 7673326042 / irinotecan; EC 3.4.21.77 / Prostate-Specific Antigen; Q20Q21Q62J / Cisplatin; XT3Z54Z28A / Camptothecin
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17. Molenaar JP, Baten A, Blokx WA, Hoogendam A: Development of carcinoid tumour in hormonally treated adenocarcinoma of the prostate. Eur Urol; 2009 Nov;56(5):874-7; quiz 876
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  • [Title] Development of carcinoid tumour in hormonally treated adenocarcinoma of the prostate.
  • We present the case of an 81-yr-old man with a prostatic adenocarcinoma and a metastatic carcinoid.
  • Simultaneous occurrence of hormonally treated adenocarcinoma of the prostate and a carcinoid has been described before.
  • The pathogenesis of this coincidence is largely unclear; however, androgen deprivation therapy might play a key role in neuroendocrine differentiation of adenocarcinoma cells.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoid Tumor / pathology. Liver Neoplasms / pathology. Neoplasms, Multiple Primary. Nitriles / therapeutic use. Prostatic Neoplasms / drug therapy. Tosyl Compounds / therapeutic use
  • [MeSH-minor] Aged, 80 and over. Biopsy. Humans. Male. Malignant Carcinoid Syndrome / drug therapy. Positron-Emission Tomography. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use

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  • (PMID = 19171417.001).
  • [ISSN] 1873-7560
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents, Hormonal; 0 / Nitriles; 0 / Tosyl Compounds; 51110-01-1 / Somatostatin; A0Z3NAU9DP / bicalutamide
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18. Wafa LA, Palmer J, Fazli L, Hurtado-Coll A, Bell RH, Nelson CC, Gleave ME, Cox ME, Rennie PS: Comprehensive expression analysis of L-dopa decarboxylase and established neuroendocrine markers in neoadjuvant hormone-treated versus varying Gleason grade prostate tumors. Hum Pathol; 2007 Jan;38(1):161-70
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  • [Title] Comprehensive expression analysis of L-dopa decarboxylase and established neuroendocrine markers in neoadjuvant hormone-treated versus varying Gleason grade prostate tumors.
  • Current hormone withdrawal therapies used for treatment of advanced prostate cancer lead to androgen-independent tumor growth.
  • Increased prostatic neuroendocrine (NE) cell density has been implicated in promoting progression of prostate cancer, but the process by which this occurs remains unclear.
  • The aim of this study was to determine whether there is an association of increased NE differentiation with neoadjuvant hormone therapy and Gleason grade.
  • Using adjacently sectioned tissue microarrays, the expression profile of novel and known NE markers were monitored.
  • L-Dopa decarboxylase (DDC), a catecholamine synthesis enzyme and androgen receptor (AR) coregulator protein, was identified as an additional NE marker of prostate cancer.
  • Immunohistochemical analysis of DDC with the established NE markers, chromogranin A and bombesin, revealed a significant increase in NE differentiation after 6 months of hormone therapy and after progression to androgen independence but no apparent correlation with Gleason grade.
  • Taken together, these results suggest that the increase of NE differentiation in prostate cancers depends specifically on duration of hormone therapy.
  • This increase may be due to the transdifferentiation of AR-expressing epithelial-derived adenocarcinoma cells into an NE cell phenotype.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Biomarkers, Tumor / biosynthesis. Dopa Decarboxylase / biosynthesis. Neurosecretory Systems / drug effects. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Bombesin / analysis. Cell Differentiation. Chromogranin A / analysis. Humans. Immunohistochemistry. Male. Middle Aged. Neoadjuvant Therapy. Neoplasm Staging. Receptors, Androgen / analysis. Severity of Illness Index

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  • (PMID = 16997353.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Receptors, Androgen; EC 4.1.1.- / Dopa Decarboxylase; PX9AZU7QPK / Bombesin
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19. Evans AJ, Humphrey PA, Belani J, van der Kwast TH, Srigley JR: Large cell neuroendocrine carcinoma of prostate: a clinicopathologic summary of 7 cases of a rare manifestation of advanced prostate cancer. Am J Surg Pathol; 2006 Jun;30(6):684-93
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  • [Title] Large cell neuroendocrine carcinoma of prostate: a clinicopathologic summary of 7 cases of a rare manifestation of advanced prostate cancer.
  • Neuroendocrine (NE) differentiation in prostate cancer is typically detected by immunohistochemistry as single cells in conventional adenocarcinoma.
  • Prostatic NE tumors, such as carcinoid or small cell carcinoma, are rare and large cell NE carcinoma (LCNEC) is described only in case reports.
  • In 6 cases, there was a history of adenocarcinoma treated with hormone therapy for a mean of 2.4 years (range: 2 to 3 y).
  • The mean patient age at diagnosis with LCNEC was 67 years (range: 43 to 81 y).
  • In 6 cases, there were foci of admixed adenocarcinoma, 4 of which showed hormone therapy effects.
  • There was strong bcl-2 overexpression, expression of MIB1, and p53 in >50% of nuclei, focally positive staining for prostate specific antigen and prostatic acid phosphatase and negative androgen receptor staining.
  • Follow-up was available for 6 patients, all of who died with metastatic disease at mean of 7 months (range: 3 to 12 mo) after platinum-based chemotherapy.
  • LCNEC of prostate is a distinct clinicopathologic entity that typically manifests after long-term hormonal therapy for prostatic adenocarcinoma and likely arises through clonal progression under the selection pressure of therapy.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Neuroendocrine / pathology. Neoplasms, Second Primary / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents, Hormonal / therapeutic use. Humans. Immunohistochemistry. Male. Middle Aged. Prostate-Specific Antigen / blood

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  • (PMID = 16723845.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; EC 3.4.21.77 / Prostate-Specific Antigen
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20. 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.
  • Metastases in the penis only occur at an advanced state of the tumour and with a high dedifferentiation, e. g., ductal adenocarcinoma.
  • 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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21. Spieth ME, Lin YG, Nguyen TT: Diagnosing and treating small-cell carcinomas of prostatic origin. Clin Nucl Med; 2002 Jan;27(1):11-7
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  • [Title] Diagnosing and treating small-cell carcinomas of prostatic origin.
  • PURPOSE: Small-cell carcinoma is very aggressive, metastasizes early and often, and does not respond to most chemotherapy regimens.
  • In approximately 50% of cases of prostate cancer, tumors are a combination of small-cell carcinoma and androgen-sensitive adenocarcinoma.
  • It is widely believed that no successful treatment exists for androgen-independent prostate cancer.
  • METHODS: A 67-year-old man had undergone androgen ablation therapy and radical prostatectomy for prostate cancer followed by bilateral orchiectomy, limited radiation therapy, and unsuccessful chemotherapy for pain-causing metastatic bone disease.
  • Biopsy and immunohistochemical analysis revealed neuroendocrine differentiation of the cancer.
  • Therapy with the cold somatostatin derivative resulted in a rapid and significant relief of pain with significant tumor shrinkage.
  • CONCLUSIONS: Somatostatin analogs and their radionuclide and cytotoxic derivatives are recommended as adjuvant treatments for prostate carcinoma, especially in those patients who are at high risk for carcinoma recurrence after radical prostatectomy and who have advanced prostate carcinoma at the time of relapse.
  • Because small-cell carcinomas of the prostate and lung are identical, these analogs may be useful in the detection and treatment of these tumors as well.
  • [MeSH-major] Carcinoma, Small Cell / diagnosis. Carcinoma, Small Cell / therapy. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Follow-Up Studies. Humans. Lung Neoplasms / diagnosis. Lung Neoplasms / secondary. Lung Neoplasms / therapy. Magnetic Resonance Imaging. Male. Prostatectomy. Radiotherapy, Adjuvant. Somatostatin / administration & dosage. Somatostatin / analogs & derivatives. Treatment Outcome

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  • (PMID = 11805477.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 51110-01-1 / Somatostatin
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22. Berruti A, Dogliotti L, Mosca A, Gorzegno G, Bollito E, Mari M, Tarabuzzi R, Poggio M, Torta M, Fontana D, Angeli A: Potential clinical value of circulating chromogranin A in patients with prostate carcinoma. Ann Oncol; 2001;12 Suppl 2:S153-7
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  • [Title] Potential clinical value of circulating chromogranin A in patients with prostate carcinoma.
  • BACKGROUND: Neuroendocrine (NE) differentiation of prostate adenocarcinoma has received increasing attention in recent years as a result of possible implications for prognosis and therapy.
  • METHODS: This article provides a review on published papers evaluating circulating CgA in prostate cancer patients.
  • RESULTS: Circulating CgA levels were found to be higher in prostate cancer patients than in patients with benign or pre-malignant prostatic diseases.
  • CgA levels did not correlate with serum prostate specific antigen (PSA) and were supranormal in the majority of advanced patients with PSA within normality.
  • CgA values were not substantially affected by either endocrine therapy or chemotherapy.
  • CONCLUSIONS: Present data suggest a potential role of circulating CgA in the management of prostate cancer patients.
  • Serial evaluation of circulating CgA could provide information on changes in the NE phenotype expression as a consequence of tumor progression and/or treatment administration.

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  • (PMID = 11762344.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Biomarkers, Tumor; 0 / CHGA protein, human; 0 / Chromogranin A; 0 / Chromogranins; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 42
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23. 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.
  • A prostatic pelvic mass was detected in 13 patients (72.2%).
  • 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.
  • The rise of the serum markers may aid in the diagnosis and follow-up of these patients.
  • [MeSH-major] Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology


24. Huss WJ, Lai L, Barrios RJ, Hirschi KK, Greenberg NM: Retinoic acid slows progression and promotes apoptosis of spontaneous prostate cancer. Prostate; 2004 Oct 1;61(2):142-52
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  • [Title] Retinoic acid slows progression and promotes apoptosis of spontaneous prostate cancer.
  • BACKGROUND: All-trans retinoic acid (ATRA) promotes terminal differentiation in epithelial cells and anti-angiogenesis and thus, may have beneficial effects in an intervention therapy for prostate cancer.
  • METHODS: We used the autochthonous spontaneous transgenic adenocarcinoma of the mouse prostate (TRAMP) model system to test the ability of ATRA to prevent initiation and progression of prostate cancer in a pre-clinical setting.
  • RESULTS: Initial studies demonstrated that exposure of TRAMP-derived C2N prostate tumor cells to ATRA in vitro decreased total viable cell numbers with a concomitant decrease in the fraction of cells in S phase.
  • However, ATRA therapy conferred no significant protection on incidence of tumors or frequency of metastasis at any dose.
  • Nevertheless, we were able to observe a significant decrease in the expression of synaptophysin, a marker of neuroendocrine differentiation, in tumors of mice receiving the highest dose of ATRA.
  • CONCLUSIONS: Collectively, our in vitro and in vivo data demonstrates that ATRA was able to slow prostate tumor cell proliferation, induce apoptosis, and block the emergence of the neuroendocrine phenotype.
  • Furthermore, our study suggests the differential regulation of p21 and p27 as a molecular mechanism whereby ATRA intervention therapy can inhibit the natural history of spontaneous prostate cancer.
  • [MeSH-major] Adenocarcinoma / physiopathology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Prostatic Neoplasms / physiopathology. Tretinoin / pharmacology
  • [MeSH-minor] Animals. Cell Cycle Proteins / drug effects. Cell Division / drug effects. Cell Line, Tumor. Disease Progression. Male. Mice

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc
  • (PMID = 15305337.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA64851; United States / NCI NIH HHS / CA / CA82847; United States / NHLBI NIH HHS / HL / HL61408
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cell Cycle Proteins; 5688UTC01R / Tretinoin
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25. Sasaki T, Komiya A, Suzuki H, Shimbo M, Ueda T, Akakura K, Ichikawa T: Changes in chromogranin a serum levels during endocrine therapy in metastatic prostate cancer patients. Eur Urol; 2005 Aug;48(2):224-9; discussion 229-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Changes in chromogranin a serum levels during endocrine therapy in metastatic prostate cancer patients.
  • INTRODUCTION: The concept of neuroendocrine (NE) differentiation in prostate cancer has become more widely recognized as its diagnostic, prognostic, and therapeutic usefulness.
  • PATIENTS AND METHODS: We enrolled 38 patients with stage D prostate cancer who underwent endocrine therapy by medical or surgical castration and oral antiandrogen.
  • According to PSA response, serum levels of CGA as a marker of NE differentiation were measured at the multiple points of time;.
  • (1) pre-treatment, (2) complete response (CR), (3) a nadir level of PSA, (4) PSA failure or hormone independent progression.
  • We compared these serum values in relation to efficacy of endocrine therapy.
  • Serum CGA increased as intervals of endocrine therapy became longer with positive correlation (p < 0.05).
  • CONCLUSION: During endocrine therapy in metastatic prostate cancer patients, serum CGA values were not related to serum PSA levels, and increased as treatment periods became longer.
  • It is suggested that CGA velocity has potential to predict androgen independent progression after endocrine therapy.
  • [MeSH-major] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Chromogranins / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Analysis of Variance. Biomarkers, Tumor / blood. Disease Progression. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Prostate-Specific Antigen / blood. Statistics, Nonparametric






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