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1. Ito H, Nishimura T, Abe H, Oka F, Miura T, Uchikoba T, Oaki Y: Adenocarcinoma of the prostate with ectopic antidiuretic hormone production: a case report. Hinyokika Kiyo; 2000 Jul;46(7):499-503
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  • [Title] Adenocarcinoma of the prostate with ectopic antidiuretic hormone production: a case report.
  • An 88-year-old patient with a poorly differentiated adenocarcinoma of the prostate gland was found to have all cardinal findings of syndrome of inappropriate antidiuretic hormone secretion (SIADH).
  • Elevated levels of antidiuretic hormone were found in the patient's serum and in the prostatic tumor and the cytoplasms of the tumor was positive for prostate specific antigen and was faintly positive for antidiuretic hormone (ADH).
  • He responded well to combination therapy of androgen blockade with leuprorelin acetate and flutamide, and laboratory findings of SIADH and serum ADH level returned to normal.
  • However, he died of sudden profuse bleeding caused by gastric ulcers 6 months after the therapy.
  • [MeSH-major] Adenocarcinoma / secretion. Paraneoplastic Endocrine Syndromes. Prostatic Neoplasms / secretion. Vasopressins / secretion
  • [MeSH-minor] Aged. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Flutamide / therapeutic use. Humans. Inappropriate ADH Syndrome / drug therapy. Inappropriate ADH Syndrome / etiology. Leuprolide / therapeutic use. Male. Treatment Outcome

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  • (PMID = 10965460.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 11000-17-2 / Vasopressins; 76W6J0943E / Flutamide; EFY6W0M8TG / Leuprolide
  • [Number-of-references] 12
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2. Minami H, Kanagawa K, Watanabe Y, Sakakura T, Ito T, Kawamura M, Nakatani T, Kishimoto T: [Complete remission of brain metastases from prostate cancer by gamma knife radiosurgery: a case report]. Hinyokika Kiyo; 2001 May;47(5):333-6
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  • [Title] [Complete remission of brain metastases from prostate cancer by gamma knife radiosurgery: a case report].
  • The serum prostate specific antigen (PSA) level was within normal limits, and intravenous pyelography and urethrocystography showed no abnormal findings.
  • Because of his urinary retention, transurethral resection of prostate was performed under a clinical diagnosis of benign prostatic hyperplasia.
  • The pathological diagnosis was poorly differentiated adenocarcinoma of the prostate.
  • Not only combination hormone therapy with goserelin acetate and flutamide, but also intermittent arterial infusion chemotherapy with cisplatin (CDDP) and pirarubicin (THP) using a reservoir system was administered.
  • Magnetic resonance imaging (MRI) demonstrated that his prostate was reduced to less than 50% in size and he had no difficulty in voiding.
  • He suddenly developed dysarthria and hemiplegia 3 months later.
  • MRI and computed tomography (CT) revealed multiple brain metastases.
  • [MeSH-major] Adenocarcinoma / surgery. Brain Neoplasms / surgery. Prostatic Neoplasms / pathology. Radiosurgery


3. Kageyama S, Narita M, Kim CJ, Hanada E, Sakano Y, Iwaki H, Yoshiki T, Okada Y: [Small cell carcinoma of the prostate: a report of three patients and a prognostic analysis of cases reported in Japan]. Hinyokika Kiyo; 2006 Oct;52(10):809-15
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  • [Title] [Small cell carcinoma of the prostate: a report of three patients and a prognostic analysis of cases reported in Japan].
  • Small cell carcinoma (SCC) originating from the prostate is rare.
  • We report three cases of SCC of the prostate.
  • Case 1: A 29-year-old man with large pelvic mass and pelvic lymph node metastases was diagnosed as having pure SCC of the prostate.
  • Although cystoprostatectomy combined with pre- and post-operative chemotherapy ended with no evidence of disease, he died after 16 months because of multiple metastases and local recurrence.
  • Case 3: A 73-year-old man was diagnosed as having SCC and poorly differentiated adenocarcinoma of the prostate simultaneously.
  • Chemo-endocrine therapy and pelvic irradiation were performed, achieving partial remission.
  • However, he developed multiple distant metastases, and died of disease 15 months after diagnosis.
  • Thirty-seven (45%) were pure SCCs and 45 (55%) were associated with adenocarcinoma.

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  • (PMID = 17131874.001).
  • [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
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4. Segawa N, Inamoto T, Ibuki N, Mizutani Y, Azuma H, Tsuji M, Katsuoka Y: [Neuroendocrine differentiation in adenocarcinoma of the prostate during hormonal treatment : a case report]. Hinyokika Kiyo; 2010 Jan;56(1):49-54
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  • [Title] [Neuroendocrine differentiation in adenocarcinoma of the prostate during hormonal treatment : a case report].
  • A case of neuroendocrine (NE) differentiated prostate cancer is reported herein, which was progressed with NE differentiation during hormonal treatment in adenocarcinoma of the prostate.
  • A 65-year-old man was admitted to our department with increased serum prostate specific antigen (PSA) (150 ng/ml).
  • A prostate biopsy was performed and histological examinations indicated poorly differentiated adenocarcinoma with a Gleason score of 5 + 4 = 9.
  • The clinical stage was T3bN0M1b and hormonal therapy using leuprorelin was started.
  • Eighteen months after hormonal therapy, the serum PSA level declined to 1.702 ng/ml.
  • Computed tomography (CT) demonstrated enlargement of the prostate and swelling of multiple pelvic lymph nodes.
  • The treatment measure was changed from hormonal therapy to combination chemotherapy comprising cisplatin (CDDP) and irinotecan (CPT-11).
  • Pelvic radiotherapy (50 Gy) was then performed.
  • Two courses of the chemotherapy resulted in a great reduction of the tumor volume.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Antineoplastic Agents, Hormonal / therapeutic use. Leuprolide / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Cell Differentiation. Humans. Male. Phosphopyruvate Hydratase / analysis. Prostate-Specific Antigen / blood

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  • (PMID = 20104011.001).
  • [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; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; EC 3.4.21.77 / Prostate-Specific Antigen; EC 4.2.1.11 / Phosphopyruvate Hydratase; EFY6W0M8TG / Leuprolide
  • [Number-of-references] 26
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5. El Touny LH, Banerjee PP: Akt GSK-3 pathway as a target in genistein-induced inhibition of TRAMP prostate cancer progression toward a poorly differentiated phenotype. Carcinogenesis; 2007 Aug;28(8):1710-7
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  • [Title] Akt GSK-3 pathway as a target in genistein-induced inhibition of TRAMP prostate cancer progression toward a poorly differentiated phenotype.
  • Anti-proliferative properties of genistein in prostate and other cancers have been studied extensively.
  • In this study, we have demonstrated that the incorporation of genistein in the diet of transgenic adenocarcinoma mouse prostate model (TRAMP/FVB) mice resulted in a reduction in prostate size and the incidence of poorly differentiated (PD) cancer ensuing in an accumulation of prostates at the prostatic intra-epithelial neoplasia (PIN) stage.
  • TRAMP/FVB prostate cancer progression and the onset of PD cancer were characterized by the activation of acutely transforming retrovirus AKT8 in rodent T cell lymphoma (Akt), phosphorylation of glycogen synthase kinase 3-beta (GSK-3beta), post-transcriptional up-regulation of cyclin D1 and repression of cadherin-1 via snail-1 up-regulation.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cell Differentiation / genetics. Dietary Supplements. Genistein / administration & dosage. Glycogen Synthase Kinase 3 / physiology. Prostatic Neoplasms / drug therapy. Proto-Oncogene Proteins c-akt / physiology. Signal Transduction / drug effects
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Disease Models, Animal. Disease Progression. Dose-Response Relationship, Drug. Drug Delivery Systems. Female. Male. Mice. Mice, Transgenic. Phenotype


6. Challagundla S, Gokden M, Viswamitra S, Kohli M: Orbital metastasis from prostate cancer: an atypical case of neuroendocrine dedifferentiation during progression from hormone-sensitive to refractory stage. Clin Prostate Cancer; 2005 Sep;4(2):134-7
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  • [Title] Orbital metastasis from prostate cancer: an atypical case of neuroendocrine dedifferentiation during progression from hormone-sensitive to refractory stage.
  • We report a case of orbital metastasis from a neuroendocrine dedifferentiated prostate cancer during progression from hormone-sensitive to hormone refractory stage.
  • A patient receiving androgen deprivation for hormone-sensitive prostate cancer presented with sudden-onset right-sided ptosis and an increasing serum prostate-specific antigen level.
  • Comparison of the metastatic histology with the original pathology confirmed a histologic change to poorly differentiated prostate adenocarcinoma with neuroendocrine features.
  • Local radiation of the lesion and palliative systemic chemotherapy resulted in marked short-term improvement of all presenting symptoms.
  • Because prostate cancer metastasis involves hematogenous and lymphatic routes, we also evaluated expression of the vascular endothelial growth factor (VEGF) and receptors (VEGFR-1, VEGFR-2, and VEGFR-3) in the metastatic deposit by immunohistochemistry.
  • We recommend a second biopsy of atypical prostate metastasis associated with sudden change to aggressive clinical behavior in order to evaluate for dedifferentiation features before planning appropriate treatment interventions especially in patients who are candidates for systemic chemotherapy.
  • [MeSH-minor] Humans. Male. Middle Aged. Neoplasms, Hormone-Dependent / drug therapy. Receptors, Vascular Endothelial Growth Factor / analysis. Synaptophysin / analysis. Vascular Endothelial Growth Factor A / analysis

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  • (PMID = 16197616.001).
  • [ISSN] 1540-0352
  • [Journal-full-title] Clinical prostate cancer
  • [ISO-abbreviation] Clin Prostate Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Synaptophysin; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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7. Nabeshima S, Kishihara Y, Nabeshima A, Yamaga S, Kinjo M, Kashiwagi S, Hayashi J: Poorly differentiated adenocarcinoma with signet-ring cells of the Vater's ampulla, without jaundice but with disseminated carcinomatosis. Fukuoka Igaku Zasshi; 2003 Jul;94(7):235-40
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  • [Title] Poorly differentiated adenocarcinoma with signet-ring cells of the Vater's ampulla, without jaundice but with disseminated carcinomatosis.
  • The histological findings from bone marrow showed metastasis of adenocarcinoma with signet-ring cells, although the primary site was unknown.
  • To reduce tumor cells in number and improve DIC, 11 cycles of 5-Fluorouracil and leucovorin therapy were done, and the patient survived for 12 months.
  • Autopsy showed a 0.8 cm diameter, poorly differentiated adenocarcinoma with the signet-ring cell type in the lamina propria of the Vater's ampulla.
  • The sections of the stomach, the gallbladder, urinary bladder, prostate, and thyroid gland showed no malignant cells.
  • This is a rare case of an ampullary tumor of poorly differentiated adenocarcinoma with the signet-ring cell type, without jaundice but with multiple metastasis.
  • 5-Fluorouracil and leucovorin were effective for increasing survival time and improving quality of life.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disseminated Intravascular Coagulation / complications. Disseminated Intravascular Coagulation / drug therapy. Fatal Outcome. Fluorouracil / administration & dosage. Humans. Jaundice. Leucovorin / administration & dosage. Male. Middle Aged. Neoplastic Cells, Circulating / pathology. Quality of Life

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  • (PMID = 14509231.001).
  • [ISSN] 0016-254X
  • [Journal-full-title] Fukuoka igaku zasshi = Hukuoka acta medica
  • [ISO-abbreviation] Fukuoka Igaku Zasshi
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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8. Singh RP, Raina K, Sharma G, Agarwal R: Silibinin inhibits established prostate tumor growth, progression, invasion, and metastasis and suppresses tumor angiogenesis and epithelial-mesenchymal transition in transgenic adenocarcinoma of the mouse prostate model mice. Clin Cancer Res; 2008 Dec 1;14(23):7773-80
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  • [Title] Silibinin inhibits established prostate tumor growth, progression, invasion, and metastasis and suppresses tumor angiogenesis and epithelial-mesenchymal transition in transgenic adenocarcinoma of the mouse prostate model mice.
  • PURPOSE: The chronic nature of prostate cancer growth and progression leading to metastasis provides a large window for intervention.
  • Herein, for the first time, we investigated the effect and associated mechanisms of silibinin phosphatidylcholine (silybin-phytosome) on established prostate tumors in transgenic adenocarcinoma of the mouse prostate (TRAMP) model.
  • EXPERIMENTAL DESIGN: Twenty-week-old TRAMP male mice having palpable prostate tumor were fed with control or 0.5% and 1%, w/w, silybin-phytosome diets for 11 weeks and then sacrificed.
  • RESULTS: Dietary silibinin inhibited the growth of prostate tumors (up to 60%, P < 0.001) and suppressed tumor progression from prostatic intraepithelial neoplasia to differentiated adenocarcinoma and poorly differentiated adenocarcinoma, with a complete absence of poorly differentiated adenocarcinoma at higher doses.
  • CONCLUSIONS: Overall, silibinin treatment of TRAMP mice bearing prostate tumor inhibited tumor growth, progression, local invasion, and distant metastasis involving suppression of tumor angiogenesis and epithelial-mesenchymal transition.
  • These findings would have greater relevance for the ongoing phase II clinical trial with silibinin-phytosome in prostate cancer patients.

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  • (PMID = 19047104.001).
  • [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 / CA102514-05; United States / NCI NIH HHS / CA / R01 CA102514; United States / NCI NIH HHS / CA / R01 CA102514-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cadherins; 0 / Silymarin; 0 / Vimentin; 0 / silybin-phytosome; EC 3.4.24.- / Matrix Metalloproteinases
  • [Other-IDs] NLM/ NIHMS82719; NLM/ PMC2639624
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9. Chuang AY, DeMarzo AM, Veltri RW, Sharma RB, Bieberich CJ, Epstein JI: Immunohistochemical differentiation of high-grade prostate carcinoma from urothelial carcinoma. Am J Surg Pathol; 2007 Aug;31(8):1246-55
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  • [Title] Immunohistochemical differentiation of high-grade prostate carcinoma from urothelial carcinoma.
  • The histologic distinction between high-grade prostate cancer and infiltrating high-grade urothelial cancer may be difficult, and has significant implications because each disease may be treated very differently (ie, hormone therapy for prostate cancer and chemotherapy for urothelial cancer).
  • Immunohistochemistry of novel and established prostatic and urothelial markers using tissue microarrays (TMAs) were studied.
  • Prostatic markers studied included: prostate-specific antigen (PSA), prostein (P501s), prostate-specific membrane antigen (PSMA), NKX3.1 (an androgen-related tumor suppressor gene), and proPSA (pPSA) (precursor form of PSA).
  • TMAs contained 38 poorly differentiated prostate cancers [Gleason score 8 (n=2), Gleason score 9 (n=18), Gleason score 10 (n=18)] and 35 high-grade invasive urothelial carcinomas from radical prostatectomy and cystectomy specimens, respectively.
  • Each case had 2 to 8 tissue spots (0.6-mm diameter).
  • The sensitivities for labeling prostate cancers were PSA (97.4%), P501S (100%), PSMA (92.1%), NKX3.1 (94.7%), and pPSA (94.7%).
  • Because of PSA's high sensitivity on the TMA, we chose 41 additional poorly differentiated primary (N=36) and metastatic (N=5) prostate carcinomas which showed variable PSA staining at the time of diagnosis and performed immunohistochemistry on routine tissue sections.
  • These urothelial markers were relatively specific with only a few prostate cancers showing scattered (<or=2%) weak-moderate positive cells.
  • In summary, PSA can be used as the first screening marker for differentiating high-grade prostate adenocarcinoma from high-grade urothelial carcinoma.
  • Immunohistochemistry for P501S, PSMA, NKX3.1, and pPSA are useful when high-grade prostate cancer is suspected based on the morphology or clinical findings, yet shows negative or equivocal PSA staining.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / analysis. Carcinoma, Transitional Cell / secondary. Immunoenzyme Techniques / methods. Prostatic Neoplasms / pathology. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Male. Predictive Value of Tests. Tissue Array Analysis

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  • (PMID = 17667550.001).
  • [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 / Biomarkers, Tumor
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10. 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.
  • When TRAMP mice were treated in vivo with ATRA for either 6 or 8 weeks at low, medium, or high dose, mice on average presented with lower grade and more differentiated tumors.
  • However, ATRA therapy conferred no significant protection on incidence of tumors or frequency of metastasis at any dose.
  • As well, expression of the cell cycle inhibitor p21 was found to be elevated only in well-differentiated tumors of mice, treated with ATRA while expression of p27, was found to be elevated only in the poorly differentiated tumors.
  • 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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11. Sargeant AM, Rengel RC, Kulp SK, Klein RD, Clinton SK, Wang YC, Chen CS: OSU-HDAC42, a histone deacetylase inhibitor, blocks prostate tumor progression in the transgenic adenocarcinoma of the mouse prostate model. Cancer Res; 2008 May 15;68(10):3999-4009
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  • [Title] OSU-HDAC42, a histone deacetylase inhibitor, blocks prostate tumor progression in the transgenic adenocarcinoma of the mouse prostate model.
  • Here, we examined the effect of dietary administration of OSU-HDAC42, a novel HDAC inhibitor, on prostate tumor progression in the transgenic adenocarcinoma of the mouse prostate (TRAMP) model.
  • Based on a series of pilot studies, an AIN-76A diet was formulated containing 208 ppm OSU-HDAC42, which was estimated to deliver approximately 25 mg/kg of drug per day to each mouse and found to cause a suppression of PC-3 xenograft tumor growth equivalent to that achieved by gavage administration of a similar dose.
  • At 6 weeks of age, TRAMP mice received this drug-containing or control diet for 4 or 18 weeks and were evaluated for prostatic intraepithelial neoplasia (PIN) and carcinoma development, respectively.
  • OSU-HDAC42 not only decreased the severity of PIN and completely prevented its progression to poorly differentiated carcinoma (74% incidence in controls versus none in drug-treated mice), but also shifted tumorigenesis to a more differentiated phenotype, suppressing absolute and relative urogenital tract weights by 86% and 85%, respectively, at 24 weeks of age.
  • With the exception of completely reversible hematologic alterations and testicular degeneration, no significant changes in body weight or other indicators of general health were observed in drug-treated mice.
  • These results suggest that OSU-HDAC42 has value in prostate cancer prevention.
  • [MeSH-major] Adenocarcinoma / drug therapy. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Phenylbutyrates / pharmacology. Prostatic Neoplasms / drug therapy

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  • (PMID = 18483287.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA112250
  • [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 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / OSU-HDAC42 compound; 0 / Phenylbutyrates; 58IFB293JI / vorinostat
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12. Goto T, Maeshima A, Oyamada Y, Kato R: Solitary pulmonary metastasis from prostate sarcomatoid cancer. World J Surg Oncol; 2010;8:101
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  • [Title] Solitary pulmonary metastasis from prostate sarcomatoid cancer.
  • BACKGROUND: Pulmonary metastasis from prostate cancer is considered to be a late event, and patients can be treated with chemotherapy or hormonal manipulation.
  • However, there has been only a few reports on surgical resection for pulmonary metastasis from prostate cancer.
  • CASE PRESENTATION: We present a surgical case of solitary pulmonary metastasis from prostate cancer.
  • A 73-year-old man underwent pelvic evisceration for prostate cancer.
  • Histopathological examination revealed a poorly differentiated adenocarcinoma with a sarcomatoid carcinoma component.
  • During postoperative follow-up, chest computed tomography showed a nodular shadow in the lung, and thoracoscopic wedge resection of the lung was performed.
  • Histopathological examination revealed a histological appearance similar to that of the prostate sarcomatoid carcinoma.
  • This is the first reported case of solitary pulmonary metastasis from prostate sarcomatoid cancer.
  • CONCLUSION: Isolated pulmonary metastasis from prostate sarcomatoid cancer is extremely rare, but surgery could be the treatment of choice.
  • [MeSH-minor] Aged. Diagnosis, Differential. Follow-Up Studies. Humans. Male. Positron-Emission Tomography. Prostatectomy. Tomography, X-Ray Computed

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  • [Cites] Cancer. 1984 Dec 15;54(12):3078-84 [6498785.001]
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  • (PMID = 21092117.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2995788
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13. Fujimoto N, Harada S, Hida T, Matsumoto T: [Long-term survival of hormone-refractory prostate cancer: a case report]. J UOEH; 2001 Mar 1;23(1):51-8
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  • [Title] [Long-term survival of hormone-refractory prostate cancer: a case report].
  • Although prostate cancer initially responds well to endocrine therapy, it becomes resistant to the therapy a few years later, and is called hormone-refractory cancer.
  • In general, hormone-refractory prostate cancer is resistant to all kinds of therapy and the prognosis is extremely poor.
  • Here we report an unusual case of a person with hormone-refractory prostate cancer, who has been surviving for more than 5 years after being diagnosed as having this type of cancer.
  • A 75-year-old man was diagnosed with prostate cancer (poorly differentiated adenocarcinoma, T3 N0 M1, stage D2) and initial endocrine therapy combined with castration and estrogen was effective.
  • Four years later, the tumor marker of prostate-specific antigen (PSA) increased and the cancer was thought to be hormone-independent, refractory state.
  • When PSA rose again, we started oral chemotherapy with tegafur.uracil.
  • After that, a rapid increase of PSA was controlled for 7 months by oral chemotherapy with estramustine phosphate sodium and VP-16.
  • This case indicates that alteration of antiandrogens or oral chemotherapy may be useful in some cases with hormone-refractory prostate cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / administration & dosage. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Aged. Chlormadinone Acetate / administration & dosage. Chlormadinone Acetate / analogs & derivatives. Combined Modality Therapy. Enzyme Inhibitors / administration & dosage. Humans. Male. Orchiectomy. Survivors. Tegafur / administration & dosage. Uracil / administration & dosage

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  • (PMID = 11279841.001).
  • [ISSN] 0387-821X
  • [Journal-full-title] Journal of UOEH
  • [ISO-abbreviation] J. UOEH
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Enzyme Inhibitors; 0SY050L61N / Chlormadinone Acetate; 1548R74NSZ / Tegafur; 3114-44-1 / chlormadinol acetate; 56HH86ZVCT / Uracil
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14. Harper CE, Patel BB, Wang J, Arabshahi A, Eltoum IA, Lamartiniere CA: Resveratrol suppresses prostate cancer progression in transgenic mice. Carcinogenesis; 2007 Sep;28(9):1946-53
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  • [Title] Resveratrol suppresses prostate cancer progression in transgenic mice.
  • We hypothesized that resveratrol would exert a chemopreventive effect against prostate cancer via regulation of sex steroid receptor and growth factor signaling pathways.
  • In the current study, Transgenic Adenocarcinoma Mouse Prostate males were fed resveratrol (625 mg resveratrol per kg AIN-76A diet) or phytoestrogen-free, control diet (AIN-76A) starting at 5 weeks of age.
  • Resveratrol in the diet significantly reduced the incidence of poorly differentiated prostatic adenocarcinoma by 7.7-fold.
  • In the dorsolateral prostate, resveratrol significantly inhibited cell proliferation, increased androgen receptor, estrogen receptor-beta, and insulin-like growth factor-1 receptor, and significantly decreased insulin-like growth factor (IGF)-1 and phospho-extracellular regulating kinase 1 (phospho-ERK 1).
  • In the ventral prostate, resveratrol significantly reduced cell proliferation and phospho-ERKs 1 and 2, but did not significantly alter insulin-like growth factor-1 receptor and IGF-1.
  • Serum total testosterone, free testosterone, estradiol, dihydrotestosterone and sex hormone-binding globulin (SHBG) concentrations and Simian Virus-40 large T antigen expression in the prostate were not altered in resveratrol-treated mice.
  • The decrease in cell proliferation and the potent growth factor, IGF-1, the down-regulation of downstream effectors, phospho-ERKs 1 and 2 and the increase in the putative tumor suppressor, estrogen receptor-beta, provide a biochemical basis for resveratrol suppressing prostate cancer development.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Prostatic Neoplasms / drug therapy. Stilbenes / therapeutic use
  • [MeSH-minor] Animals. Cell Division / drug effects. Crosses, Genetic. Disease Progression. Female. Heterozygote. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic

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  • (PMID = 17675339.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 47888; United States / NCI NIH HHS / CA / P30 CA-13148-34
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Stilbenes; Q369O8926L / resveratrol
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15. Huss WJ, Barrios RJ, Greenberg NM: SU5416 selectively impairs angiogenesis to induce prostate cancer-specific apoptosis. Mol Cancer Ther; 2003 Jul;2(7):611-6
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  • [Title] SU5416 selectively impairs angiogenesis to induce prostate cancer-specific apoptosis.
  • We have previously demonstrated the differential expression in tumor-associated blood vessels of two vascular endothelial growth factor receptors (VEGFRs), VEGFR1 and VEGFR2, during initiation and progression of prostate cancer in the genetically engineered transgenic adenocarcinoma of the mouse prostate (TRAMP) mouse model.
  • In our "progression switch" model, expression of VEGFR1 is associated with early and more differentiated disease, whereas expression of VEGFR2 is associated with advanced and more poorly differentiated disease.
  • To test the hypothesis that stage-specific inhibition of vascular endothelial growth factor signaling could be used as therapy for autochthonous prostate cancer, we initiated a preclinical trial with SU5416, a potent antiangiogenic small molecule inhibitor of VEGFR associated tyrosine kinase activity.
  • In our early intervention trial, administration of SU5416 to TRAMP mice did not appear to influence angiogenesis or tumor progression between 10 and 16 weeks of age, a time corresponding to high levels of VEGFR1 expression.
  • In our late intervention trial, however, we observed a significant decrease in tumor-associated mean vessel density, increased apoptotic index, and pronounced regions of cell death when SU5416 was administered to TRAMP mice between 16 and 22 weeks of age, a time corresponding to high levels of VEGFR2 expression.
  • These results clearly demonstrate that therapy directed specifically against the VEGFR signaling axis can dramatically impair angiogenesis and induce apoptosis of autochthonous spontaneous and progressive prostate cancer.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Apoptosis / drug effects. Indoles / therapeutic use. Neovascularization, Pathologic / drug therapy. Prostatic Neoplasms / blood supply. Prostatic Neoplasms / pathology. Pyrroles / therapeutic use
  • [MeSH-minor] Animals. Cell Differentiation / physiology. Disease Models, Animal. Disease Progression. Drug Evaluation, Preclinical. Gene Expression Regulation, Neoplastic. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Microcirculation / pathology. Protein-Tyrosine Kinases / antagonists & inhibitors. Up-Regulation. Vascular Endothelial Growth Factor Receptor-1. Vascular Endothelial Growth Factor Receptor-2

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  • (PMID = 12883033.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA64851; United States / NCI NIH HHS / CA / CA84926
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Indoles; 0 / Pyrroles; 71IA9S35AJ / Semaxinib; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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16. Isayeva T, Chanda D, Kallman L, Eltoum IE, Ponnazhagan S: Effects of sustained antiangiogenic therapy in multistage prostate cancer in TRAMP model. Cancer Res; 2007 Jun 15;67(12):5789-97
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  • [Title] Effects of sustained antiangiogenic therapy in multistage prostate cancer in TRAMP model.
  • Antiangiogenic therapy is a promising alternative for prostate cancer growth and metastasis and holds great promise as an adjuvant therapy.
  • The present study evaluated the potential of stable expression of angiostatin and endostatin before the onset of neoplasia and during the early and late stages of prostate cancer progression in transgenic adenocarcinoma of mouse prostate (TRAMP) mice.
  • The effects of therapy were determined by sacrificing groups of treated mice at defined stages of tumor progression and following cohorts of similarly treated mice for long-term survival.
  • Results indicated remarkable survival after recombinant adeno-associated virus-(E+A) therapy only when the treatment was given at an earlier time, before the onset of high-grade neoplasia, compared with treatment given for invasive cancer.
  • Interestingly, early-stage antiangiogenic therapy arrested the progression of moderately differentiated carcinoma to poorly differentiated state and distant metastasis.
  • Immunohistochemical analysis of the prostate from treated mice indicated significantly lower endothelial cell proliferation and increased tumor cell apoptosis.
  • Vascular endothelial growth factor receptor (VEGFR)-2 expression was significantly down-regulated in tumor endothelium after treatment but not VEGFR-1.
  • Analysis of the neuroendocrine marker synaptophysin expression indicated that antiangiogenic therapy given at an early-stage disease reduced neuroendocrine transition of the epithelial tumors.
  • These studies indicate that stable endostatin and angiostatin gene therapy may be more effective for minimally invasive tumors rather than advanced-stage disease.
  • [MeSH-major] Adenocarcinoma / therapy. Angiogenesis Inhibitors / administration & dosage. Angiostatins / administration & dosage. Endostatins / administration & dosage. Prostatic Neoplasms / therapy
  • [MeSH-minor] Adenoviridae / genetics. Animals. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. Genetic Therapy / methods. Genetic Vectors. Immunohistochemistry. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Receptors, Vascular Endothelial Growth Factor / drug effects. Receptors, Vascular Endothelial Growth Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Synaptophysin / drug effects. Synaptophysin / metabolism

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  • (PMID = 17575146.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA98817
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Endostatins; 0 / Synaptophysin; 86090-08-6 / Angiostatins; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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17. 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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  • [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.
  • 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%).
  • 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


18. Uemura H, Hasumi H, Kawahara T, Sugiura S, Miyoshi Y, Nakaigawa N, Teranishi J, Noguchi K, Ishiguro H, Kubota Y: Pilot study of angiotensin II receptor blocker in advanced hormone-refractory prostate cancer. Int J Clin Oncol; 2005 Dec;10(6):405-10
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  • [Title] Pilot study of angiotensin II receptor blocker in advanced hormone-refractory prostate cancer.
  • BACKGROUND: We previously demonstrated that an angiotensin II receptor blocker (ARB) had the potential to inhibit cell proliferation of prostate cancer.
  • In this study, we examined whether an ARB could elicit an antiproliferative effect on hormone-refractory prostate cancer, clinically.
  • METHODS: Twenty-three patients with advanced hormone-refractory prostate cancer who had already received secondary hormonal therapy using dexamethasone, and who were no longer receiving conventional therapy, were enrolled.
  • Change in prostate-specific antigen (PSA) was determined as the primary endpoint.
  • To investigate angiotensin II type 1 (AT1) receptor expression in prostate cancer tissue, real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was performed, using specimens, from untreated patients with prostate cancer.
  • The mean time to PSA progression (TTPP) in responders was 8.3 months (range, 1-24 months).
  • Half of the patients showed stable or improved PS during treatment.
  • With regard to toxic effects, only one patient showed hypotension during treatment.
  • The RT-PCR showed that AT1 receptor expression in well-differentiated adenocarcinoma was higher than that in poorly differentiated adenocarcinoma.
  • CONCLUSION: These data showed that an ARB had potential biological effects on prostate cancer, suggesting the usefulness of the cytostatic activity of such agents on recurrent prostate cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Angiotensin II Type 1 Receptor Blockers / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Benzimidazoles / administration & dosage. Benzimidazoles / therapeutic use. Drug Resistance, Neoplasm. Humans. Male. Middle Aged. Pilot Projects. Prostate-Specific Antigen / metabolism. RNA, Messenger / metabolism. Receptor, Angiotensin, Type 1 / genetics. Receptor, Angiotensin, Type 1 / metabolism. Tetrazoles / administration & dosage. Tetrazoles / therapeutic use

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  • (PMID = 16369744.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; 0 / Antineoplastic Agents, Hormonal; 0 / Benzimidazoles; 0 / RNA, Messenger; 0 / Receptor, Angiotensin, Type 1; 0 / Tetrazoles; EC 3.4.21.77 / Prostate-Specific Antigen; S8Q36MD2XX / candesartan
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19. Huss WJ, Gray DR, Greenberg NM, Mohler JL, Smith GJ: Breast cancer resistance protein-mediated efflux of androgen in putative benign and malignant prostate stem cells. Cancer Res; 2005 Aug 01;65(15):6640-50
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  • [Title] Breast cancer resistance protein-mediated efflux of androgen in putative benign and malignant prostate stem cells.
  • Malignantly transformed stem cells represent a potential common nidus for the primary cancer and the recurrent cancer that arises after treatment failure.
  • Putative prostate stem cells and prostate tumor stem cells in benign and malignant human prostate tissue, in primary human prostate xenografts, and in the transgenic adenocarcinoma of the mouse prostate (TRAMP) mouse model of prostate cancer, are defined by expression of breast cancer resistance protein (BCRP), a marker of pluripotent hematopoietic, muscle, and neural stem cells, and by an absence of androgen receptor (AR) protein.
  • Inhibition of BCRP-mediated efflux of dihydrotestosterone by novobiocin or fumitremorgin C in a rat prostate progenitor cell line that expresses BCRP and AR mRNAs, but minimal AR protein, results in stabilization and nuclear translocation of AR protein, providing a mechanism for lack of AR protein in BCRP-expressing stem cells.
  • In both benign and malignant human prostate tissue, the rare epithelial cells that express BCRP and lack AR protein are localized in the basal cell compartment, survive androgen deprivation, and maintain proliferative potential in the hypoxic, androgen-deprived prostate.
  • Putative prostate tumor stem cells that express BCRP but not AR protein in TRAMP are the source of a BCRP-negative and AR-negative, Foxa2- and SV40Tag-expressing, transit amplifying compartment that progresses to the poorly differentiated carcinomas that arise rapidly after castration.
  • Therefore, BCRP expression isolates prostate stem/tumor stem cells from the prostate tissue microenvironment through constitutive efflux of androgen, protecting the putative tumor stem cells from androgen deprivation, hypoxia, or adjuvant chemotherapy, and providing the nidus for recurrent prostate cancer.
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Animals. Cell Line. Cell Nucleus / metabolism. Humans. Indoles / pharmacology. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Novobiocin / pharmacology. Prostate / metabolism. Protein Processing, Post-Translational. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Rats. Receptors, Androgen / biosynthesis. Receptors, Androgen / deficiency. Receptors, Androgen / genetics. Receptors, Androgen / metabolism. Transplantation, Heterologous

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  • (PMID = 16061644.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA84296; United States / NCI NIH HHS / CA / P01 CA077739; United States / NCI NIH HHS / CA / CA77739; United States / NCI NIH HHS / CA / CA64851; United States / NIEHS NIH HHS / ES / ES07017; United States / NCI NIH HHS / CA / CA64865
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; 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 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Androgens; 0 / Indoles; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Receptors, Androgen; 17EC19951N / Novobiocin; CW5S8OP3VO / tryptoquivaline
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20. Sakai H, Tsuruta T, Wajiki M: [Small cell carcinoma of the prostate: a case report]. Hinyokika Kiyo; 2004 Apr;50(4):269-71
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  • [Title] [Small cell carcinoma of the prostate: a case report].
  • He had undergone anti-androgen therapy for prostate cancer for 8 months at another hospital.
  • His serum prostate specific antigen (PSA) level was 14.4 ng/ml.
  • We performed a prostate biopsy and identified poorly differentiated adenocarcinoma with Gleason score 4 + 5.
  • After 4 months, his serum PSA level increased to 24.8 ng/ml, and we started maximum androgen blockade therapy using additional luteinizing hormone-releasing hormone (LH-RH) analogue.
  • The autopsy pathology of his prostate revealed small cell carcinoma.
  • We reviewed the initial biopsy specimens and found both small cell carcinoma and adenocarcinoma histologic types of prostate cancer.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma, Small Cell / drug therapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Fatal Outcome. Gonadotropin-Releasing Hormone / antagonists & inhibitors. Gonadotropin-Releasing Hormone / therapeutic use. Humans. Male. Prostate-Specific Antigen / blood

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  • (PMID = 15188622.001).
  • [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 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone; EC 3.4.21.77 / Prostate-Specific Antigen
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21. Kabeer MA, Lloyd-Davies E, Maskell G, Hohle R, Mathew J: Metastatic prostate cancer masquerading clinically and radiologically as a primary caecal carcinoma. World J Surg Oncol; 2007;5:2
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  • [Title] Metastatic prostate cancer masquerading clinically and radiologically as a primary caecal carcinoma.
  • We describe the case of a patient with metastatic prostate cancer to the bowel presenting clinically and radiologically as a primary caecal cancer.
  • Histology showed a poorly differentiated adenocarcinoma which was PSA positive, confirming metastatic prostatic adenocarcinoma to the caecum.
  • The patient underwent adjuvant chemotherapy and is free from recurrence a year later.
  • The treatment for metastatic prostate cancer is mainly palliative.
  • [MeSH-major] Adenocarcinoma / secondary. Cecal Neoplasms / secondary. Cecal Neoplasms / therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biopsy, Needle. Chemotherapy, Adjuvant. Colectomy / methods. Diagnosis, Differential. Follow-Up Studies. Gastrointestinal Hemorrhage / diagnosis. Gastrointestinal Hemorrhage / etiology. Humans. Immunohistochemistry. Male. Neoplasm Staging. Prostatectomy / methods. Rectum. Risk Assessment. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17207288.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1779271
  • [General-notes] NLM/ Original DateCompleted: 20070802
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22. Willman JH, Holden JA: Immunohistochemical staining for DNA topoisomerase II-alpha in benign, premalignant, and malignant lesions of the prostate. Prostate; 2000 Mar 1;42(4):280-6
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  • [Title] Immunohistochemical staining for DNA topoisomerase II-alpha in benign, premalignant, and malignant lesions of the prostate.
  • BACKGROUND: The DNA topoisomerase II-alpha (topo II-alpha)-targeting drug etoposide was recently shown to be an active agent in the combined chemotherapy of hormone-insensitive prostatic carcinoma.
  • Much experimental data indicate that cells sensitive to topo II-targeting chemotherapeutic drugs are rapidly proliferating and show elevated topo II expression.
  • There is little information concerning topo II expression in lesions of the prostate.
  • RESULTS: The average topo II-alpha index for well-differentiated prostatic adenocarcinomas (Gleason scores 2-4) was 1.5 +/- 0.9; for moderately differentiated tumors (Gleason scores 5-7), 3.1 +/- 2.4; and for poorly differentiated tumors (Gleason scores 8-10), 6.7 +/- 5.5.
  • The average topo II-alpha index of 2.3 (range, 0-8.6) for high-grade prostatic intraepithelial neoplasia was intermediate between the invasive tumors and benign prostate.
  • CONCLUSIONS: Topo II-alpha expression in carcinoma of the prostate correlates with Gleason score.
  • The carcinomas with the highest expression of enzyme are more poorly differentiated and have the highest Gleason scores.
  • [MeSH-major] Adenocarcinoma / enzymology. DNA Topoisomerases, Type II / analysis. Isoenzymes / analysis. Prostate / enzymology. Prostatic Hyperplasia / enzymology. Prostatic Intraepithelial Neoplasia / enzymology. Prostatic Neoplasms / enzymology

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10679757.001).
  • [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 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / Isoenzymes; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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23. Sato N, Kotake T, Masai M, Sakai S, Ito H: [Preventive effect of chlormadinone acetate on flare-up phenomenon in advanced prostate cancer administered with a luteinizing hormone-releasing hormone analogue]. Hinyokika Kiyo; 2000 Jan;46(1):1-7
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  • [Title] [Preventive effect of chlormadinone acetate on flare-up phenomenon in advanced prostate cancer administered with a luteinizing hormone-releasing hormone analogue].
  • To investigate whether chlormadinone acetate (CMA) could prevent the flare-up phenomenon induced by a luteinizing hormone-releasing hormone analogue (LH-RHa), we treated 4 cases of stage C and 17 cases of stage D prostate cancer with CMA for 4 weeks and CMA plus monthly injection of LH-RHa for following 24 weeks.
  • Serum LH, testosterone, and prostate-specific antigen (PSA) levels were closely monitored before and 3 days, 1-, 2-, and 4-weeks after LH-RHa injection.
  • Out of 21 cases, 3 cases (14%) consisting of 2 poorly and 1 moderately differentiated adenocarcinoma showed increased serum PSA levels 1 week after LH-RHa injection in spite of suppressed serum testosterone levels.
  • The objective response of these 2 poorly differentiated cases was progressive disease at 24 weeks.
  • CMA seemed to be capable of preventing flare-up phenomenon in advanced prostate cancer.
  • [MeSH-major] Acute-Phase Reaction / prevention & control. Adenocarcinoma / drug therapy. Antineoplastic Agents, Hormonal / adverse effects. Chlormadinone Acetate / administration & dosage. Prostatic Neoplasms / drug therapy. Triptorelin Pamoate / adverse effects
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / blood. Drug Therapy, Combination. Humans. Luteinizing Hormone / blood. Male. Neoplasm Staging. Prostate-Specific Antigen / blood. Testosterone / blood

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  • (PMID = 10723656.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0SY050L61N / Chlormadinone Acetate; 3XMK78S47O / Testosterone; 57773-63-4 / Triptorelin Pamoate; 9002-67-9 / Luteinizing Hormone; EC 3.4.21.77 / Prostate-Specific Antigen
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24. Donald CD, Cooper CR, Harris-Hooker S, Emmett N, Scanlon M, Cooke DB 3rd: Cytoskeletal organization and cell motility correlates with metastatic potential and state of differentiation in prostate cancer. Cell Mol Biol (Noisy-le-grand); 2001 Sep;47(6):1033-8
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  • [Title] Cytoskeletal organization and cell motility correlates with metastatic potential and state of differentiation in prostate cancer.
  • Correlations were found between metastatic potential phenotypic properties such as cell motility, cell spreading and cytoskeletal organization in prostate cancer.
  • As a cell progresses from a normal state to a malignant state, it loses its ability to function normally and also become poorly differentiated.
  • Differentiation therapy is concerned with the redirection of malignant cells toward a terminal, non-dividing state using non-cytotoxic agents.
  • Two well acknowledged differentiation agents, retinoic acid (RA) and diflouromethylomithine (DFMO) were examined for their ability to alter cellular phenotypes associated with metastatic potential in rat prostate cancer cell lines.
  • We also show that treatment of highly metastatic cells with either RA or DFMO significantly alters cell morphology, cell morphometry and motility to states similar to non-metastatic cells.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Movement. Cytoskeleton / ultrastructure. Prostatic Neoplasms / pathology
  • [MeSH-minor] Actins / analysis. Animals. Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. Eflornithine / pharmacology. Male. Microscopy, Confocal. Neoplasm Metastasis. Phenotype. Rats. Rats, Inbred Strains. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 11785653.001).
  • [ISSN] 0145-5680
  • [Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)
  • [ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Actins; 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin; ZQN1G5V6SR / Eflornithine
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25. Castilla C, Congregado B, Conde JM, Medina R, Torrubia FJ, Japón MA, Sáez C: Immunohistochemical expression of Hsp60 correlates with tumor progression and hormone resistance in prostate cancer. Urology; 2010 Oct;76(4):1017.e1-6
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  • [Title] Immunohistochemical expression of Hsp60 correlates with tumor progression and hormone resistance in prostate cancer.
  • OBJECTIVES: To investigate the expression of Hsp60 protein in prostate cancer biopsy samples, and its association with prognostic clinical parameters and hormone resistance and survival.
  • METHODS: We selected 107 patients with localized and locally advanced prostate cancer at our hospital from 1999 through 2004.
  • We performed an analysis by western blot and immunohistochemistry on paraffin-embedded tissue sections.
  • CONCLUSIONS: Hsp60 protein is overexpressed in poorly differentiated prostate cancers.
  • Identification of such markers could be of relevance in the clinical management of prostate cancer.
  • [MeSH-major] Adenocarcinoma / chemistry. Antineoplastic Agents, Hormonal / therapeutic use. Biomarkers, Tumor / analysis. Chaperonin 60 / analysis. Drug Resistance, Neoplasm. Neoplasm Proteins / analysis. Prostatic Neoplasms / chemistry
  • [MeSH-minor] Androgens. Cell Differentiation. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Kaplan-Meier Estimate. Lymphatic Metastasis. Male. Neoplasms, Hormone-Dependent / chemistry. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / pathology. Proportional Hazards Models. Prostate-Specific Antigen / blood. Survival Analysis

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20708221.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Chaperonin 60; 0 / Neoplasm Proteins; EC 3.4.21.77 / Prostate-Specific Antigen
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26. Ishizu K, Hirata H, Naito K, Sasaguri Y, Saito A: [Signet ring cell carcinoma of the prostate successfully treated with endocrine therapy: a case report]. Hinyokika Kiyo; 2003 May;49(5):281-3
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  • [Title] [Signet ring cell carcinoma of the prostate successfully treated with endocrine therapy: a case report].
  • The prostate was enlarged and stony hard.
  • The serum level of prostate specific antigen was abnormally high (46.2 ng/ml).
  • Prostatic biopsy showed signet ring cells which were stained positive for prostate specific antigen and poorly differentiated adenocarcinoma.
  • Endocrine therapy with luteinizing hormone-releasing hormone agonist was started.
  • After two months, the serum level of prostate specific antigen decreased to the normal range.
  • The pathological findings and the good response to endocrine therapy in our case suggest that signet ring cell carcinoma of the prostate is only a morphologic variant of ordinary prostatic adenocarcinoma.
  • [MeSH-major] Carcinoma, Signet Ring Cell / drug therapy. Gonadotropin-Releasing Hormone / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Drug Administration Schedule. Humans. Male

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  • (PMID = 12822458.001).
  • [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] 33515-09-2 / Gonadotropin-Releasing Hormone
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27. Tian Y, Leung W, Yue K, Mak N: Cell death induced by MPPa-PDT in prostate carcinoma in vitro and in vivo. Biochem Biophys Res Commun; 2006 Sep 22;348(2):413-20
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  • [Title] Cell death induced by MPPa-PDT in prostate carcinoma in vitro and in vivo.
  • Lack of effective photosensitizers has become a major limit for extensive application of photodynamic therapy.
  • In this study, the photocytotoxicity and mode of death induced by a newly developed photosensitizer MPPa, a derivative of chlorophyll a, were investigated in PC-3M cell line, a highly metastatic variant of poorly differentiated androgen-independent proctanec adenocarcinoma PC-3.
  • The photocytotoxicity of MPPa showed both light- and drug-dose dependent characteristics and no significant dark cytotoxicity was observed in PC-3M cells.
  • These results indicate the death way of cells induced by MPPa is mainly via mild apoptotic and the cure effect is obvious, suggesting that MPPa is a potential photosensitizer of photodynamic therapy for prostate cancer.
  • [MeSH-major] Photochemotherapy / methods. Porphyrins / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Apoptosis. Caspase 3. Caspase 8. Caspase 9. Caspases / metabolism. Cell Death / drug effects. Cell Line, Tumor. Darkness. Endothelium, Vascular / cytology. Endothelium, Vascular / drug effects. Humans. Male. Microscopy, Electron, Transmission

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  • (PMID = 16889752.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Porphyrins; 0 / pyropheophorbide-a methylester; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases
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28. Nakamura K, Teshima T, Takahashi Y, Imai A, Koizumi M, Mitsuhashi N, Inoue T, Japanese PCS Working Subgroup of Prostate Cancer: Radical radiation therapy for prostate cancer in Japan: a Patterns of Care Study report. Jpn J Clin Oncol; 2003 Mar;33(3):122-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radical radiation therapy for prostate cancer in Japan: a Patterns of Care Study report.
  • BACKGROUND: The patterns of radical radiation therapy for prostate cancer are unclear in Japan.
  • A Patterns of Care Study was performed throughout Japan to examine the patterns of radiation therapy for prostate cancer.
  • Detailed information was collected on a total of 311 prostate cancer patients without evidence of distant metastases, who were treated by radiation therapy between 1996 and 1998.
  • RESULTS: Eighty percent of the patients had high-risk diseases defined as T3 or T4 tumors, a pretreatment prostate-specific antigen level >20 ng/ml or poorly differentiated adenocarcinoma.
  • Androgen ablation was performed in 85.8% of patients and the median duration of hormonal therapy before and after radiation therapy was 5.3 and 21.4 months, respectively.
  • The median total dose of radiation therapy to the prostate was 65.0 Gy (range: 20-74 Gy).
  • CONCLUSIONS: The majority of the patients who received radical radiation therapy in Japan have high-risk disease.
  • Androgen ablation plus radiation therapy was commonly used to treat these patients and resulted in high rates of initial control with a low risk of complications.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / mortality. Adenocarcinoma / radiotherapy. Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Combined Modality Therapy. Humans. Male. Medical Audit. Middle Aged. Practice Patterns, Physicians'. Prostate-Specific Antigen / blood. Radiotherapy, Conformal. Radiotherapy, High-Energy. Survival Rate

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  • (PMID = 12672788.001).
  • [ISSN] 0368-2811
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; EC 3.4.21.77 / Prostate-Specific Antigen
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29. Mazzucchelli R, Montironi R, Santinelli A, Lucarini G, Pugnaloni A, Biagini G: Vascular endothelial growth factor expression and capillary architecture in high-grade PIN and prostate cancer in untreated and androgen-ablated patients. Prostate; 2000 Sep 15;45(1):72-9
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  • [Title] Vascular endothelial growth factor expression and capillary architecture in high-grade PIN and prostate cancer in untreated and androgen-ablated patients.
  • BACKGROUND: Recent studies have demonstrated that angiogenesis is a potent prognostic indicator for patients with prostate cancer (PCa) and have pointed out that the evaluation of vascular endothelial growth factor (VEGF) is useful in assessing the angiogenic phenotype in PCa.
  • The aim of the study was to investigate immunohistochemically the expression of VEGF and its correlation with the pattern of capillary architecture in prostate cancer and high-grade prostatic intraepithelial neoplasia (PIN), in untreated and androgen-ablated patients.
  • METHODS: Forty-five patients who underwent radical prostatectomy (RP) for localized prostate carcinoma were recruited for this study.
  • The study population included two groups: 35 patients who did not receive chemo-, hormone, or radiation therapy before surgery, and 10 patients who were under complete androgen blockade (CAB) for 3 months at time of surgery.
  • VEGF was examined by immunohistochemistry, and its tissue expression was compared with the pattern of capillary architecture evaluated by immunostaining the endothelial antigen CD34.
  • RESULTS: In normal tissue, the intensity of the VEGF immunoreactivity in the cytoplasm of secretory cells ranged from negative to low.
  • All prostate cancer specimens stained positively, the intensity of the immunoreaction ranging from low to strong and being correlated with the Gleason score.
  • The other, characterized by a strong cytoplasmic immunoreaction similar to that of poorly differentiated tumors, was defined as pattern B.
  • CONCLUSIONS: Our immunohistochemical results indicate that significant levels of VEGF are present in prostate cancer and in a population of PIN lesions, expression being highest in association with NE cells.
  • [MeSH-major] Adenocarcinoma / blood supply. Androgen Antagonists / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Endothelial Growth Factors / biosynthesis. Lymphokines / biosynthesis. Neovascularization, Pathologic / physiopathology. Prostatic Intraepithelial Neoplasia / blood supply. Prostatic Neoplasms / blood supply
  • [MeSH-minor] Aged. Anilides / administration & dosage. Capillaries / anatomy & histology. Capillaries / drug effects. Capillaries / physiopathology. Goserelin / administration & dosage. Humans. Immunohistochemistry. Male. Middle Aged. Nitriles. Prostatectomy. Tosyl Compounds. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10960845.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Nitriles; 0 / Tosyl Compounds; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 0F65R8P09N / Goserelin; A0Z3NAU9DP / bicalutamide
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30. deVere White RW, Hackman RM, Soares SE, Beckett LA, Li Y, Sun B: Effects of a genistein-rich extract on PSA levels in men with a history of prostate cancer. Urology; 2004 Feb;63(2):259-63
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of a genistein-rich extract on PSA levels in men with a history of prostate cancer.
  • OBJECTIVES: To determine whether supplemental amounts of soy isoflavone (genistein-rich extract) would lower prostate-specific antigen (PSA) levels more than 50% in patients with prostate cancer (CaP).
  • An open-label pilot study was conducted for 6 months in which the patients took capsules containing the genistein-rich extract three times daily by mouth.
  • The subjects were in one of five groups: after radical retropubic prostatectomy (n = 9), after radiotherapy (n = 17), after both radical retropubic prostatectomy and radiotherapy (n = 6), off-cycle during hormonal therapy (intermittent hormones; n = 14), or active surveillance (n = 16).
  • The primary endpoint for the trial was a 50% reduction in the PSA level at 6 months compared with before treatment.
  • All 8 patients with lower PSA levels at 6 months were in the active surveillance (watchful waiting) treatment subgroup.
  • In the 9 patients with a partial response, 6 had pathologic findings that were moderately differentiated, 2 had well-differentiated findings, and 1 had poorly differentiated findings.
  • CONCLUSIONS: A genistein-rich extract as the sole treatment for CaP did not reduce PSA levels by 50% or more in 51 of 52 subjects.
  • Thus, it does not appear to be an effective treatment for CaP when given alone.
  • [MeSH-major] Adenocarcinoma / drug therapy. Biomarkers, Tumor / blood. Enzyme Inhibitors / therapeutic use. Genistein / therapeutic use. Neoplasm Proteins / blood. Phytotherapy. Plant Extracts / therapeutic use. Prostate-Specific Antigen / blood. Prostatic Neoplasms / drug therapy. Soybeans / chemistry
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Combined Modality Therapy. Disease Progression. Drugs, Chinese Herbal / therapeutic use. Follow-Up Studies. Humans. Male. Middle Aged. Pilot Projects. Prostatectomy. Protein-Tyrosine Kinases / antagonists & inhibitors. Reishi / chemistry. Testosterone / blood. Treatment Failure


31. Hamasaki T, Kondo Y, Ogata Y, Yoshida K, Kimura G, Shimizu H, Nishimura T: Advanced carcinoma of the prostatic urethra in a patient with marked response to chemotherapy, leading to preservation of the bladder. Int J Clin Oncol; 2010 Feb;15(1):109-11
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advanced carcinoma of the prostatic urethra in a patient with marked response to chemotherapy, leading to preservation of the bladder.
  • We performed transurethral resection of the prostate (TUR-P) for a 66-year-old man with benign prostatic hyperplasia.
  • Pathological examination diagnosed poorly differentiated urothelial carcinoma of the urethra with broad prostatic permeation.
  • Random bladder biopsies showed no malignancy, but a second TUR-P revealed urothelial carcinoma in the prostate and bladder neck.
  • Computed tomography (CT) showed lymph node metastases from para-aortic to right/left external iliac and left obturator nodes, so clinical stage T3N2M0 carcinoma of the prostatic urethra was diagnosed.
  • Given the presence of lymph node metastases, neoadjuvant chemotherapy using cisplatin 70 mg/m(2), ifosfamide 1.2 g/m(2) and docetaxel 70 mg/m(2) (PIT) was considered.
  • After chemotherapy, CT showed complete response (CR) of all lymph nodes.
  • Pathological findings of surgical specimens showed no residual carcinoma in the prostatic urethra or lymph nodes, although prostatic adenocarcinoma was recognized.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Prostatic Neoplasms / secondary. Urethral Neoplasms / drug therapy
  • [MeSH-minor] Aged. Humans. Lymph Node Excision. Lymphatic Metastasis. Male. Neoadjuvant Therapy. Prostatectomy. Prostatic Hyperplasia / surgery

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  • (PMID = 20087614.001).
  • [ISSN] 1437-7772
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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32. Dodiuk-Gad R, Ziv M, Loven D, Schafer J, Shani-Adir A, Dyachenko P, Rozenman D: Sister Mary Joseph's nodule as a presenting sign of internal malignancy. Skinmed; 2006 Sep-Oct;5(5):256-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A skin biopsy from the nodule showed mucinous adenocarcinoma.
  • The mass was removed and diagnosed as a poorly differentiated adenocarcinoma, staining positively for carcinoembryonic antigen, and negatively for CK20, CK7, prostate-specific antigen, and prostatic acid phosphatase.
  • On bronchoscopy, it was found to be an invasive adenocarcinoma, consistent with a primary tumor of the lung.
  • The patient received 4 cycles of combined chemotherapy with carboplatine and gemcitabine, with no improvement.
  • Following demonstration of intra-abdominal spread of disease by CT scan, a second line chemotherapy was instituted with paclitaxel.
  • The patient died 3 weeks later, 9 months after the diagnosis of adenocarcinoma of the lung.

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  • (PMID = 16957443.001).
  • [ISSN] 1540-9740
  • [Journal-full-title] Skinmed
  • [ISO-abbreviation] Skinmed
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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