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1. Zellweger T, Ninck C, Bloch M, Mirlacher M, Koivisto PA, Helin HJ, Mihatsch MJ, Gasser TC, Bubendorf L: Expression patterns of potential therapeutic targets in prostate cancer. Int J Cancer; 2005 Feb 10;113(4):619-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression patterns of potential therapeutic targets in prostate cancer.
  • Androgen withdrawal is the only effective therapy for patients with advanced prostate cancer, but progression to androgen independence ultimately occurs in almost all patients.
  • Here, we aimed to evaluate the expression of potential therapeutic targets in advanced prostate cancer.
  • A tissue microarray (TMA) containing samples from 535 tissue blocks was constructed, including benign prostatic hyperplasia as controls (n = 65), prostatic intraepithelial neoplasia (PIN; n = 78), clinically localized prostate cancers (n = 181), as well as hormone-refractory local recurrences (n = 120) and distant metastases (n = 91).
  • Significant overexpression in hormone-refractory prostate cancer and metastatic tissue compared to localized prostate cancer was found for Ki67 (64% vs. 9%), Bcl-2 (11% vs. 1%), p53 (35% vs. 4%), Syndecan-1 (38% vs. 3%), EGFR (16% vs. 1%) and HER2/neu (16% vs. 0%).
  • Taken together, p53, Bcl-2, Syndecan-1, EGFR and HER2/neu are preferentially expressed in hormone-refractory and metastatic prostate cancer.
  • Treatment decisions should not be based on findings in primary tumors but rather on tissues from recurrent or metastatic lesions.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / metabolism. Neoplasms, Hormone-Dependent / metabolism. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Humans. Immunoenzyme Techniques. Male. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology. Prostate / metabolism. Prostate / pathology. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial Neoplasia / metabolism. Prostatic Intraepithelial Neoplasia / pathology



2. Schmitz M, Grignard G, Margue C, Dippel W, Capesius C, Mossong J, Nathan M, Giacchi S, Scheiden R, Kieffer N: Complete loss of PTEN expression as a possible early prognostic marker for prostate cancer metastasis. Int J Cancer; 2007 Mar 15;120(6):1284-92
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  • [Title] Complete loss of PTEN expression as a possible early prognostic marker for prostate cancer metastasis.
  • The EGF/IGF growth factors are potent mitogens that regulate cell proliferation and cell survival and are involved in prostate cancer development.
  • Using laser microdissection technology and real-time PCR, together with immunohistochemistry, we have explored the growth factor and integrin dependent PI3-kinase/PTEN/Akt signalling pathway in prostate cell lines and tumour samples by analysing EGF-R, IGF1-R, ILK, beta3 integrin, PTEN and p-Akt protein expression.
  • We provide evidence that loss of PTEN expression rather than upregulated EGF/IGF1 receptor expression was responsible for increased p-Akt in neoplastic prostate cells.
  • In Study II, 25 of the 42 patients (59%) with lymph node metastasis had complete loss of PTEN expression in both the neoplastic glands of the prostate and the invasive prostate cancer cells in the lymph node, and of these 13 (52%) exhibited already loss of PTEN expression at first diagnosis.
  • These findings demonstrate that loss of PTEN expression is an important factor in progression towards metastatic disease and could potentially serve as an early prognostic marker for prostate cancer metastasis.
  • [MeSH-major] Adenocarcinoma / secondary. Biomarkers, Tumor / analysis. PTEN Phosphohydrolase / analysis. Prostate / pathology. Prostatic Neoplasms / pathology



3. Tan WW: Novel agents and targets in managing patients with metastatic prostate cancer. Cancer Control; 2006 Jul;13(3):194-8
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  • [Title] Novel agents and targets in managing patients with metastatic prostate cancer.
  • BACKGROUND: Docetaxel has recently been found to improve survival in patients with metastatic androgen-independent prostate cancer (AIPC).
  • METHODS: Clinically relevant articles focusing on chemotherapy drugs for metastatic prostate cancer and their mechanism of action and efficacy were reviewed from January 2004 through April 2006.
  • CONCLUSIONS: Docetaxel should be considered for first-line treatment of metastatic AIPC.
  • [MeSH-major] Adenocarcinoma / therapy. Bone Neoplasms / therapy. Prostatic Neoplasms / therapy



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4. Boyiadzis M, Nam M, Dahut W: Fulminant hepatic failure secondary to metastatic prostate cancer. Urol Int; 2005;74(2):185-7
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  • [Title] Fulminant hepatic failure secondary to metastatic prostate cancer.
  • The most common sites of metastatic disease from prostate cancer include the bones, lymph nodes and less commonly the lungs, adrenal glands, brain and kidneys.
  • We describe a case of fatal liver failure in a 71-year-old male due to metastases to the liver from a prostatic adenocarcinoma.
  • Thus in patients with metastatic cancer and elevated liver function tests, the possibility of hepatic involvement by the cancer should be considered as a possible cause of hepatic failure.
  • [MeSH-major] Adenocarcinoma / complications. Liver Failure, Acute / etiology. Liver Neoplasms / complications. Prostatic Neoplasms / pathology



5. Mimeault M, Johansson SL, Henichart JP, Depreux P, Batra SK: Cytotoxic effects induced by docetaxel, gefitinib, and cyclopamine on side population and nonside population cell fractions from human invasive prostate cancer cells. Mol Cancer Ther; 2010 Mar;9(3):617-30
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  • [Title] Cytotoxic effects induced by docetaxel, gefitinib, and cyclopamine on side population and nonside population cell fractions from human invasive prostate cancer cells.
  • The present study has been undertaken to establish the therapeutic benefit of cotargeting epidermal growth factor receptor (EGFR) and sonic hedgehog pathways by using gefitinib and cyclopamine, respectively, for improving the efficacy of the current chemotherapeutic drug docetaxel to counteract the prostate cancer progression from locally invasive to metastatic and recurrent disease stages.
  • The data from immuofluorescence analyses revealed that EGFR/Tyr(1173)-pEGFR, sonic hedgehog ligand, smoothened coreceptor, and GLI-1 were colocalized with the CD133(+) stem cell-like marker in a small subpopulation of prostate cancer cells.
  • These signaling molecules were also present in the bulk tumor mass of CD133(-) prostate cancer cells with a luminal phenotype detected in patient's adenocarcinoma tissues.
  • Altogether, these observations suggest that EGFR and sonic hedgehog cascades may represent the potential therapeutic targets of great clinical interest to eradicate the total prostate cancer cell mass and improve the current docetaxel-based therapies against locally advanced and invasive prostate cancers, and thereby prevent metastases and disease relapse.
  • [MeSH-major] Adenocarcinoma / pathology. Prostate / drug effects. Prostate / pathology. Prostatic Neoplasms / pathology. Quinazolines / pharmacology. Taxoids / pharmacology. Veratrum Alkaloids / pharmacology

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  • (PMID = 20179163.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA138791; United States / NCI NIH HHS / CA / R01 CA138791-03
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytotoxins; 0 / GLI1 protein, human; 0 / Quinazolines; 0 / Taxoids; 0 / Transcription Factors; 0 / Veratrum Alkaloids; 15H5577CQD / docetaxel; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib; ZH658AJ192 / cyclopamine
  • [Other-IDs] NLM/ NIHMS173400; NLM/ PMC3228252
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6. Moura FM, Garcia LT, Castro LP, Ferrari TC: Prostate adenocarcinoma manifesting as generalized lymphadenopathy. Urol Oncol; 2006 May-Jun;24(3):216-9
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  • [Title] Prostate adenocarcinoma manifesting as generalized lymphadenopathy.
  • Generalized lymphadenopathy is a rare manifestation of metastatic prostate cancer.
  • There were no urinary symptoms, and the serum prostate-specific antigen (PSA) was only mildly increased with a normal free PSA.
  • A biopsy of the supraclavicular lymph node was compatible with adenocarcinoma, whose prostatic origin was shown by immunohistochemical staining with PSA.
  • The origin of the primary tumor was confirmed by directed prostate biopsy.
  • We emphasize that a suspicion of prostate cancer in men with adenocarcinoma of undetermined origin is important for an adequate diagnostic and therapeutic approach.
  • [MeSH-major] Adenocarcinoma / diagnosis. Lymphatic Diseases / diagnosis. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Humans. Male. Prostate-Specific Antigen / analysis. Tomography, X-Ray Computed



7. Stanko C, Grandinetti L, Baldassano M, Mahmoodi M, Kantor GR: Epidermotropic metastatic prostate carcinoma presenting as an umbilical nodule-Sister Mary Joseph nodule. Am J Dermatopathol; 2007 Jun;29(3):290-2
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  • [Title] Epidermotropic metastatic prostate carcinoma presenting as an umbilical nodule-Sister Mary Joseph nodule.
  • Carcinoma of the prostate accounts for fewer than 1% of all skin metastases.
  • Cutaneous metastases from prostate carcinoma most often involve the penis, the anterior aspect of the thighs, the suprapubic area, and the perineum, but they also have been reported in the scalp, the chest, the back, and even the face.
  • We report an unusual case of metastatic prostate adenocarcinoma that presented as an umbilical nodule (Sister Mary Joseph nodule) and demonstrated significant epidermotropism histologically.
  • A review of the literature has found only one documented case of prostatic carcinoma metastasizing to the umbilicus, and one other documented case of epidermotropic metastatic prostate carcinoma.
  • [MeSH-major] Adenocarcinoma / secondary. Prostatic Neoplasms / pathology. Skin Neoplasms / secondary. Umbilicus / pathology

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  • (PMID = 17519629.001).
  • [ISSN] 0193-1091
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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8. Haidar A, Yassin A, Saad F, Shabsigh R: Effects of androgen deprivation on glycaemic control and on cardiovascular biochemical risk factors in men with advanced prostate cancer with diabetes. Aging Male; 2007 Dec;10(4):189-96
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  • [Title] Effects of androgen deprivation on glycaemic control and on cardiovascular biochemical risk factors in men with advanced prostate cancer with diabetes.
  • INTRODUCTION AND OBJECTIVE: Androgen deprivation therapy of prostate cancer with luteinizing hormone releasing hormone agonists may result in loss of bone mass, changes in body composition and a deterioration of arterial stiffness.
  • All men had insulin-dependent diabetes mellitus prior to being diagnosed with metastatic prostate cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / epidemiology. Blood Glucose / analysis. Diabetes Mellitus, Type 2 / epidemiology. Gonadotropin-Releasing Hormone / agonists. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / epidemiology

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  • (PMID = 18033628.001).
  • [ISSN] 1368-5538
  • [Journal-full-title] The aging male : the official journal of the International Society for the Study of the Aging Male
  • [ISO-abbreviation] Aging Male
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Hemoglobin A, Glycosylated; 0 / Triglycerides; 33515-09-2 / Gonadotropin-Releasing Hormone; 9001-32-5 / Fibrinogen; 9007-41-4 / C-Reactive Protein; 97C5T2UQ7J / Cholesterol
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9. Hainsworth JD, Meluch AA, Spigel DR, Yost K, Meng C, Greco FA: Weekly docetaxel/estramustine phosphate in patients with increasing serum prostate- specific antigen levels after primary treatment for prostate cancer: a phase II trial of the Minnie Pearl Cancer Research Network. Clin Genitourin Cancer; 2006 Mar;4(4):287-92
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  • [Title] Weekly docetaxel/estramustine phosphate in patients with increasing serum prostate- specific antigen levels after primary treatment for prostate cancer: a phase II trial of the Minnie Pearl Cancer Research Network.
  • PURPOSE: Docetaxel alone or in combination with estramustine prolongs survival in patients with metastatic hormone-refractory prostate cancer.
  • The role of chemotherapy is undefined in the treatment of patients who develop an increasing serum prostate-specific antigen (PSA) level after primary therapy but have no detectable metastases.
  • This phase II study was performed as a preliminary evaluation of the feasibility and efficacy of weekly docetaxel/estramustine in patients with prostate cancer and increasing serum PSA levels.
  • All patients had biopsy-proven adenocarcinoma of the prostate and had increasing PSA levels but no clinically or radiographically detected metastases after primary therapy.
  • CONCLUSION: Treatment with weekly docetaxel and estramustine is feasible and active in patients with prostate cancer and increasing serum PSA levels.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / drug therapy

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  • (PMID = 16729913.001).
  • [ISSN] 1558-7673
  • [Journal-full-title] Clinical genitourinary cancer
  • [ISO-abbreviation] Clin Genitourin Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel; 35LT29625A / Estramustine; EC 3.4.21.77 / Prostate-Specific Antigen
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10. Dorff TB, Shazer RL, Nepomuceno EM, Tucker SJ: Successful treatment of metastatic androgen-independent prostate carcinoma in a transsexual patient. Clin Genitourin Cancer; 2007 Jun;5(5):344-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of metastatic androgen-independent prostate carcinoma in a transsexual patient.
  • The occurrence of prostate carcinoma in transsexual patients has rarely been reported.
  • By definition, their disease is androgen-independent prostate cancer, and the role of local therapy is undefined.
  • We report on a male-to-female transsexual patient with metastatic prostate cancer treated successfully with combination chemotherapy after previous standard therapy failed.
  • [MeSH-major] Adenocarcinoma / drug therapy. Prostatic Neoplasms / drug therapy. Salvage Therapy. Transsexualism / pathology
  • [MeSH-minor] Aged. Androgen Antagonists / therapeutic use. Combined Modality Therapy. Female. Humans. Male. Prostate-Specific Antigen / blood

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  • (PMID = 17645834.001).
  • [ISSN] 1558-7673
  • [Journal-full-title] Clinical genitourinary cancer
  • [ISO-abbreviation] Clin Genitourin Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; EC 3.4.21.77 / Prostate-Specific Antigen
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11. Flannery T, Kano H, Niranjan A, Monaco EA 3rd, Flickinger JC, Lunsford LD, Kondziolka D: Stereotactic radiosurgery as a therapeutic strategy for intracranial metastatic prostate carcinoma. J Neurooncol; 2010 Feb;96(3):369-74
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  • [Title] Stereotactic radiosurgery as a therapeutic strategy for intracranial metastatic prostate carcinoma.
  • Intracranial metastatic prostate carcinoma is rare.
  • We sought to determine the clinical outcomes after Gamma Knife stereotactic radiosurgery (GKSRS) for patients with intracranial prostate carcinoma metastases.
  • The primary pathology was adenocarcinoma (eight patients) and small cell carcinoma (two patients).
  • SRS was a well tolerated and effective therapy either alone or as a boost to fractionated radiation therapy in the management of patients with intracranial prostate carcinoma metastases.
  • [MeSH-minor] Aged. Aged, 80 and over. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Magnetic Resonance Imaging / methods. Male. Middle Aged. Prostatic Neoplasms / pathology. Radiotherapy Dosage. Survival Rate

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  • (PMID = 19609490.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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12. Zhang J, Wilkinson JE, Gonit M, Keck R, Selman S, Ratnam M: Expression and sub-cellular localization of the CCAAT/enhancer binding protein alpha in relation to postnatal development and malignancy of the prostate. Prostate; 2008 Aug 1;68(11):1206-14
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  • [Title] Expression and sub-cellular localization of the CCAAT/enhancer binding protein alpha in relation to postnatal development and malignancy of the prostate.
  • There, is a paucity of information on the expression and sub-cellular localization of C/EBPalpha in normal mouse and human prostate and in prostate cancer.
  • RESULTS: In the mouse prostate epithelium, C/EBPalpha was present at 1 week postnatal localized in the cytosol, began to show nuclear localization at 8 weeks and continued to show prominent nuclear expression at 10 weeks and beyond; C/EBPalpha mRNA was expressed at all ages.
  • Most prostate adenocarcinomas expressed a range of levels of C/EBPalpha mRNA and protein that were relatively high in metastatic tumors in a manner that correlated with AR expression; however, most cells showed C/EBPalpha sequestered in the cytosol.
  • CONCLUSIONS: Temporal changes in sub-cellular localization of C/EBPalpha are consistent with a role in prostate differentiation and as a prostate tumor suppressor; the cytoplasmic sequestration of C/EBPalpha, unique to older human prostates, is arguably a permissive condition for the greater frequency of proliferative disorders of the prostate.
  • In malignant prostate C/EBPalpha may be available to regulate AR signaling through transient changes in its sub-cellular localization.

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  • [Copyright] Copyright (c) 2008 Wiley-Liss, Inc.
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  • (PMID = 18481268.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA103964; United States / NCI NIH HHS / CA / 5R01CA103964
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / RNA, Messenger; 0 / Receptors, Androgen
  • [Other-IDs] NLM/ NIHMS546003; NLM/ PMC3911780
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13. Ruiz-Martín I, Rodríguez-Sánchez CA, Ocaña-Fernández A, del Valle-Zapico J, Soto de Prado-Otero D, Cruz-Hernández JJ: Metastatic prostate cancer with a normal prostate-specific antigen level. Clin Transl Oncol; 2005 Oct;7(9):412-3
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  • [Title] Metastatic prostate cancer with a normal prostate-specific antigen level.
  • Prostate-specific antigen (PSA) is the most commonly used tumour marker for prostate cancer, both in screening and in follow-up.
  • However, there are many false positive increases in the presence of other prostate diseases and, currently, there is no consensus regarding sensitivity and specificity of the PSA test, nor what constitutes the upper limit of normality.
  • We report a case of a 67-year-old patient with metastatic prostate cancer who, with increased level of alkaline phosphatase and normal PSA, showed clinical and radiological evidence of progression of the disease.
  • [MeSH-major] Adenocarcinoma / blood. Bone Neoplasms / secondary. Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood



14. Kolias AG, Derham C, Mankad K, Hasegawa H, O'Kane R, Ismail A, Phillips NI: Multiple cranial neuropathy as the initial presentation of metastatic prostate adenocarcinoma: case report and review of literature. Acta Neurochir (Wien); 2010 Jul;152(7):1251-5
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  • [Title] Multiple cranial neuropathy as the initial presentation of metastatic prostate adenocarcinoma: case report and review of literature.
  • The skull base is an atypical metastatic site for prostate carcinoma.
  • However, skull base involvement causing cranial nerve palsies may rarely be the presenting sign of prostate carcinoma.
  • Here, we describe an unusual case of prostate adenocarcinoma presenting as a central skull base tumour with multiple cranial neuropathy.

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  • (PMID = 20379748.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Austria
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15. Andreoiu M, Cheng L: Multifocal prostate cancer: biologic, prognostic, and therapeutic implications. Hum Pathol; 2010 Jun;41(6):781-93
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  • [Title] Multifocal prostate cancer: biologic, prognostic, and therapeutic implications.
  • Prostatic adenocarcinoma is the most common cancer diagnosed in men and is often multifocal.
  • This review examines recent progress in the pathogenesis of multifocal prostatic adenocarcinoma and its biologic, pathologic, prognostic, and therapeutic implications.
  • Prostatic cancer multifocality makes accurate clinical staging difficult, and repeated revisions have been undertaken in an effort to optimize prognostic accuracy.
  • The clinical significance of smaller secondary tumors and the relationship between extent of chromosomal abnormalities and the metastatic potential of an individual tumor focus were reviewed.
  • [MeSH-major] Adenocarcinoma. Neoplasms, Multiple Primary. Prostatic Neoplasms

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20466122.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 125
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16. Sciarra A, Lichtner M, Autran GA, Mastroianni C, Rossi R, Mengoni F, Cristini C, Gentilucci A, Vullo V, Di Silverio F: Characterization of circulating blood dendritic cell subsets DC123+ (lymphoid) and DC11C+ (myeloid) in prostate adenocarcinoma patients. Prostate; 2007 Jan 1;67(1):1-7
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  • [Title] Characterization of circulating blood dendritic cell subsets DC123+ (lymphoid) and DC11C+ (myeloid) in prostate adenocarcinoma patients.
  • PURPOSE: We verified whether prostate adenocarcinoma produces specific modifications in DC subsets count.
  • METHODS: Twenty-one untreated prostate adenocarcinomas were divided on the basis of clinical stage in localized and metastatic disease.
  • RESULTS: We showed a statistically significant reduction in pDCs count in prostate cancer population when compared to healthy controls (P = 0.002).
  • Comparing each clinical stage with healthy controls, significant differences were found between controls and the metastatic group in both pDCs and mDCs (P = 0.005 and P = 0.023 respectively) but not between controls and the localized group (P = 0.055 and P = 0.829 respectively).
  • CONCLUSIONS: We showed that DCs count in PB is significantly affected by prostate adenocarcinoma progression in a metastatic disease.
  • [MeSH-major] Adenocarcinoma / pathology. Dendritic Cells / pathology. Prostatic Neoplasms / pathology

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17075798.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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17. Chua CW, Chiu YT, Yuen HF, Chan KW, Wang X, Ling MT, Wong YC: Differential expression of MSX2 in nodular hyperplasia, high-grade prostatic intraepithelial neoplasia and prostate adenocarcinoma. APMIS; 2010 Dec;118(12):918-26
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  • [Title] Differential expression of MSX2 in nodular hyperplasia, high-grade prostatic intraepithelial neoplasia and prostate adenocarcinoma.
  • One of the common features in advanced prostate cancer is bone metastasis.
  • In this study, we investigated the clinical relevance of a bone factor, MSX2, in predicting the metastatic ability of prostate adenocarcinoma.
  • Evaluation of MSX2 expression was performed using prostate cell lines as well as patient specimens.
  • A sharp decrease in MSX2 was found in primary prostate cancer cells, 22Rv1, when compared with the non-malignant counterparts, followed by a gradual increase in more aggressive prostate cancer cell lines.
  • Interestingly, the MSX2 protein was upregulated and predominantly expressed in the nucleus in aggressive prostate cancer cell line, C4-2b, compared with the less aggressive 22Rv1.
  • Consistent with the in vitro results, MSX2 nuclear expression was significantly higher in nodular hyperplasia when compared with high-grade prostatic intraepithelial neoplasia (PIN), while MSX2 nuclear expression in prostate adenocarcinoma was higher than that in high-grade PIN.
  • Taken together, MSX2 may serve as a potential biomarker in predicting primary prostate tumors with higher metastatic capability.
  • [MeSH-major] Adenocarcinoma / metabolism. Homeodomain Proteins / biosynthesis. Prostatic Hyperplasia / metabolism. Prostatic Intraepithelial Neoplasia / metabolism. Prostatic Neoplasms / metabolism

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  • [Copyright] © 2010 The Authors. Journal Compilation © 2010 APMIS.
  • (PMID = 21091772.001).
  • [ISSN] 1600-0463
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MSX2 protein
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18. Chiosea S, Jelezcova E, Chandran U, Acquafondata M, McHale T, Sobol RW, Dhir R: Up-regulation of dicer, a component of the MicroRNA machinery, in prostate adenocarcinoma. Am J Pathol; 2006 Nov;169(5):1812-20
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  • [Title] Up-regulation of dicer, a component of the MicroRNA machinery, in prostate adenocarcinoma.
  • In prostate adenocarcinoma, 39 microRNAs are up-regulated, and six microRNAs are down-regulated.
  • From a gene array analysis of 16 normal prostate tissue samples, 64 organ-confined, and four metastatic prostate adenocarcinomas, we identified an up-regulation of major components of the microRNA machinery, including Dicer, in metastatic prostate adenocarcinoma.
  • Immunohistochemical studies on a tissue microarray consisting of 232 prostate specimens confirmed up-regulation of Dicer in prostatic intraepithelial neoplasia and in 81% of prostate adenocarcinoma.
  • The increased Dicer level in prostate adenocarcinoma correlated with clinical stage, lymph node status, and Gleason score.
  • Western blot analysis of benign and neoplastic prostate cell lines further confirmed Dicer up-regulation in prostate adenocarcinoma.
  • Dicer up-regulation may explain an almost global increase of microRNA expression in prostate adenocarcinoma.
  • The presence of up-regulated microRNA machinery may predict the susceptibility of prostate adenocarcinoma to RNA interference-based therapy.
  • [MeSH-major] Adenocarcinoma / enzymology. Adenocarcinoma / pathology. DEAD-box RNA Helicases / metabolism. Endoribonucleases / metabolism. MicroRNAs / metabolism. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / pathology. Up-Regulation
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Blotting, Western. Cell Line, Tumor. Epithelium / pathology. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Microarray Analysis. Middle Aged. Prostate / cytology. Prostate / enzymology. Prostate / pathology. Ribonuclease III

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  • (PMID = 17071602.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; EC 3.1.- / Endoribonucleases; EC 3.1.26.3 / DICER1 protein, human; EC 3.1.26.3 / Ribonuclease III; EC 3.6.4.13 / DEAD-box RNA Helicases
  • [Other-IDs] NLM/ PMC1780192
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19. Gravdal K, Halvorsen OJ, Haukaas SA, Akslen LA: Proliferation of immature tumor vessels is a novel marker of clinical progression in prostate cancer. Cancer Res; 2009 Jun 1;69(11):4708-15
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  • [Title] Proliferation of immature tumor vessels is a novel marker of clinical progression in prostate cancer.
  • Including vascular endothelial growth factor (VEGF)-A and hypoxia-inducible factor-1alpha (HIF-1alpha) expression, we studied relation to disease progression in prostate cancer.
  • Sections from 104 radical prostatectomies with long follow-up, 33 castration-resistant prostate cancers, 28 nonskeletal metastases, 13 skeletal metastases, and 41 benign prostatic hyperplasias were immunostained for Nestin/Ki-67, VEGF-A, and HIF-1alpha.
  • Median vascular proliferation counts were 4- to 5-fold higher in castration-resistant prostate cancers and metastases versus localized cancers and prostatic hyperplasias (P < 0.0005).
  • Thus, vascular proliferation was of independent prognostic importance among prostate cancers.
  • When compared with localized cancers, vascular proliferation was significantly increased in castration-resistant cases and metastatic lesions.
  • These novel data might have an effect on clinical evaluation and treatment of prostate cancer patients.
  • [MeSH-major] Adenocarcinoma / blood supply. Biomarkers, Tumor. Blood Vessels / pathology. Neovascularization, Pathologic / pathology. Prostatic Neoplasms / blood supply

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  • [ErratumIn] Cancer Res. 2009 Jul 15;69(14):6005
  • (PMID = 19487287.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Intermediate Filament Proteins; 0 / Ki-67 Antigen; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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20. Azios NG, Krishnamoorthy L, Harris M, Cubano LA, Cammer M, Dharmawardhane SF: Estrogen and resveratrol regulate Rac and Cdc42 signaling to the actin cytoskeleton of metastatic breast cancer cells. Neoplasia; 2007 Feb;9(2):147-58
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  • [Title] Estrogen and resveratrol regulate Rac and Cdc42 signaling to the actin cytoskeleton of metastatic breast cancer cells.

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  • (PMID = 17356711.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5 F31 CA111486-02; United States / NCI NIH HHS / CA / R03 CA109913; United States / NCI NIH HHS / CA / CA109913-03; United States / NCI NIH HHS / CA / R03 CA109913-03; United States / NCI NIH HHS / CA / F31 CA111486; United States / NCRR NIH HHS / RR / 2G12RR003035; United States / NCI NIH HHS / CA / 5R03CA109913-03; United States / NCRR NIH HHS / RR / G12 RR003035
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Estrogens; 0 / Recombinant Fusion Proteins; 0 / Stilbenes; 4TI98Z838E / Estradiol; 62229-50-9 / Epidermal Growth Factor; EC 3.6.5.2 / cdc42 GTP-Binding Protein; EC 3.6.5.2 / rac GTP-Binding Proteins; Q369O8926L / resveratrol
  • [Other-IDs] NLM/ PMC1813930
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21. McMorris TC, Chimmani R, Alisala K, Staake MD, Banda G, Kelner MJ: Structure-activity studies of urea, carbamate, and sulfonamide derivatives of acylfulvene. J Med Chem; 2010 Feb 11;53(3):1109-16
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  • The lead acylfulvene (4), irofulven (5), in a randomized phase IIB clinical trial significantly increased overall survival in patients with metastatic hormone-refractory prostate cancer who failed prior treatment with two different standard chemotherapeutic regimens.
  • [MeSH-major] Adenocarcinoma / pathology. B-Lymphocytes / drug effects. Carbamates / chemistry. Lung Neoplasms / pathology. Sulfonamides / chemistry. Urea / chemistry

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  • (PMID = 20067264.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbamates; 0 / Sesquiterpenes; 0 / Spiro Compounds; 0 / Sulfonamides; 0 / acylfulvene; 8W8T17847W / Urea
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22. Rojiani MV, Alidina J, Esposito N, Rojiani AM: Expression of MMP-2 correlates with increased angiogenesis in CNS metastasis of lung carcinoma. Int J Clin Exp Pathol; 2010;3(8):775-81
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  • Matrix metalloproteinases (MMP) have been implicated in increased invasive and metastatic potential of tumors, possibly via interactions with the extracellular matrix and angiogenesis.
  • This study investigates the relationship between MMP-2 immunoexpression and angiogenesis in a series of lung carcinomas metastatic to the central nervous system (CNS).
  • Twenty eight metastatic carcinoma cases with adequate brain-tumor interface were identified from the archives at the Moffitt Cancer Center.
  • Sixteen (57.14%) metastatic tumors were strongly immunoreac-tive for MMP-2, while 12 (42.86%) were negative.
  • [MeSH-major] Adenocarcinoma / blood supply. Brain Neoplasms / blood supply. Lung Neoplasms / blood supply. Matrix Metalloproteinase 2 / metabolism. Neovascularization, Pathologic / enzymology

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  • (PMID = 21151391.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; EC 3.4.24.24 / Matrix Metalloproteinase 2
  • [Other-IDs] NLM/ PMC2993228
  • [Keywords] NOTNLM ; CNS metastasis / Matrix metalloproteinases (MMP) / angiogenesis / lung cancer
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23. Prawettongsopon C, Asawakarn S, Suthiphongchai T: Suppression of prometastatic phenotype of highly metastatic androgen-independent rat prostate cancer MLL cell line by PI3K inhibitor LY294002. Oncol Res; 2009;17(7):301-9
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  • [Title] Suppression of prometastatic phenotype of highly metastatic androgen-independent rat prostate cancer MLL cell line by PI3K inhibitor LY294002.
  • Upregulation of the PI3K pathway has often been reported in androgen-independent prostate cancer and is implicated in cancer cell survival and proliferation in the absence of androgen.
  • Inhibition of PI3K by LY294002 suppressed cell invasion and motility of the highly metastatic androgen-independent Dunning rat prostate cancer MLL cell line with similar IC50 values and inhibition profile.
  • [MeSH-major] Androgens / pharmacology. Chromones / pharmacology. Enzyme Inhibitors / pharmacology. Morpholines / pharmacology. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / secondary. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Animals. Cell Movement / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Male. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 2 / metabolism. Phosphorylation / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Tumor Cells, Cultured. Urokinase-Type Plasminogen Activator / genetics. Urokinase-Type Plasminogen Activator / metabolism

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  • (PMID = 19408575.001).
  • [ISSN] 0965-0407
  • [Journal-full-title] Oncology research
  • [ISO-abbreviation] Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / RNA, Messenger; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; EC 3.4.24.24 / Matrix Metalloproteinase 2
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24. Schlomm T, Iwers L, Kirstein P, Jessen B, Köllermann J, Minner S, Passow-Drolet A, Mirlacher M, Milde-Langosch K, Graefen M, Haese A, Steuber T, Simon R, Huland H, Sauter G, Erbersdobler A: Clinical significance of p53 alterations in surgically treated prostate cancers. Mod Pathol; 2008 Nov;21(11):1371-8
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  • [Title] Clinical significance of p53 alterations in surgically treated prostate cancers.
  • Despite the high number of previous studies, the role of p53 alterations in prostate cancer is not clearly defined.
  • To address the role of p53 alterations in prostate cancer biology, a total of 2514 cancers treated by radical prostatectomy were successfully analyzed by immunohistochemistry in a tissue microarray format.
  • These data suggest a high sensitivity of our immunohistochemistry approach and confirm the overall low frequency of p53 alterations in clinically localized prostate cancer.
  • A higher rate of positive p53 immunostaining was detected in late-stage diseases including metastatic prostate cancer (P=0.0152) and hormone-refractory tumors (P=0.0003).
  • In summary, the results of this study show that p53 mutations characterize a small biologically aggressive subgroup of prostate cancers with a high risk of progression after prostatectomy.
  • The rate of p53 alterations increases with prostate cancer progression.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Prostatic Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18552821.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Tumor Suppressor Protein p53
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25. Kuttan NA, Flemming DK, Dane JN, Ang DB: Metastatic lesion of the anterior mandible with an occult primary: a case report. Spec Care Dentist; 2006 Mar-Apr;26(2):76-80
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  • [Title] Metastatic lesion of the anterior mandible with an occult primary: a case report.
  • Metastatic tumors to the oral cavity are relatively uncommon and account for about 1% of all oral cancers.
  • The leading common primary sites for these lesions are the breast in females and the lung in males followed by the adrenals, kidneys, prostate, thyroid and colon.
  • In 30% of all cancers, a metastatic lesion could be the first sign of a primary tumor elsewhere in the body.
  • Metastatic lesions to the jaws are known to simulate periodontal and pulpal disease and other radiolucent lesions that can occur in the jaws.
  • Microscopic evaluation with concurrent radiographic skeletal survey is warranted in patients where a metastatic lesion is suspected.
  • [MeSH-major] Adenocarcinoma / secondary. Colonic Neoplasms / pathology. Mandibular Neoplasms / secondary. Neoplasms, Unknown Primary / pathology

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  • (PMID = 16681243.001).
  • [ISSN] 0275-1879
  • [Journal-full-title] Special care in dentistry : official publication of the American Association of Hospital Dentists, the Academy of Dentistry for the Handicapped, and the American Society for Geriatric Dentistry
  • [ISO-abbreviation] Spec Care Dentist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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26. Tollefson M, Magera J, Sebo T, Cohen J, Drauch A, Maier J, Frank I: Raman spectral imaging of prostate cancer: can Raman molecular imaging be used to augment standard histopathology? BJU Int; 2010 Aug;106(4):484-8
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  • [Title] Raman spectral imaging of prostate cancer: can Raman molecular imaging be used to augment standard histopathology?
  • OBJECTIVE: To evaluate whether Raman molecular imaging (RMI, which combines digital imaging and analytical spectroscopy to evaluate the biochemical composition of interrogated material) can be used to identify biochemical differences in patients with Gleason 7 prostate cancer who progress to metastatic disease and die from prostate cancer.
  • PATIENTS AND METHODS: We identified 38 patients who had a radical prostatectomy for Gleason 7 adenocarcinoma of the prostate.
  • Half progressed to metastatic disease and half had no evidence of disease after treatment.
  • Patients were matched for preoperative prostate-specific antigen level, surgical margin status, pathological stage, tumour volume, age at surgery, year of surgery and DNA ploidy.
  • In Gleason 7 disease, RMI shows distinctive chemical differences in patients who progress to metastatic disease in both Gleason pattern 3 and 4 regions.
  • This preliminary work lays the foundation for the further study of RMI for evaluating prostate tissue.
  • [MeSH-major] Adenocarcinoma / pathology. Prostatectomy / methods. Prostatic Neoplasms / pathology. Spectrum Analysis, Raman



27. Comstock CE, Revelo MP, Buncher CR, Knudsen KE: Impact of differential cyclin D1 expression and localisation in prostate cancer. Br J Cancer; 2007 Mar 26;96(6):970-9
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  • [Title] Impact of differential cyclin D1 expression and localisation in prostate cancer.
  • Cyclin D1 is a critical regulator of androgen-dependent transcription and cell cycle progression in prostate cancer cells.
  • Despite the influence of D-type cyclins on prostate cancer proliferation, few studies have examined the expression of cyclin D1 in localised tumours or challenged its relevance to disease progression.
  • Cyclin D1 status was characterised using immunohistochemistry in 38 non-neoplastic prostate samples, 138 primary human prostate carcinomas, and three lymph node metastatic specimens.
  • Relevance of cyclin D1 to preoperative prostate-specific antigen (PSA) levels, Ki-67 index, and p21Cip1 status was also examined.
  • These data demonstrate that differential cyclin D1 status may influence clinicopathological parameters, and reveal new insight as to the regulation and potential consequence of cyclin D1 expression in prostate cancer.

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  • (PMID = 17375037.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA099996; United States / NCI NIH HHS / CA / CA 099996
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Ki-67 Antigen; 136601-57-5 / Cyclin D1; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Other-IDs] NLM/ PMC2360090
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28. Carducci MA, Saad F, Abrahamsson PA, Dearnaley DP, Schulman CC, North SA, Sleep DJ, Isaacson JD, Nelson JB, Atrasentan Phase III Study Group Institutions: A phase 3 randomized controlled trial of the efficacy and safety of atrasentan in men with metastatic hormone-refractory prostate cancer. Cancer; 2007 Nov 01;110(9):1959-66
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  • [Title] A phase 3 randomized controlled trial of the efficacy and safety of atrasentan in men with metastatic hormone-refractory prostate cancer.
  • BACKGROUND: The objective of this study was to evaluate the efficacy and safety of atrasentan (Xinlay), a selective endothelin-A receptor antagonist, in patients with metastatic hormone-refractory prostate cancer (HRPC).
  • METHODS: This multinational, double-blind, placebo-controlled trial enrolled 809 men with metastatic HRPC.
  • In exploratory analyses, increases from baseline to final bone alkaline phosphatase (BAP) and prostate-specific antigen (PSA) levels were significantly lower with atrasentan treatment (P < .05 for each).
  • CONCLUSIONS: Atrasentan did not delay disease progression in men with metastatic HRPC despite evidence of biologic effects on PSA and BAP as markers of disease burden.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Antineoplastic Agents / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Pyrrolidines / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Alkaline Phosphatase / blood. Alkaline Phosphatase / drug effects. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Disease Progression. Double-Blind Method. Drug Resistance, Neoplasm. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prostate-Specific Antigen / blood. Prostate-Specific Antigen / drug effects



29. Jantscheff P, Esser N, Graeser R, Ziroli V, Kluth J, Unger C, Massing U: Liposomal gemcitabine (GemLip)-efficient drug against hormone-refractory Du145 and PC-3 prostate cancer xenografts. Prostate; 2009 Aug 1;69(11):1151-63
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  • [Title] Liposomal gemcitabine (GemLip)-efficient drug against hormone-refractory Du145 and PC-3 prostate cancer xenografts.
  • BACKGROUND: Gemcitabine (Gemc) is an efficient chemotherapeutic drug in various cancer types (e.g., pancreas) but has only limited effects on hormone-refractory prostate cancer (HRPCa).
  • METHODS: Anti-tumoral and anti-metastatic activity of GemLip and Gemc were investigated in two luciferase-expressing, human hormone-refractory PC-3 and Du145 HRPCa xenograft models in immunodeficient mice.
  • Anti-metastatic effects of treatment were determined by in vitro luciferase assay of the tissues.
  • GemLip has, even at very low doses, a significant anti-tumoral and anti-metastatic therapeutic effect in HRPCa xenografts in vivo and was beneficial even when the conventional Gemc failed.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / therapeutic use. Deoxycytidine / analogs & derivatives. Prostatic Neoplasms / drug therapy. Transplantation, Heterologous

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  • (PMID = 19399788.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Liposomes; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 1.13.12.- / Luciferases
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30. Jennbacken K, Gustavsson H, Welén K, Vallbo C, Damber JE: Prostate cancer progression into androgen independency is associated with alterations in cell adhesion and invasivity. Prostate; 2006 Nov 1;66(15):1631-40
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  • [Title] Prostate cancer progression into androgen independency is associated with alterations in cell adhesion and invasivity.
  • BACKGROUND: Mortality in prostate cancer is primarily due to failure to cure hormone refractory patients with metastatic disease.
  • CONCLUSIONS: The results show that LNCaP-19 mimics hormone refractory prostate cancer and therefore is an excellent tool for studies on androgen-independent cancer and invasion.
  • [MeSH-major] Adenocarcinoma / pathology. Androgens / metabolism. Cell Transformation, Neoplastic / pathology. Prostatic Neoplasms / pathology



31. Wong SY, Haack H, Crowley D, Barry M, Bronson RT, Hynes RO: Tumor-secreted vascular endothelial growth factor-C is necessary for prostate cancer lymphangiogenesis, but lymphangiogenesis is unnecessary for lymph node metastasis. Cancer Res; 2005 Nov 1;65(21):9789-98
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  • [Title] Tumor-secreted vascular endothelial growth factor-C is necessary for prostate cancer lymphangiogenesis, but lymphangiogenesis is unnecessary for lymph node metastasis.
  • Dissemination to draining lymph nodes is a frequent first step in prostate cancer metastasis.
  • Here, we inhibit intratumoral lymphangiogenesis in s.c. and surgical orthotopic implantation mouse models of human prostate cancer using several strategies.
  • Combination of soluble Flt4 and VEGF-C siRNA yielded >92% reduction of intratumoral lymphatics in orthotopic prostate tumors.
  • We also analyzed the lymphatics in spontaneous transgenic adenocarcinomas of the mouse prostate which metastasize to lymph nodes.
  • Progression from well-differentiated prostate intraepithelial neoplasia to metastatic, undifferentiated adenocarcinoma was accompanied by loss of lymphatics.
  • These results suggest that tumor-secreted VEGF-C and, to a lesser extent, VEGF-A, are important for inducing prostate cancer intratumoral lymphangiogenesis but are unnecessary for lymph node metastasis.
  • [MeSH-major] Adenocarcinoma / pathology. Lymph Nodes / pathology. Prostatic Neoplasms / pathology. Vascular Endothelial Growth Factor C / physiology

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  • (PMID = 16267000.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA17007
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / VEGFA protein, human; 0 / VEGFC protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C
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32. Plotnikov A, Niego B, Ophir R, Korenstein R, Keisari Y: Effective treatment of mouse metastatic prostate cancer by low electric field enhanced chemotherapy. Prostate; 2006 Nov 1;66(15):1620-30
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  • [Title] Effective treatment of mouse metastatic prostate cancer by low electric field enhanced chemotherapy.
  • In the present study we investigated its efficacy against prostate metastatic transgenic adenocarcinoma of mice (TRAMP).
  • METHODS: Mice with 5, 10, and 13 mm in diameter intracutaneous tumors received Low Electric Field Cancer Treatment-Enhanced Chemotherapy (LEFCT-EC) with doxorubicin (10 mg/kg), and monitored for survival, and primary and metastatic tumors growth.
  • CONCLUSION: Our results suggest that LEFCT-EC is an effective method for the destruction of metastatic prostate tumors.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antibiotics, Antineoplastic / therapeutic use. Doxorubicin / therapeutic use. Electrochemotherapy. Prostatic Neoplasms / drug therapy

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  • (PMID = 16941466.001).
  • [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 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
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33. Castellana D, Zobairi F, Martinez MC, Panaro MA, Mitolo V, Freyssinet JM, Kunzelmann C: Membrane microvesicles as actors in the establishment of a favorable prostatic tumoral niche: a role for activated fibroblasts and CX3CL1-CX3CR1 axis. Cancer Res; 2009 Feb 1;69(3):785-93
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  • [Title] Membrane microvesicles as actors in the establishment of a favorable prostatic tumoral niche: a role for activated fibroblasts and CX3CL1-CX3CR1 axis.
  • To elucidate their role in cancer-to-fibroblast cell communication, TMV obtained from two prostate carcinoma cell lines with high and weak metastatic potential (PC3 and LnCaP, respectively) have been characterized.
  • Moreover, TMV not only induce the activation of fibroblasts assessed through extracellular signal-regulated kinase 1/2 phosphorylation and MMP-9 up-regulation, increase motility and resistance to apoptosis but also promote MV shedding from activated fibroblasts able in turn to increase migration and invasion of highly metastatic PC3 cells but not LnCaP cells.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Communication / physiology. Chemokine CX3CL1 / metabolism. Prostatic Neoplasms / pathology. Receptors, Chemokine / metabolism

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  • (PMID = 19155311.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CX3CL1 protein, human; 0 / CX3CR1 protein, human; 0 / Chemokine CX3CL1; 0 / Receptors, Chemokine; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.24.35 / Matrix Metalloproteinase 9
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34. Grenader T, Shavit L, Lossos A, Pizov G, Wygoda M: Brain metastases: a rare initial presentation of prostate cancer. Int Urol Nephrol; 2007;39(2):537-9
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  • [Title] Brain metastases: a rare initial presentation of prostate cancer.
  • Although brain metastases are common in cancer patients, carcinoma of the prostate rarely metastasizes to the brain.
  • Cerebral metastases as an initial clinical presentation of prostate carcinoma are extremely rare.
  • The pathological diagnosis of the tumor was consistent with metastatic prostate carcinoma.
  • Further evaluation revealed widespread bony metastases by technetium 99 bone scan and high level of prostate-specific antigen.
  • [MeSH-major] Adenocarcinoma / secondary. Brain Neoplasms / secondary. Prostatic Neoplasms / pathology



35. Mackler NJ, Pienta KJ, Dunn RL, Cooney KA, Redman BG, Olson KB, Fardig JE, Smith DC: Phase II evaluation of oral estramustine, oral etoposide, and intravenous paclitaxel in patients with hormone-sensitive prostate adenocarcinoma. Clin Genitourin Cancer; 2007 Jun;5(5):318-22
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  • [Title] Phase II evaluation of oral estramustine, oral etoposide, and intravenous paclitaxel in patients with hormone-sensitive prostate adenocarcinoma.
  • PURPOSE: The primary objective of this study was to assess the feasibility and efficacy of administering etoposide/estramustine/paclitaxel in hormone-sensitive metastatic prostate cancer responding to hormonal therapy.
  • PATIENTS AND METHODS: Eligible patients had metastatic prostate cancer and had received combined androgen blockade for 6-8 months with a > or = 80% decrease in prostate-specific antigen from pretreatment.
  • Although the TTF of 21.7 months by prostate-specific antigen criteria is similar to historical controls in the emergence of clinically evident androgen-independent disease after starting hormone therapy, direct comparisons cannot be made.
  • More trials are needed to investigate the timing of chemotherapy in patients with prostate cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasms, Hormone-Dependent / drug therapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Aged. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Disease Progression. Estramustine / administration & dosage. Etoposide / administration & dosage. Feasibility Studies. Humans. Injections, Intravenous. Male. Middle Aged. Paclitaxel / administration & dosage. Prostate-Specific Antigen / blood. Survival Rate. Treatment Outcome

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  • (PMID = 17645828.001).
  • [ISSN] 1558-7673
  • [Journal-full-title] Clinical genitourinary cancer
  • [ISO-abbreviation] Clin Genitourin Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 P30 CA 46592
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 35LT29625A / Estramustine; 6PLQ3CP4P3 / Etoposide; EC 3.4.21.77 / Prostate-Specific Antigen; P88XT4IS4D / Paclitaxel
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36. Chiappino I, Destefanis P, Addeo A, Galetto A, Cucchiarale G, Munoz F, Zitella A, Ferrando U, Fontana D, Ricardi U, Tizzani A, Bertetto O: Activity of weekly paclitaxel in advanced hormone-refractory prostate cancer. Am J Clin Oncol; 2007 Jun;30(3):234-8
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  • [Title] Activity of weekly paclitaxel in advanced hormone-refractory prostate cancer.
  • OBJECTIVE: We evaluated efficacy and toxicity of weekly paclitaxel in metastatic hormone-refractory prostate cancer (HRPC).
  • RESULTS: The study enrolled 43 patients with metastatic HRPC diagnosed a median of 10.5 months before.
  • Five had previous radioisotopes treatment for bone pain, 15 had previous treatment of metastatic hormone-refractory disease, mainly estramustine.
  • CONCLUSION: Docetaxel every 3 weeks is the standard of care for metastatic HRPC, but our results suggest some activity and an acceptable toxicity of weekly paclitaxel.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents, Phytogenic / administration & dosage. Paclitaxel / administration & dosage. Prostatic Neoplasms / drug therapy

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  • (PMID = 17551298.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; P88XT4IS4D / Paclitaxel
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37. Idelevich E, Kashtan H, Mavor E, Brenner B: Small bowel obstruction caused by secondary tumors. Surg Oncol; 2006 Jul;15(1):29-32
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  • Linitis plastica caused by metastatic lobular carcinoma of the breast.
  • Small bowel intussusception due to metastatic malignant melanoma.
  • Rectal obstruction secondary to carcinoma of the prostate treated by transanal resection of the prostate.
  • Unusual presentation of rectal adenocarcinoma.
  • A case of jejunal intussusception with gastrointestinal bleeding caused by metastatic testicular germ cell cancer.

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  • (PMID = 16905310.001).
  • [ISSN] 0960-7404
  • [Journal-full-title] Surgical oncology
  • [ISO-abbreviation] Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 22
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38. 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.
  • 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.
  • [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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39. Tarján M: Prognostic significance of focal neuroendocrine differentiation in prostate cancer: cases with autopsy-verified cause of death. Indian J Urol; 2010 Jan-Mar;26(1):41-5
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  • [Title] Prognostic significance of focal neuroendocrine differentiation in prostate cancer: cases with autopsy-verified cause of death.
  • AIMS: This study was designed to evaluate the prognostic significance of focal chromogranin A (cgA) expression in prostate cancer in a series of cases with autopsy-verified cause of death.
  • METHODS AND RESULTS: Seventy seven autopsy-verified cases of prostate cancer were identified, 41 cases with metastatic disease and 36 with nonmetastatic disease at autopsy.
  • After exclusion of a single case of carcinoid tumor, 14 of the 18 (78%) metastatic and none of the 21 (0%) nonmetastatic tumors showed focal neuroendocrine differentiation (NED).
  • The Gleason score and focal cgA expression further increased the accuracy of the prediction of the outcome, as all the cases with focal NED associated with high Gleason score had metastatic disease in contrast to cases without cgA-expression and low Gleason score, all of which were non-metastatic.
  • CONCLUSIONS: Focal NED seems to be a powerful negative prognostic parameter in prostate adenocarcinomas.
  • The outcome of the disease in prostate cancer can be accurately predicted based on focal NED of the tumor cells either alone or in combination with Gleason score.

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  • (PMID = 20535283.001).
  • [ISSN] 1998-3824
  • [Journal-full-title] Indian journal of urology : IJU : journal of the Urological Society of India
  • [ISO-abbreviation] Indian J Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2878436
  • [Keywords] NOTNLM ; Adenocarcinoma / neuroendocrine differentiation / prognosis / prostate
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40. Stein ME, Boehmer D, Kuten A: Radiation therapy in prostate cancer. Recent Results Cancer Res; 2007;175:179-99
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  • [Title] Radiation therapy in prostate cancer.
  • Adenocarcinoma of the prostate is one of the most frequently diagnosed cancers of men in the Western hemisphere and is second only to lung cancer for male cancer mortality.
  • Innovative methods such as brachytherapy, three-dimensional conformal radiotherapy (3D-CRT), and IMRT (intensity modulated radiotherapy) are able to deliver very high tumoricidal doses to the diseased prostate, with minimal side effects to the surrounding tissue.
  • Radiation therapy is also very effective in alleviating symptoms of metastatic prostate cancer (bone metastases, spinal cord compression, and bladder outlet obstruction).
  • [MeSH-major] Prostatic Neoplasms / radiotherapy

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  • (PMID = 17432560.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 103
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41. Wong SY, Haack H, Kissil JL, Barry M, Bronson RT, Shen SS, Whittaker CA, Crowley D, Hynes RO: Protein 4.1B suppresses prostate cancer progression and metastasis. Proc Natl Acad Sci U S A; 2007 Jul 31;104(31):12784-9
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  • [Title] Protein 4.1B suppresses prostate cancer progression and metastasis.
  • In a screen for genes involved with prostate cancer metastasis, we found that 4.1B expression is reduced in highly metastatic tumors.
  • Down-regulation of 4.1B increased the metastatic propensity of poorly metastatic cells in an orthotopic model of prostate cancer.
  • Furthermore, 4.1B-deficient mice displayed increased susceptibility for developing aggressive, spontaneous prostate carcinomas.
  • Because expression of Protein 4.1B is frequently down-regulated in human clinical prostate cancer, as well as in a spectrum of other tumor types, these results suggest a more general role for Protein 4.1B as a negative regulator of cancer progression to metastatic disease.

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  • (PMID = 17640904.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE7930
  • [Grant] United States / NCI NIH HHS / CA / R01 CA017007; United States / NCI NIH HHS / CA / U54 CA112967; United States / NCI NIH HHS / CA / R01 CA 17007; United States / NCI NIH HHS / CA / U54 CA 112967
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EPB41L3 protein, human; 0 / Epb4.1l3 protein, mouse; 0 / Membrane Proteins; 0 / Microfilament Proteins; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC1924789
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42. Berezovska OP, Glinskii AB, Yang Z, Li XM, Hoffman RM, Glinsky GV: Essential role for activation of the Polycomb group (PcG) protein chromatin silencing pathway in metastatic prostate cancer. Cell Cycle; 2006 Aug;5(16):1886-901
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  • [Title] Essential role for activation of the Polycomb group (PcG) protein chromatin silencing pathway in metastatic prostate cancer.
  • Another PcG protein, Ezh2, was implicated in metastatic prostate and breast cancers, suggesting that PcG pathway activation is relevant for epithelial malignancies.
  • Here we demonstrate that activation of the BMI1 oncogene-associated PcG pathway plays an essential role in metastatic prostate cancer, thus mechanistically linking the pathogenesis of leukemia, self-renewal of stem cells, and prostate cancer metastasis.
  • To characterize the functional status of the PcG pathway in metastatic prostate cancer, we utilized advanced cell- and whole animal-imaging technologies, gene and protein expression profiling, stable siRNA-gene targeting, and tissue microarray (TMA) analysis in relevant experimental and clinical settings.
  • We demonstrate that in multiple experimental models of metastatic prostate cancer both BMI1 and Ezh2 genes are amplified and gene amplification is associated with increased expression of corresponding mRNAs and proteins.
  • For the first time, we provide images of human prostate carcinoma metastasis precursor cells isolated from blood and shown to overexpress both BMI1 and Ezh2 oncoproteins.
  • Consistent with the PcG pathway activation hypothesis, increased BMI1 and Ezh2 expression in metastatic cancer cells is associated with elevated levels of H2AubiK119 and H3metK27 histones.
  • Quantitative immunofluorescence colocalization analysis and expression profiling experiments documented increased BMI1 and Ezh2 expression in clinical prostate carcinoma samples and demonstrated that high levels of BMI1 and Ezh2 expression are associated with markedly increased likelihood of therapy failure and disease relapse after radical prostatectomy.
  • Gene-silencing analysis reveals that activation of the PcG pathway is mechanistically linked with highly malignant behavior of human prostate carcinoma cells and is essential for in vivo growth and metastasis of human prostate cancer.
  • We conclude that the results of experimental and clinical analyses indicate the important biological role of the PcG pathway activation in metastatic prostate cancer.
  • Our work suggests that the PcG pathway activation is a common oncogenic event in pathogenesis of metastatic solid tumors and provides justification for development of small molecule inhibitors of the PcG chromatin silencing pathway as a novel therapeutic modality for treatment of metastatic prostate cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Chromatin Assembly and Disassembly. Gene Silencing. Neoplastic Cells, Circulating / metabolism. Prostatic Neoplasms / metabolism. Repressor Proteins / biosynthesis

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  • (PMID = 16963837.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5R01 CA89827
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Polycomb-Group Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 0 / Transcription Factors; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2; EC 6.3.2.19 / Polycomb Repressive Complex 1
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43. Chen HL, Chang WH, Shih SC, Pang KK, Bair MJ: Trismus and trigeminal neuralgia in one patient with colon cancer. J Natl Med Assoc; 2008 Jun;100(6):740-2
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  • Metastatic tumors to the oral cavity are relatively uncommon.
  • They are found most commonly in the mandible, and 70% of cases are adenocarcinoma-most commonly from breast and lung, followed by adrenals, kidneys, prostate, thyroid and colon.
  • [MeSH-major] Adenocarcinoma / secondary. Colonic Neoplasms / pathology. Mandibular Neoplasms / secondary. Trigeminal Neuralgia / etiology. Trismus / etiology

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  • (PMID = 18595580.001).
  • [ISSN] 1943-4693
  • [Journal-full-title] Journal of the National Medical Association
  • [ISO-abbreviation] J Natl Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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44. Senzer N, Arsenau J, Richards D, Berman B, MacDonald JR, Smith S: Irofulven demonstrates clinical activity against metastatic hormone-refractory prostate cancer in a phase 2 single-agent trial. Am J Clin Oncol; 2005 Feb;28(1):36-42
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  • [Title] Irofulven demonstrates clinical activity against metastatic hormone-refractory prostate cancer in a phase 2 single-agent trial.
  • BACKGROUND: The primary objective of this study was to assess the antitumor activity of irofulven in patients with hormone-refractory prostate cancer by measuring a sustained decrease of 50% or greater in serum prostate-specific antigen (PSA) levels.
  • Eligible patients had pathologically confirmed metastatic hormone-refractory adenocarcinoma of the prostate and had not received prior cytotoxic chemotherapy.
  • CONCLUSION: Irofulven shows activity in hormone-refractory prostate cancer and has an acceptable safety profile, warranting further investigation of this drug, particularly in combination therapies.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents, Alkylating / therapeutic use. Prostatic Neoplasms / drug therapy. Sesquiterpenes / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Humans. Male. Middle Aged. Prostate-Specific Antigen / blood. Survival Analysis

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  • (PMID = 15685033.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Sesquiterpenes; 6B799IH05A / irofulven; EC 3.4.21.77 / Prostate-Specific Antigen
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45. Narayanan BA, Narayanan NK, Pttman B, Reddy BS: Adenocarcina of the mouse prostate growth inhibition by celecoxib: downregulation of transcription factors involved in COX-2 inhibition. Prostate; 2006 Feb 15;66(3):257-65
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  • [Title] Adenocarcina of the mouse prostate growth inhibition by celecoxib: downregulation of transcription factors involved in COX-2 inhibition.
  • BACKGROUND: Epidemiological studies have shown a decreased risk of prostate cancer among men who regularly take aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs).
  • In this study, we examined a dose-dependent effect of a cyclooxygenase-2 (COX-2) inhibitor, celecoxib against transgenic adenocarcinoma of the mouse prostate.
  • METHODS: Efficacy of four different doses in parts per million of celecoxib, such as 200 ppm, 400 ppm, 600 ppm, and 1,000 ppm representing very low, moderate, and high doses, respectively were tested against adenocarcinoma of the mouse prostate using a transgenic adenocarcinoma of the mouse prostate (TRAMP) model assay.
  • RESULTS: Dietary supplement of celecoxib at doses of 400 ppm, 600 ppm, and 1,000 ppm are most effective against mPIN (mouse prostatic intraepithelial neoplasia) and adenocarcinoma of the prostate.
  • At 1,000 ppm, a complete inhibition of the PIN lesions was extended to limit the growth of adenocarcinoma (from 85% to 15%) and metastasis of the mouse prostate.
  • CONCLUSIONS: Dietary supplementation of celecoxib at different doses provides evidence for the suppression of prostate adenocarcinoma tumor growth in a dose-dependent manner.
  • Suppression of adenocarcinoma by celecoxib further limits the growth of metastatic prostate cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cyclooxygenase 2 / metabolism. Cyclooxygenase Inhibitors / pharmacology. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Neoplasms / drug therapy. Pyrazoles / pharmacology. Sulfonamides / pharmacology. Transcription Factor RelA / antagonists & inhibitors

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16175586.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA107813-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Transcription Factor RelA; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib
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46. Higano CS, Corman JM, Smith DC, Centeno AS, Steidle CP, Gittleman M, Simons JW, Sacks N, Aimi J, Small EJ: Phase 1/2 dose-escalation study of a GM-CSF-secreting, allogeneic, cellular immunotherapy for metastatic hormone-refractory prostate cancer. Cancer; 2008 Sep 1;113(5):975-84
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  • [Title] Phase 1/2 dose-escalation study of a GM-CSF-secreting, allogeneic, cellular immunotherapy for metastatic hormone-refractory prostate cancer.
  • BACKGROUND: This open-label, multicenter, dose-escalation study evaluated multiple dose levels of immunotherapy in patients with metastatic hormone-refractory prostate cancer (HRPC).
  • The immunotherapy, based on the GVAX platform, consisted of 2 allogeneic prostate-carcinoma cell lines modified to secrete granulocyte-macrophage-colony-stimulating factor (GM-CSF).
  • Endpoints included safety, immunogenicity, overall survival, radiologic response, prostate-specific antigen (PSA) kinetics, and serum GM-CSF pharmacokinetics.
  • Two phase 3 trials in patients with metastatic HRPC are underway.
  • [MeSH-major] Adenocarcinoma / therapy. Cancer Vaccines / therapeutic use. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Immunotherapy / methods. Prostatic Neoplasms / therapy



47. Whang PG, Schwarz EM, Gamradt SC, Dougall WC, Lieberman JR: The effects of RANK blockade and osteoclast depletion in a model of pure osteoblastic prostate cancer metastasis in bone. J Orthop Res; 2005 Nov;23(6):1475-83
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  • [Title] The effects of RANK blockade and osteoclast depletion in a model of pure osteoblastic prostate cancer metastasis in bone.
  • Adenocarcinoma of the prostate exhibits a clear propensity for bone and is associated with the formation of osteoblastic metastases.
  • Here we investigate the effects of complete in vivo osteoclast depletion via the blockade of receptor activator of NF:kappaB (RANK) on the establishment and progression of purely osteoblastic (LAPC-9 cells) bone lesions induced by human prostate cancer cells using a SCID mouse intratibial injection model.
  • These results indicate that in vivo RANK blockade may not be effective for the prevention of osteoblastic metastasis but may potentially represent a novel therapy that limits the growth of established metastatic CaP lesions in bone.
  • [MeSH-major] Bone Neoplasms / pathology. Bone Neoplasms / secondary. Glycoproteins / antagonists & inhibitors. Osteoblasts / pathology. Osteoclasts / physiology. Prostatic Neoplasms / pathology. Receptors, Cytoplasmic and Nuclear / antagonists & inhibitors. Receptors, Tumor Necrosis Factor / antagonists & inhibitors. Recombinant Fusion Proteins / therapeutic use

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  • (PMID = 16005175.001).
  • [ISSN] 0736-0266
  • [Journal-full-title] Journal of orthopaedic research : official publication of the Orthopaedic Research Society
  • [ISO-abbreviation] J. Orthop. Res.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / R01 AR46789-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glycoproteins; 0 / Immunoglobulin Fc Fragments; 0 / Osteoprotegerin; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Fusion Proteins; 0 / TNFRSF11B protein, human; 0 / Tnfrsf11b protein, mouse
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48. You YN, Wolff BG, Boardman LA, Riegert-Johnson DL, Qin R: Peutz-Jeghers syndrome: a study of long-term surgical morbidity and causes of mortality. Fam Cancer; 2010 Dec;9(4):609-16
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  • Two malignancies were found intra-operatively (duodenal and rectal adenocarcinoma).
  • Twenty-one additional cancers were treated in 19 patients: gynecologic (11), lung (3), and prostate (2) being the most common.
  • The cause of death was unknown in 4 patients, but was due exclusively to malignancies in all other patients, most commonly due to metastatic gynecologic cancer (5).

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  • (PMID = 20571886.001).
  • [ISSN] 1573-7292
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Netherlands
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49. Pallini R, Sabatino G, Doglietto F, Lauretti L, Fernandez E, Maira G: Clivus metastases: report of seven patients and literature review. Acta Neurochir (Wien); 2009 Apr;151(4):291-6; discussion 296
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  • The primary tumours associated were lung adenocarcinoma (n = 2), prostate carcinoma (n = 2), skin melanoma (n = 1), hepatocarcinoma (n = 1) and lung squamous cell carcinoma (n = 1).
  • Including our series, the most common primary tumours were prostate cancer (26.4%), thyroid carcinoma (11.7%) and hepatocarcinoma (11.7%).
  • The metastatic lesion might be a late and single expression of the primary tumour.
  • [MeSH-minor] Abducens Nerve Diseases / etiology. Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Liver Neoplasms / pathology. Lung Neoplasms / pathology. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Metastasis. Prognosis. Prostatic Neoplasms / pathology. Skin Neoplasms / pathology. Survival Rate. Tomography, X-Ray Computed

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  • (PMID = 19259614.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Austria
  • [Number-of-references] 30
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50. Kasper S: Survey of genetically engineered mouse models for prostate cancer: analyzing the molecular basis of prostate cancer development, progression, and metastasis. J Cell Biochem; 2005 Feb 1;94(2):279-97
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  • [Title] Survey of genetically engineered mouse models for prostate cancer: analyzing the molecular basis of prostate cancer development, progression, and metastasis.
  • Genetically engineered mouse models have been generated to study the molecular basis of prostate cancer (PCa) development, progression, and metastasis.
  • Selection of a prostate-specific promoter, such as the probasin (PB) and prostate specific antigen (PSA) promoters, is critical for generating sufficient levels of transgene expression to elicit a phenotypic response.
  • Furthermore, the effects of gene disruption on promoting low- and high-grade intraepithelial neoplasia (LGPIN and HGPIN, respectively), locally invasive carcinoma and metastatic lesions will be discussed.
  • To date, the PB-Cre4 x PTENloxp/loxp model appears to be the only model that represents the entire continuum of prostate adenocarcinoma development, tumor progression, and metastasis, although models that develop prostatic neuroendocrine (NE) cancer can be generated by disrupting one genetic event.
  • Indeed, analysis of bigenic mouse models indicates that two genetic events are generally required for progression from HGPIN to locally invasive adenocarcinoma and that two to five genetic events can promote metastasis to distant sites.
  • [MeSH-major] Adenocarcinoma / secondary. Disease Models, Animal. Mice, Transgenic. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology



51. Hainsworth JD, Meluch AA, Spigel DR, Barton J Jr, Simons L, Meng C, Gould B, Greco FA: Weekly docetaxel and bortezomib as first-line treatment for patients with hormone-refractory prostate cancer: a Minnie Pearl Cancer Research Network phase II trial. Clin Genitourin Cancer; 2007 Mar;5(4):278-83
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  • [Title] Weekly docetaxel and bortezomib as first-line treatment for patients with hormone-refractory prostate cancer: a Minnie Pearl Cancer Research Network phase II trial.
  • BACKGROUND: Docetaxel is currently the standard first-line treatment in patients with hormone-refractory prostate cancer (HRPC).
  • Bortezomib, the first proteasome inhibitor in clinical use, demonstrated activity against prostate cancer in phase I trials.
  • All patients had metastatic adenocarcinoma of the prostate that had progressed on hormonal therapy.
  • Fifteen patients (25%; 95% confidence interval, 15%-38%) had a > 50% decrease in serum prostate-specific antigen level with treatment; the median response duration was 8 months.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / administration & dosage. Boronic Acids / administration & dosage. Prostatic Neoplasms / drug therapy. Pyrazines / administration & dosage. Taxoids / administration & dosage

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  • (PMID = 17553208.001).
  • [ISSN] 1558-7673
  • [Journal-full-title] Clinical genitourinary cancer
  • [ISO-abbreviation] Clin Genitourin Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 0 / Taxoids; 15H5577CQD / docetaxel; 69G8BD63PP / Bortezomib
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52. Hu SY, Liu T, Liu ZZ, Ledet E, Velasco-Gonzalez C, Mandal DM, Koochekpour S: Identification of a novel germline missense mutation of the androgen receptor in African American men with familial prostate cancer. Asian J Androl; 2010 May;12(3):336-43
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  • [Title] Identification of a novel germline missense mutation of the androgen receptor in African American men with familial prostate cancer.
  • Race, family history and age are the unequivocally accepted risk factors for prostate cancer (PCa).
  • Androgen receptor (AR)-dependent signaling is an important element in prostate carcinogenesis and its progression to metastatic disease.

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  • (PMID = 20173765.001).
  • [ISSN] 1745-7262
  • [Journal-full-title] Asian journal of andrology
  • [ISO-abbreviation] Asian J. Androl.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / 1P20 RR021970; United States / NCI NIH HHS / CA / R21 CA149137; United States / NCI NIH HHS / CA / R21 CA120625; United States / NIMHD NIH HHS / MD / R01 MD005824-01; United States / NCI NIH HHS / CA / R21 CA149137-01; United States / NCRR NIH HHS / RR / RR021970-056085; United States / NCI NIH HHS / CA / CA120625-01; United States / NIMHD NIH HHS / MD / R01 MD005824; United States / NCRR NIH HHS / RR / P20 RR021970; United States / NCI NIH HHS / CA / R03 CA097778; United States / NIMHD NIH HHS / MD / MD005824-01; United States / NCI NIH HHS / CA / 1 R03 CA97778-01; United States / NCRR NIH HHS / RR / P20 RR021970-056085; United States / NCI NIH HHS / CA / R21 CA143589; United States / NCI NIH HHS / CA / CA149137-01; United States / NCI NIH HHS / CA / R21 CA120625-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Receptors, Androgen
  • [Other-IDs] NLM/ NIHMS224601; NLM/ PMC3008322
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53. Morris MJ, Pandit-Taskar N, Carrasquillo J, Divgi CR, Slovin S, Kelly WK, Rathkopf D, Gignac GA, Solit D, Schwartz L, Stephenson RD, Hong C, Delacruz A, Curley T, Heller G, Jia X, O'Donoghue J, Larson S, Scher HI: Phase I study of samarium-153 lexidronam with docetaxel in castration-resistant metastatic prostate cancer. J Clin Oncol; 2009 May 20;27(15):2436-42
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  • [Title] Phase I study of samarium-153 lexidronam with docetaxel in castration-resistant metastatic prostate cancer.
  • PURPOSE: Early studies of patients with castration-resistant metastatic prostate cancer (CRMPC) suggest that chemotherapy administered with a dose of a bone-seeking radiopharmaceutical is superior to chemotherapy alone.
  • Fifteen patients demonstrated a more than 50% decline in prostate-specific antigen.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Analgesics, Non-Narcotic / administration & dosage. Analgesics, Non-Narcotic / adverse effects. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Bone and Bones / drug effects. Drug Resistance, Neoplasm. Humans. Male. Maximum Tolerated Dose. Middle Aged. Organometallic Compounds / administration & dosage. Organometallic Compounds / adverse effects. Organophosphorus Compounds / administration & dosage. Organophosphorus Compounds / adverse effects. Prostate-Specific Antigen / blood. Prostate-Specific Antigen / drug effects. Radiopharmaceuticals / administration & dosage. Radiopharmaceuticals / adverse effects. Taxoids / administration & dosage. Taxoids / adverse effects

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  • (PMID = 19364960.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K23 CA102544; United States / NCI NIH HHS / CA / CA102544
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics, Non-Narcotic; 0 / Organometallic Compounds; 0 / Organophosphorus Compounds; 0 / Radiopharmaceuticals; 0 / Taxoids; 15H5577CQD / docetaxel; 745X144DZY / samarium Sm-153 lexidronam; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Other-IDs] NLM/ PMC2684850
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54. Morey SR, Smiraglia DJ, James SR, Yu J, Moser MT, Foster BA, Karpf AR: DNA methylation pathway alterations in an autochthonous murine model of prostate cancer. Cancer Res; 2006 Dec 15;66(24):11659-67
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  • [Title] DNA methylation pathway alterations in an autochthonous murine model of prostate cancer.
  • We examined the DNA methylation pathway in an autochthonous murine prostate cancer model, transgenic adenocarcinoma of mouse prostate (TRAMP).
  • We observed that, compared with strain-matched normal prostates, primary and metastatic TRAMP tumors display increased cytosine DNA methyltransferase (Dnmt) activity, Dnmt1 and Dnmt3b protein expression, and Dnmt1, Dnmt3a, and Dnmt3b mRNA expression.
  • In summary, our data reveal a systemic DNA methylation pathway defect in TRAMP reminiscent of human prostate cancer, supporting the use of this model to investigate the functional role of DNA methylation pathway alterations in prostate cancer development.

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  • (PMID = 17178860.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5T32CA009072-31; United States / NCI NIH HHS / CA / R21 CA128062-01; United States / NCI NIH HHS / CA / R21 CA121216; United States / NCI NIH HHS / CA / P30 CA016056; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / R21 CA128062; United States / NCI NIH HHS / CA / CA128062-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Neoplasm Proteins; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase
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55. Kundranda MN, Muslimani A, Daw HA, Spiro TP: Complete remission of metastatic carcinoma of the prostate with bicalutamide withdrawal. Clin Genitourin Cancer; 2007 Sep;5(6):401-2
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  • [Title] Complete remission of metastatic carcinoma of the prostate with bicalutamide withdrawal.
  • An 83-year-old man was diagnosed with stage 4 prostate cancer with a Gleason score of 7 (3+4).
  • His initial prostate-specific antigen (PSA) level was 965 ng/dL, and he demonstrated extensive metastatic disease of the thoracic spine.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / administration & dosage. Anilides / administration & dosage. Nitriles / administration & dosage. Prostatic Neoplasms / drug therapy. Tosyl Compounds / administration & dosage
  • [MeSH-minor] Aged. Aged, 80 and over. Humans. Male. Prostate-Specific Antigen / blood. Remission Induction. Retrospective Studies

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  • (PMID = 17956714.001).
  • [ISSN] 1558-7673
  • [Journal-full-title] Clinical genitourinary cancer
  • [ISO-abbreviation] Clin Genitourin Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide; EC 3.4.21.77 / Prostate-Specific Antigen
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56. Hizli F, Berkmen F: Penile metastasis from other malignancies. A study of ten cases and review of the literature. Urol Int; 2006;76(2):118-21
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  • Furthermore, isolated metastatic penile carcinomas are exceptionally rare.
  • The rarity of the event prompted this study, which describes 10 cases of metastatic tumors of the penis including 7 cases with transitional cell carcinoma of the bladder, and in 1 case each of squamous cell carcinoma of the lung, adenocarcinoma of the prostate and leukemia.

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  • (PMID = 16493210.001).
  • [ISSN] 0042-1138
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 26
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57. Ide H, Hatake K, Terado Y, Tsukino H, Okegawa T, Nutahara K, Higashihara E, Horie S: Serum level of macrophage colony-stimulating factor is increased in prostate cancer patients with bone metastasis. Hum Cell; 2008 Feb;21(1):1-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum level of macrophage colony-stimulating factor is increased in prostate cancer patients with bone metastasis.
  • Recent evaluation of human prostate tissues has shown predominantly high expression of the macrophage colony-stimulating factor receptor in prostatic intra-epithelial neoplasia or prostate cancer.
  • However, the expression of its ligand, the macrophage colony-stimulating factor (M-CSF), and the biological role of this signaling in prostate cancer has not been analyzed.
  • In this research we determined the relationship of serum M-CSF level to clinical parameters of prostate cancer progression.
  • We measured the serum level of M-CSF in 170 patients with histologically confirmed prostatic adenocarcinoma and in 54 patients in whom prostate cancer was not detected.
  • We also investigated the M-CSF expression in prostate cancer tissues by immunohistochemistry.
  • The serum levels of M-CSF in bone metastatic prostate cancer patients was significantly higher than those in non-metastatic patients, while M-CSF did not differ with regards to histological grade, Gleason score or local tumor progression.
  • M-CSF expression was detected in prostate cancer cells themselves by immunohistochemistry.
  • These results suggest that M-CSF may have a functional role in prostate cancer progression.
  • [MeSH-major] Adenocarcinoma / secondary. Bone Neoplasms / secondary. Macrophage Colony-Stimulating Factor / blood. Macrophage Colony-Stimulating Factor / physiology. Prostatic Neoplasms / etiology. Prostatic Neoplasms / pathology

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  • (PMID = 18190394.001).
  • [ISSN] 0914-7470
  • [Journal-full-title] Human cell
  • [ISO-abbreviation] Hum. Cell
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 81627-83-0 / Macrophage Colony-Stimulating Factor
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58. Wang SQ, Mecca PS, Myskowski PL, Slovin SF: Scrotal and penile papules and plaques as the initial manifestation of a cutaneous metastasis of adenocarcinoma of the prostate: case report and review of the literature. J Cutan Pathol; 2008 Jul;35(7):681-4
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  • [Title] Scrotal and penile papules and plaques as the initial manifestation of a cutaneous metastasis of adenocarcinoma of the prostate: case report and review of the literature.
  • Cutaneous metastasis of prostatic adenocarcinoma is a rare phenomenon.
  • We present a 56-year-old African American man with metastatic disease in the skin and subcutis of the suprapubic and scrotal area 2 years after his initial diagnosis presenting as scrotal and penile edema and plaque like scrotal rash.
  • [MeSH-major] Adenocarcinoma / secondary. Genital Neoplasms, Male / secondary. Lymphedema / etiology. Penis / pathology. Prostatic Neoplasms / pathology. Scrotum / pathology. Skin Neoplasms / secondary

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  • (PMID = 18201228.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 45
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59. Adley BP, Maxwell K, Dalton DP, Yang XJ: Urothelial-type adenocarcinoma of the prostate mimicking metastatic colorectal adenocarcinoma. Int Braz J Urol; 2006 Nov-Dec;32(6):681-7; discussion 687-8
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  • [Title] Urothelial-type adenocarcinoma of the prostate mimicking metastatic colorectal adenocarcinoma.
  • Adenocarcinoma arising in urinary bladder or prostatic urethra is uncommon.
  • When they occur, the tumor can be mistaken for metastatic lesions, especially from the colon.
  • Here we report the fifth case of a primary urothelial-type adenocarcinoma arising in the prostate which showed enteric differentiation.
  • The patient was a 55 year-old male whose prostatic needle core biopsy showed a high grade adenocarcinoma which was initially thought to be metastatic colon cancer.
  • Subsequent prostatectomy revealed a high grade adenocarcinoma which was positive for cytokeratins 7 and 20, carcinoembryonic antigen, CDX2, and high molecular weight cytokeratin, and negative for prostate specific antigen, prostate specific acid phosphatase and AMACR.
  • A diagnosis of urothelial-type adenocarcinoma of the prostate was rendered.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Colorectal Neoplasms / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 17201946.001).
  • [ISSN] 1677-5538
  • [Journal-full-title] International braz j urol : official journal of the Brazilian Society of Urology
  • [ISO-abbreviation] Int Braz J Urol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
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60. Sonpavde G, Hutson TE, Berry WR, Boehm KA, Asmar L: Phase II trial of sunitinib for the therapy of progressive metastatic castration-refractory prostate cancer after previous docetaxel chemotherapy. Clin Genitourin Cancer; 2008 Sep;6(2):134-7
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  • [Title] Phase II trial of sunitinib for the therapy of progressive metastatic castration-refractory prostate cancer after previous docetaxel chemotherapy.
  • Effective options are lacking for progressive castration-refractory prostate cancer (CRPC) after conventional chemotherapy.
  • A phase II trial was conducted to examine the efficacy and toxicities of sunitinib in metastatic CRPC progressing after 1-2 previous chemotherapy regimens including docetaxel.
  • Secondary objectives included prostate-specific antigen (PSA) response, modulation of PSA kinetics, objective response, quality of life, pain, survival, and toxicities.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / therapeutic use. Indoles / therapeutic use. Prostatic Neoplasms / drug therapy. Pyrroles / therapeutic use
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Castration. Disease-Free Survival. Humans. Male. Neoplasm Metastasis. Prostate-Specific Antigen / analysis. Quality of Life



61. Gasco J, Kew Y, Livingston A, Rose J, Zhang YJ: Dissemination of prostate adenocarcinoma to the skull base mimicking giant trigeminal schwannoma: anatomic relevance of the extradural neural axis component. Skull Base; 2009 Nov;19(6):425-30
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  • [Title] Dissemination of prostate adenocarcinoma to the skull base mimicking giant trigeminal schwannoma: anatomic relevance of the extradural neural axis component.
  • We report an unusual case of a large metastatic lesion from prostate adenocarcinoma with its epicenter located in Meckel's cave.
  • The anatomic relevance the extradural neural axis component in the process of dissemination of prostate adenocarcinoma to the skull base is highlighted.

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  • (PMID = 20436844.001).
  • [ISSN] 1532-0065
  • [Journal-full-title] Skull base : official journal of North American Skull Base Society ... [et al.]
  • [ISO-abbreviation] Skull Base
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2793894
  • [Keywords] NOTNLM ; EDNAC / Meckel's cave / Prostate / brain metastases / schwannoma
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62. Jonsson E, Sigbjarnarson HP, Tomasson J, Benediktsdottir KR, Tryggvadottir L, Hrafnkelsson J, Olafsdottir EJ, Tulinius H, Jonasson JG: Adenocarcinoma of the prostate in Iceland: a population-based study of stage, Gleason grade, treatment and long-term survival in males diagnosed between 1983 and 1987. Scand J Urol Nephrol; 2006;40(4):265-71
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  • [Title] Adenocarcinoma of the prostate in Iceland: a population-based study of stage, Gleason grade, treatment and long-term survival in males diagnosed between 1983 and 1987.
  • OBJECTIVE: To investigate adenocarcinoma of the prostate in a single population with an extended follow-up period.
  • MATERIAL AND METHODS: Using the Icelandic Cancer Registry, we identified all Icelandic men diagnosed with prostate cancer between 1983 and 1987.
  • A critical evaluation was made of the accuracy of the death certificates regarding prostate cancer.
  • RESULTS: A total of 414 men were diagnosed with adenocarcinoma of the prostate.
  • Four stage groups were defined: focal incidental (n=50); localized (n=164); local advanced (n=32); and metastatic disease (n=124).
  • A total of 334 patients died during the follow-up period, of whom 168 (50%) died of prostate cancer.
  • Prostate cancer-specific survival at 10 and 15 years was 100% and 90.6%, respectively for focal incidental cancer; 73.1% and 60.8% for men with localized disease; 23.4% and 11.7% for local advanced disease; and 6.81% and 5.45% for metastatic disease.
  • A Cox multivariate analysis showed age, stage and Gleason score to be independent predictors of prostate cancer death.
  • Death certificates were judged to be accurate with regard to prostate cancer in nearly all instances (96%).
  • CONCLUSIONS: During an extended follow-up period, half of all patients with prostate cancer died from the disease.
  • However, a higher stage and grade were associated with substantial prostate cancer mortality.
  • Death certificates were accurate as far as prostate cancer was concerned.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / therapy. Prostatic Neoplasms / pathology. Prostatic Neoplasms / therapy

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  • (PMID = 16916765.001).
  • [ISSN] 0036-5599
  • [Journal-full-title] Scandinavian journal of urology and nephrology
  • [ISO-abbreviation] Scand. J. Urol. Nephrol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Sweden
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63. Mannweiler S, Amersdorfer P, Trajanoski S, Terrett JA, King D, Mehes G: Heterogeneity of prostate-specific membrane antigen (PSMA) expression in prostate carcinoma with distant metastasis. Pathol Oncol Res; 2009 Jun;15(2):167-72
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  • [Title] Heterogeneity of prostate-specific membrane antigen (PSMA) expression in prostate carcinoma with distant metastasis.
  • Prostate-specific membrane antigen (PSMA) is a transmembrane protein that is overexpressed in advanced stage prostate adenocarcinomas.
  • As a novel target for in vivo prognostic and therapeutic approaches, the distribution pattern of PSMA in primary and metastatic tumors is of significant interest.
  • Paraffin-embedded sections of 51 patients with primary prostate carcinoma and distant metastases were evaluated.
  • A significant number of the primary tumors (7/51) and metastases (6/51) presented with highly heterogeneous PSMA expression and in further 2 primary, and 8 metastatic tumors the staining was in the negative range (<10% positive tumor cells).
  • Our findings clearly support the feasibility but also direct to potential failures of PSMA-targeted in vivo diagnostic and therapeutic approaches in prostate cancer patients with distant metastasis.
  • [MeSH-major] Adenocarcinoma / metabolism. Antigens, Surface / metabolism. Cell Membrane / metabolism. Cytoplasm / metabolism. Glutamate Carboxypeptidase II / metabolism. Prostatic Neoplasms / metabolism

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  • (PMID = 18802790.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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64. Karanikolas BD, Figueiredo ML, Wu L: Comprehensive evaluation of the role of EZH2 in the growth, invasion, and aggression of a panel of prostate cancer cell lines. Prostate; 2010 May 1;70(6):675-88
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  • [Title] Comprehensive evaluation of the role of EZH2 in the growth, invasion, and aggression of a panel of prostate cancer cell lines.
  • BACKGROUND: Although most prostate cancers respond well to initial treatments, a fraction of prostate cancers are more aggressive and will recur and metastasize.
  • Polycomb Group protein enhancer of zeste 2 (EZH2) was found to be overexpressed in metastatic prostate tumors, and is considered an excellent candidate for such a biomarker.
  • Scattered studies have found that EZH2 overexpression causes neoplastic transformation, invasion, and growth of prostate cells.
  • METHODS: In this study, a comprehensive evaluation of the phenotypic effects of EZH2 in a panel of five prostate cancer cell lines was performed.
  • By using multiple cell lines, and examining overexpression and knockdown of EZH2 concurrently, a broad view of EZH2's role in prostate cancer was achieved.
  • RESULTS: Overexpression of EZH2 led to more aggressive behaviors in all prostate cell lines tested.
  • In contrast, downregulation of EZH2 reduced invasion and tumorigenicity of androgen-independent (AI) cell lines CWR22Rv1, PC3, and DU145, but not of androgen-dependent (AD) cell lines LAPC4 and LNCaP.
  • CONCLUSIONS: Findings from this study suggest that AI prostate tumors are more dependent on EZH2 expression than AD tumors.
  • Our observations provide an explanation for the strong correlation between EZH2 overexpression and advanced stage, aggressive prostate cancers.

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  • (PMID = 20087897.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI028697-17; United States / NCI NIH HHS / CA / CA092131-080007; United States / NIAID NIH HHS / AI / P30 AI028697-17; United States / NCI NIH HHS / CA / P50 CA092131; United States / NCI NIH HHS / CA / P30 CA016042; United States / NIAID NIH HHS / AI / P30 AI028697; United States / NCI NIH HHS / CA / R01 CA101904-07; United States / NCI NIH HHS / CA / P30 CA016042-34; United States / NCI NIH HHS / CA / R01 CA101904; United States / NCI NIH HHS / CA / P50 CA092131-080007; United States / NCI NIH HHS / CA / CA016042-34; United States / NCI NIH HHS / CA / CA101904-07
  • [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 / Androgens; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Transcription Factors; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2
  • [Other-IDs] NLM/ NIHMS179057; NLM/ PMC2848714
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65. Patil S, Veron A, Hosseini P, Bates R, Brown B, Guthikonda B, DeSouza R: Metastatic prostate cancer mimicking chronic subdural hematoma: a case report and review of the literature. J La State Med Soc; 2010 Jul-Aug;162(4):203-5
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  • [Title] Metastatic prostate cancer mimicking chronic subdural hematoma: a case report and review of the literature.
  • Cancer of the prostate is extremely common and is well known to metastasize to the pelvic lymph nodes and axial skeleton (vertebral column, pelvis, cranium, and proximal femur).
  • Moreover, metastatic lesions mimicking subdural hematoma are extremely rare and are uncommonly reported in the literature.
  • We present a unique case of metastatic prostate cancer presenting with headaches after head trauma with classic radiologic findings of subdural hematoma.
  • [MeSH-major] Adenocarcinoma / secondary. Hematoma, Subdural, Chronic / diagnosis. Meningeal Neoplasms / secondary. Prostatic Neoplasms / pathology

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  • (PMID = 20882812.001).
  • [ISSN] 0024-6921
  • [Journal-full-title] The Journal of the Louisiana State Medical Society : official organ of the Louisiana State Medical Society
  • [ISO-abbreviation] J La State Med Soc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
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66. Mavis CK, Morey Kinney SR, Foster BA, Karpf AR: Expression level and DNA methylation status of glutathione-S-transferase genes in normal murine prostate and TRAMP tumors. Prostate; 2009 Sep 1;69(12):1312-24
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  • [Title] Expression level and DNA methylation status of glutathione-S-transferase genes in normal murine prostate and TRAMP tumors.
  • BACKGROUND: Glutathione-S-transferase (Gst) genes are downregulated in human prostate cancer, and GSTP1 silencing is mediated by promoter DNA hypermethylation in this malignancy.
  • We examined Gst gene expression and Gst promoter DNA methylation in normal murine prostates and Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) tumors.
  • METHODS: Primary and metastatic tumors were obtained from TRAMP mice, and normal prostates were obtained from strain-matched WT mice (n = 15/group).
  • RESULTS: Of the genes analyzed, GstM1 and GstP1 were expressed at highest levels in normal prostate.
  • All five Gst genes showed greatly reduced expression in primary tumors compared to normal prostate, but not in tumor metastases.
  • Gst promoter methylation was unchanged in TRAMP tumors compared to normal prostate.
  • CONCLUSIONS: Gst genes are extensively downregulated in primary but not metastatic TRAMP tumors.

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  • (PMID = 19444856.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA128062-01; United States / NCI NIH HHS / CA / P30 CA016056; United States / NCI NIH HHS / CA / R21CA128062; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / R21 CA128062; United States / NCI NIH HHS / CA / R21 CA128062-02; United States / NCI NIH HHS / CA / CA128062-02; United States / NCI NIH HHS / CA / CA128062-01; United States / NCI NIH HHS / CA / 5T32CA009072; United States / NCI NIH HHS / CA / T32 CA009072
  • [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 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0 / Hydroxamic Acids; 0 / RNA, Messenger; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / Gstp1 protein, mouse; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ NIHMS182170; NLM/ PMC2836025
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67. Kaplan-Lefko PJ, Sutherland BW, Evangelou AI, Hadsell DL, Barrios RJ, Foster BA, Demayo F, Greenberg NM: Enforced epithelial expression of IGF-1 causes hyperplastic prostate growth while negative selection is requisite for spontaneous metastogenesis. Oncogene; 2008 May 1;27(20):2868-76
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  • [Title] Enforced epithelial expression of IGF-1 causes hyperplastic prostate growth while negative selection is requisite for spontaneous metastogenesis.
  • The insulin-like growth factor-1 (IGF-1) signaling axis is important for cell growth, differentiation and survival and increased serum IGF is a risk factor for prostate and other cancers.
  • To study IGF-1 action on the prostate, we created transgenic (PB-Des) mice that specifically express human IGF-1(des) in prostate epithelial cells.
  • Expression of IGF-1(des) was sufficient to cause hyperplastic lesions in all mice, however the well-differentiated lesions did not progress to adenocarcinoma within a year.
  • Remarkably, crossing the PB-Des mice to an established model of prostate cancer delayed progression of organ-confined tumors and emergence of metastatic lesions in young mice.
  • While dissemination of metastatic lesions was widespread in old bigenic mice we did not detect IGF-1(des) in poorly differentiated primary tumors or metastatic lesions.
  • [MeSH-major] Insulin-Like Growth Factor I / biosynthesis. Insulin-Like Growth Factor I / genetics. Prostate / metabolism. Prostate / pathology. Prostatic Hyperplasia / pathology. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / secondary. Animals. Brain Neoplasms / secondary. Cell Differentiation / physiology. Epithelium / metabolism. Epithelium / pathology. Heart Neoplasms / secondary. Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Male. Mice. Mice, Transgenic. Splenic Neoplasms / secondary. Thymus Neoplasms / secondary. Urologic Neoplasms / secondary



68. Massoud W, Paparel P, Lopez JG, Perrin P, Daumont M, Ruffion A: Discovery of a pituitary adenoma following treatment with a gonadotropin-releasing hormone agonist in a patient with prostate cancer. Int J Urol; 2006 Jan;13(1):87-8
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  • [Title] Discovery of a pituitary adenoma following treatment with a gonadotropin-releasing hormone agonist in a patient with prostate cancer.
  • We report the case of a T3 prostate cancer in a 70-year-old white man.
  • Hormone therapy represents a prominent branch in the treatment of locally advanced and metastatic prostate cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenoma / chemically induced. Antineoplastic Agents, Hormonal / adverse effects. Gonadotropin-Releasing Hormone / agonists. Leuprolide / adverse effects. Pituitary Neoplasms / chemically induced. Prostatic Neoplasms / drug therapy

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  • (PMID = 16448441.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone; EFY6W0M8TG / Leuprolide
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69. Yagihashi Y, Okinami T, Fukuzawa S, Kuriki K: [Pericardial effusion due to metastatic prostate cancer: a case report]. Hinyokika Kiyo; 2008 May;54(5):369-72
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  • [Title] [Pericardial effusion due to metastatic prostate cancer: a case report].
  • We describe a patient whose complaints were related to pericardial effusion due to prostatic carcinoma.
  • Cytologic study suggested metastatic adenocarcinoma or malignant mesothelioma.
  • At autopsy, the major finding was poorly differentiated adenocarcinoma of the prostate with metastases to the mediastinum.
  • [MeSH-major] Adenocarcinoma / pathology. Mediastinal Neoplasms / secondary. Pericardial Effusion / etiology. Prostatic Neoplasms / pathology



70. Lee DK: Prostate cancer metastases to the leg, ankle, and foot. J Am Podiatr Med Assoc; 2008 May-Jun;98(3):242-5
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  • [Title] Prostate cancer metastases to the leg, ankle, and foot.
  • Metastases to the bones of the lower extremities from prostate carcinomas are rare and are usually associated with diffuse metastatic disease or primary tumors of the abdomen and lungs.
  • I present the case of a patient who presented with lower leg pain and had undiagnosed prostate carcinoma.
  • Unlike previous reports of prostate carcinoma, this rare case includes magnetic resonance imaging, histology, and medical management.
  • [MeSH-major] Adenocarcinoma / secondary. Lower Extremity. Prostatic Neoplasms / pathology

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  • (PMID = 18487599.001).
  • [ISSN] 8750-7315
  • [Journal-full-title] Journal of the American Podiatric Medical Association
  • [ISO-abbreviation] J Am Podiatr Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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71. Ajani JA, Safran H, Bokemeyer C, Shah MA, Lenz HJ, Van Cutsem E, Burris HA 3rd, Lebwohl D, Mullaney B: A multi-center phase II study of BMS-247550 (Ixabepilone) by two schedules in patients with metastatic gastric adenocarcinoma previously treated with a taxane. Invest New Drugs; 2006 Sep;24(5):441-6
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  • [Title] A multi-center phase II study of BMS-247550 (Ixabepilone) by two schedules in patients with metastatic gastric adenocarcinoma previously treated with a taxane.
  • With the primary endpoint of assessing ixabepilone's response rate against metastatic gastric cancer previously treated with a taxane, we performed a multi-center phase II trial.
  • PATIENTS AND METHODS: Patients with histologically documented metastatic gastric or gastroesophageal adenocarcinoma, who had previously received a taxane, were eligible.
  • CONCLUSIONS: Ixabepilone, on a once every 21-day schedule, is modestly active against metastatic gastric cancer previously treated with a taxane.
  • The results of this study suggest that once every 21-day ixabepilone schedule should be pursued further in untreated gastric or gastroesophageal adenocarcinoma patients.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / therapeutic use. Epothilones / therapeutic use. Stomach Neoplasms / drug therapy

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  • (PMID = 16586011.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bridged-Ring Compounds; 0 / Epothilones; 0 / Taxoids; 1605-68-1 / taxane; K27005NP0A / ixabepilone
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72. Sung MT, Jiang Z, Montironi R, MacLennan GT, Mazzucchelli R, Cheng L: Alpha-methylacyl-CoA racemase (P504S)/34betaE12/p63 triple cocktail stain in prostatic adenocarcinoma after hormonal therapy. Hum Pathol; 2007 Feb;38(2):332-41
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  • [Title] Alpha-methylacyl-CoA racemase (P504S)/34betaE12/p63 triple cocktail stain in prostatic adenocarcinoma after hormonal therapy.
  • Alpha-methylacyl-CoA racemase (AMACR) has recently been shown to be a highly sensitive marker for the diagnosis of prostate cancer.
  • However, there is limited information concerning its utility as a marker for prostate carcinoma after hormonal therapy.
  • Our current investigation was conducted to evaluate the expression of AMACR in patients with prostate carcinoma after hormonal therapy and assess its diagnostic utility in combination with p63 and high molecular weight cytokeratin (34betaE12) staining.
  • Prostate tissues from 49 patients who had been treated with hormonal therapy were immunohistochemically analyzed for AMACR, 34betaE12, and p63 expression by a triple antibody cocktail stain.
  • The correlations between AMACR expression and metastatic status, associated hormonal therapy regimens, and the extent of hormone therapy effect were analyzed.
  • alpha-methylacyl-CoA racemase expression may be substantially diminished or entirely lost in prostate carcinoma after hormonal therapy.
  • This variation in AMACR expression does not correlate with the metastatic status, the modality of hormonal therapy, or the extent of therapy-related effect.
  • It is important that pathologists be aware that some hormonally treated prostate carcinomas do not express AMACR, and that immunostaining in such cases must be interpreted with caution.
  • A triple cocktail stain using AMACR, 34betaE12, and p63 can be helpful in evaluating prostate specimens for the presence of residual or recurrent carcinoma after hormonal therapy for cancer.
  • [MeSH-major] Adenocarcinoma / pathology. DNA-Binding Proteins / analysis. Keratins / analysis. Prostatic Neoplasms / pathology. Racemases and Epimerases / analysis. Trans-Activators / analysis. Tumor Suppressor Proteins / analysis

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  • (PMID = 17134736.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / CK-34 beta E12; 0 / DNA-Binding Proteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 68238-35-7 / Keratins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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73. Deb P, Chander Y, Rai RS: Testicular metastasis from carcinoma of prostate: report of two cases. Prostate Cancer Prostatic Dis; 2007;10(2):202-4
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  • [Title] Testicular metastasis from carcinoma of prostate: report of two cases.
  • Despite the high incidence of prostatic adenocarcinoma and its ability for wide dissemination, metastatic involvement of testis is rather uncommon.
  • We report two cases (aged 76 and 55 years, respectively), where unilateral testicular metastasis was incidentally discovered after bilateral orchiectomy following detection of adenocarcinoma prostate in six-quadrant trucut specimen.
  • Both patients had obstructive voiding symptoms, hard nodular prostate on direct rectal examination and raised serum prostate-specific antigen levels, without associated systemic or testicular symptoms.
  • [MeSH-major] Adenocarcinoma / pathology. Prostatic Neoplasms / pathology. Testicular Neoplasms / secondary

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  • (PMID = 17224911.001).
  • [ISSN] 1365-7852
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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74. Heebøll S, Borre M, Ottosen PD, Andersen CL, Mansilla F, Dyrskjøt L, Orntoft TF, Tørring N: SMARCC1 expression is upregulated in prostate cancer and positively correlated with tumour recurrence and dedifferentiation. Histol Histopathol; 2008 09;23(9):1069-76
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  • [Title] SMARCC1 expression is upregulated in prostate cancer and positively correlated with tumour recurrence and dedifferentiation.
  • BACKGROUND: The identification of new prognostic markers in prostate cancer (PC) is essential to improve patient treatment and management.
  • MATERIALS: Expression of SMARCC1 immunostaining was analysed on a tissue microarray containing specimens from 327 patients with prostate cancer and clinical follow-up information.
  • Furthermore, 30 specimens from patients with benign prostate hyperplasia were included as controls as well as 30 specimens of benign prostate tissue from PC patients.
  • In contrast, 20% of the specimens from patients with non-metastatic and non-recurrent disease showed moderate to marked staining.
  • In 31% of the patients with recurrent disease and in 31% of the patients with metastatic disease we found moderate to strong SMARCC1 immunostaining.
  • In a logistic regression analysis, patients with a marked SMARCC1 immunostaining had a significantly elevated odds ratio (OR) of 16 for recurrent cancer and an OR of 4.5 for metastatic disease.
  • Conclusions. Our present results demonstrate an increased expression of SMARCC1 protein in prostate cancer and reveal a positive correlation with tumour dedifferentiation, progression, metastasis and time to recurrence.
  • [MeSH-major] Adenocarcinoma / metabolism. Prostatic Neoplasms / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. COS Cells. Cell Dedifferentiation. Cell Nucleus / metabolism. Cell Nucleus / pathology. Cercopithecus aethiops. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Lymph Nodes / metabolism. Lymph Nodes / pathology. Lymphatic Metastasis. Male. Neoplasm Recurrence, Local. Odds Ratio. Prostate / metabolism. Prostate / pathology. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology. Tissue Array Analysis. Up-Regulation

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  • (PMID = 18581278.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / SMARCC1 protein, human; 0 / Transcription Factors
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75. Hardie C, Parker C, Norman A, Eeles R, Horwich A, Huddart R, Dearnaley D: Early outcomes of active surveillance for localized prostate cancer. BJU Int; 2005 May;95(7):956-60
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  • [Title] Early outcomes of active surveillance for localized prostate cancer.
  • OBJECTIVE: To describe the preliminary clinical outcomes of active surveillance (AS), a new strategy aiming to individualize the management of early prostate cancer by selecting only those men with significant cancers for curative therapy, and illustrate the contrast with a policy of watchful waiting (WW).
  • PATIENTS AND METHODS: Eighty men with early prostate cancer began AS at the authors' institution between 1993 and 2002.
  • Eligibility included histologically confirmed prostatic adenocarcinoma, fitness for radical treatment, clinical stage T1/T2, N0/X, M0/X, a prostate specific antigen (PSA) level of < or = 20 ng/mL, and a Gleason score of < or = 7.
  • During the same period, 32 men with localized prostate cancer (any T stage, N0/X, M0/X, any PSA, Gleason score < or = 7) were managed by WW; hormonal treatment was indicated for symptomatic prostate cancer progression.
  • No patient developed evidence of metastatic disease, none started palliative hormone therapy, and there were no deaths from prostate cancer.
  • Twenty (62%) of the 32 patients on WW remained on observation, eight (25%) received palliative hormonal therapy and four (12%) died, including one from prostate cancer.
  • CONCLUSIONS: AS is feasible in selected men with early prostate cancer.
  • [MeSH-major] Adenocarcinoma / therapy. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Clinical Protocols. Disease-Free Survival. Feasibility Studies. Follow-Up Studies. Humans. Male. Middle Aged. Prognosis. Prostate-Specific Antigen / blood. Prostatectomy / methods



76. Taplin ME, George DJ, Halabi S, Sanford B, Febbo PG, Hennessy KT, Mihos CG, Vogelzang NJ, Small EJ, Kantoff PW: Prognostic significance of plasma chromogranin a levels in patients with hormone-refractory prostate cancer treated in Cancer and Leukemia Group B 9480 study. Urology; 2005 Aug;66(2):386-91
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  • [Title] Prognostic significance of plasma chromogranin a levels in patients with hormone-refractory prostate cancer treated in Cancer and Leukemia Group B 9480 study.
  • OBJECTIVES: To test the hypothesis that chromogranin A (CgA) levels are prognostic in patients with metastatic hormone-refractory prostate cancer (HRPC).
  • The extent of neuroendocrine differentiation in prostate cancer correlates with aggressive disease and with progression to HRPC.
  • Plasma CgA levels in patients with prostate cancer may reflect the extent of the tumor neuroendocrine phenotype.
  • METHODS: Pretreatment plasma was collected from 390 patients with metastatic HRPC enrolled in the Cancer and Leukemia Group B (CALGB) 9480 trial, a study of three different doses of suramin.
  • In multivariate models (adjusting for performance status, prostate-specific antigen, and lactate dehydrogenase), the plasma CgA levels remained predictive of overall survival.
  • [MeSH-major] Adenocarcinoma / blood. Adenocarcinoma / mortality. Chromogranins / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / mortality



77. Théodore C: [Chemotherapy indications in the treatment of metastases from urological malignancies]. Prog Urol; 2008 Nov;18 Suppl 7:S219-22
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  • [Transliterated title] Indications de la chimiothérapie dans le traitement des cancers urologiques métastatiques.
  • Chemotherapy is useful for many metastatic urological cancer treatments.
  • Very efficient for testis tumors, it is at present the best weapon against metastatic urothelial tumors, especially for transitional cell carcinoma of the bladder.
  • For prostate cancer, chemotherapy is used when metastatic adenocarcinoma has become refractory to hormonal treatment.

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  • (PMID = 19070795.001).
  • [ISSN] 1166-7087
  • [Journal-full-title] Progrès en urologie : journal de l'Association française d'urologie et de la Société française d'urologie
  • [ISO-abbreviation] Prog. Urol.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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78. Bonkhoff H: [Differential diagnosis of prostate cancer: impact of pattern analysis and immunohistochemistry]. Pathologe; 2005 Nov;26(6):405-21
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  • [Title] [Differential diagnosis of prostate cancer: impact of pattern analysis and immunohistochemistry].
  • [Transliterated title] Differenzialdiagnose des Prostatakarzinoms. Rolle der Mustererkennung und der Immunhistochemie.
  • Prostate cancer offers a wide range of growth patterns depicted in the classical Gleason diagram.
  • For each Gleason pattern exist a number of benign and malignant mimickers that can simulate prostatic adenocarcinoma.
  • In the present review, the use of immunohistochemical markers is discussed with emphasis to a pattern-based approach to differential diagnosis in prostate pathology.
  • AMACR (P504 s) is helpful not only in identifying small amount of cancer in needle biopsies but also in the diagnosis of high grade prostatic intra epithelial neoplasia (HGPIN).
  • A number of lesions which may be confused with small acinar adenocarcinoma (Cowper's gland, nephrogenic metaplasia, mesonephric glands) and poorly differentiated prostate cancer (urothelial neoplasia, mucinous colon cancer and other metastatic lesions) lacks convincing PSA immunoreactivity.
  • Basal cell markers and the nuclear androgen receptors are important markers to differentiate Gleason grade 5 A und 5 B patterns from prostatic involvement by transitional cell carcinoma.
  • Finally, a selected panel of markers is useful to classify prostatic stromal lesions.
  • [MeSH-major] Biomarkers, Tumor / analysis. Prostate / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Carcinoma, Basal Cell / pathology. Cell Division / physiology. Diagnosis, Differential. Humans. Male. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial Neoplasia / pathology



79. Roca Edreira A, Aguilera Tubet C, Villanueva Peña A, Ballestero Diego R, Zubillaga Guerrero S: [Mediastinal lymph nodes during the course of a metastatic prostate cancer]. Actas Urol Esp; 2007 Jun;31(6):693-5; discussion 695
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  • [Title] [Mediastinal lymph nodes during the course of a metastatic prostate cancer].
  • [Transliterated title] Adenopatías mediastínicas en la evolución de un cancer de próstata metastásico.
  • Prostate carcinoma is one of the most frecuent cancers in men.
  • We report the case of a patient with prostate cancer who develops mediastinal lymphadenopathy, pulmonary nodules and cutaneous metastases 8 years after the diagnosis.
  • [MeSH-major] Adenocarcinoma / secondary. Androgens. Lymphatic Metastasis. Mediastinum / pathology. Neoplasms, Hormone-Dependent / secondary. Prostatic Neoplasms / pathology

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  • (PMID = 17896567.001).
  • [ISSN] 0210-4806
  • [Journal-full-title] Actas urologicas españolas
  • [ISO-abbreviation] Actas Urol Esp
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / Diphosphonates; 0 / Imidazoles; 35LT29625A / Estramustine; 57773-63-4 / Triptorelin Pamoate; 6XC1PAD3KF / zoledronic acid; 76W6J0943E / Flutamide; E61Q31EK2F / Cyproterone; R9400W927I / Ketoconazole
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80. Merrick GS, Butler WM, Wallner KE, Galbreath RW, Allen Z, Lief JH, Adamovich E: Influence of body mass index on biochemical outcome after permanent prostate brachytherapy. Urology; 2005 Jan;65(1):95-100
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  • [Title] Influence of body mass index on biochemical outcome after permanent prostate brachytherapy.
  • OBJECTIVES: To evaluate the impact of body mass index (BMI) on the 8-year biochemical outcome after permanent prostate brachytherapy with or without the addition of supplemental external beam radiotherapy and/or androgen deprivation therapy (ADT).
  • METHODS: From April 1995 through February 2001, 686 consecutive patients underwent brachytherapy using either palladium-103 or iodine-125 for clinical Stage T1b-T3aNxM0 (2002 American Joint Committee on Cancer) prostate cancer.
  • Biochemical progression-free survival was defined by a prostate-specific antigen (PSA) level of 0.4 ng/mL or less after a nadir.
  • The clinical, treatment, and dosimetric parameters evaluated for biochemical progression-free survival included BMI, patient age, clinical T stage, Gleason score, preimplant PSA level, risk group, percentage of positive biopsies, isotope, use of supplemental external beam radiotherapy, use of ADT, prostate volume, planning volume, percentage of target volume receiving 100%, 150%, and 200% of the prescribed dose, minimal percentage of dose covering 90% of the target volume, tobacco use, and the presence of hypertension and diabetes.
  • At last follow-up, 5 patients (0.7%) had died of metastatic prostate cancer.
  • CONCLUSIONS: Prostate brachytherapy results in a high probability of 8-year biochemical progression-free survival for low, intermediate, and high-risk patients.
  • [MeSH-major] Adenocarcinoma / radiotherapy. Body Mass Index. Brachytherapy. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Aged. Antineoplastic Agents, Hormonal / therapeutic use. Biomarkers, Tumor / blood. Combined Modality Therapy. Disease-Free Survival. Follow-Up Studies. Humans. Life Tables. Male. Middle Aged. Neoplasm Proteins / blood. Obesity / complications. Proportional Hazards Models. Prostate-Specific Antigen / blood. Radiotherapy, High-Energy. Risk. Treatment Outcome

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  • (PMID = 15667872.001).
  • [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 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; EC 3.4.21.77 / Prostate-Specific Antigen
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81. Balanathan P, Williams ED, Wang H, Pedersen JS, Horvath LG, Achen MG, Stacker SA, Risbridger GP: Elevated level of inhibin-alpha subunit is pro-tumourigenic and pro-metastatic and associated with extracapsular spread in advanced prostate cancer. Br J Cancer; 2009 Jun 2;100(11):1784-93
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  • [Title] Elevated level of inhibin-alpha subunit is pro-tumourigenic and pro-metastatic and associated with extracapsular spread in advanced prostate cancer.
  • The biological function of inhibin-alpha subunit (INH alpha) in prostate cancer (PCa) is currently unclear.
  • This prompted us to use clinical specimens and functional studies to investigate the pro-tumourigenic and pro-metastatic function of INH alpha.
  • This study is the first to demonstrate a pro-tumourigenic and pro-metastatic function for INH alpha associated with androgen-independent stage of metastatic prostate disease.
  • Our results also suggest that INH alpha expression in the primary prostate tumour can be used as a predictive factor for prognosis of PCa.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Inhibins / metabolism. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Cell Line, Tumor. Cell Separation. Gene Expression Regulation, Neoplastic. Humans. Male. Neoplasm Metastasis / genetics. Neoplasm Metastasis / pathology. Neoplasm Staging

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  • (PMID = 19436293.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
  • [Other-IDs] NLM/ PMC2695696
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82. Saleem M, Kweon MH, Johnson JJ, Adhami VM, Elcheva I, Khan N, Bin Hafeez B, Bhat KM, Sarfaraz S, Reagan-Shaw S, Spiegelman VS, Setaluri V, Mukhtar H: S100A4 accelerates tumorigenesis and invasion of human prostate cancer through the transcriptional regulation of matrix metalloproteinase 9. Proc Natl Acad Sci U S A; 2006 Oct 3;103(40):14825-30
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  • [Title] S100A4 accelerates tumorigenesis and invasion of human prostate cancer through the transcriptional regulation of matrix metalloproteinase 9.
  • We previously showed that the calcium-binding protein S100A4 is overexpressed during the progression of prostate cancer (CaP) in humans and in the TRAMP (transgenic adenocarcinoma of the mouse prostate) mouse model.
  • We tested a hypothesis that the S100A4 gene plays a role in the invasiveness of human CaP and may be associated with its metastatic spread.
  • We evaluated the mechanism through which the S100A4 gene controls invasiveness of cells by using a macroarray containing 96 well characterized metastatic genes.

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  • (PMID = 16990429.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P50 DK065303; United States / NCI NIH HHS / CA / R01 CA 101039; United States / NCI NIH HHS / CA / R01 CA078809; United States / NCI NIH HHS / CA / R01 CA 78809; United States / NCI NIH HHS / CA / R01 CA101039; United States / NIDDK NIH HHS / DK / P50 DK 65303
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / S100 Proteins; 0 / Tissue Inhibitor of Metalloproteinase-1; 142662-27-9 / S100A4 protein, human; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC1595436
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83. Veshapidze N, Alibegashvili M, Gabunia N, Ramishvili L, Kotrikadze N: Erythrocyte membrane permeability in the men with metastatic adenocarcinoma of the prostate. Georgian Med News; 2009 Jan;(166):9-12
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  • [Title] Erythrocyte membrane permeability in the men with metastatic adenocarcinoma of the prostate.
  • The aim of our study was to investigate the alterations of the erythrocyte membrane permeability in the men with metastatic adenocarcinoma of the prostate before and six months after castration.
  • For experimental research were used the erythrocytes of 15 men with metastatic prostate cancer (Pca) (before and after 6 months from castration) and of the 15 practically healthy men (control group).
  • Investigations revealed the changes of Na(+)/K(+)-ATP-ase activity and the changes of Na(+) and K(+) ions concentration in metastatic Pca patients before and six months after castration.
  • [MeSH-major] Adenocarcinoma / metabolism. Cell Membrane Permeability / physiology. Erythrocyte Membrane / metabolism. Prostatic Neoplasms / metabolism. Sodium-Potassium-Exchanging ATPase / metabolism

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  • (PMID = 19202209.001).
  • [ISSN] 1512-0112
  • [Journal-full-title] Georgian medical news
  • [ISO-abbreviation] Georgian Med News
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Georgia (Republic)
  • [Chemical-registry-number] 9NEZ333N27 / Sodium; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase; RWP5GA015D / Potassium
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84. Müller Arteaga C, Egea Camacho J, Alvarez Gago T, Cortiñas González JR, Gonzalo Rodríguez V, Fernández del Busto E: [Spermatic cord liposarcoma. Association with prostate cancer. Report of a case and review of literature]. Actas Urol Esp; 2005 Jul-Aug;29(7):700-3
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  • [Title] [Spermatic cord liposarcoma. Association with prostate cancer. Report of a case and review of literature].
  • [Transliterated title] Liposarcoma de cordón espermático. Asociación con carcinoma de próstata. Comunicación de un caso y revisión de la literatura.
  • We describe and relation between liposarcoma and prostate cancer in a 66 years old patient who had a left paratesticular tumor with low speed growth and 12 cm of length; nodule in prostate gland was detected.
  • Ecography demostrate an hipoecoic tumor in the spermatic cord; Prostate Specific Antigen (PSA) was 1276 ng.
  • /ml. and bone gammagraphy reported metastatic lesions.
  • [MeSH-major] Adenocarcinoma / complications. Liposarcoma / complications. Prostatic Neoplasms / complications. Spermatic Cord / pathology



85. Gurel B, Iwata T, Koh CM, Jenkins RB, Lan F, Van Dang C, Hicks JL, Morgan J, Cornish TC, Sutcliffe S, Isaacs WB, Luo J, De Marzo AM: Nuclear MYC protein overexpression is an early alteration in human prostate carcinogenesis. Mod Pathol; 2008 Sep;21(9):1156-67
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  • [Title] Nuclear MYC protein overexpression is an early alteration in human prostate carcinogenesis.
  • A region on chromosome 8q24 encompassing the MYC locus is amplified in prostate cancer, but this occurs mostly in advanced disease suggesting that MYC alterations occur late in prostate cancer.
  • In contrast, MYC mRNA is elevated in most prostate cancers, even those of relatively low stage and grade (eg Gleason score 6) suggesting that MYC plays a role in initiation.
  • Thus, it is critical to determine whether MYC protein is elevated in human prostate cancer, and if so, at what stage of the disease this elevation occurs.
  • We utilized a new anti-MYC antibody coupled with genetically defined control experiments to localize MYC protein within human tissue microarrays consisting of normal, atrophy, PIN, primary adenocarcinoma, and metastatic adenocarcinoma.
  • Nuclear overexpression of MYC protein occurred frequently in luminal cells of PIN, as well as in most primary carcinomas and metastatic disease.
  • These results provide evidence that upregulation of nuclear MYC protein expression is a highly prevalent and early change in prostate cancer and suggest that increased nuclear MYC may be a critical oncogenic event driving human prostate cancer initiation and progression.

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  • (PMID = 18567993.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA058236; United States / NCI NIH HHS / CA / P50 CA058236-11; United States / NCI NIH HHS / CA / P50CA58236
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger
  • [Other-IDs] NLM/ NIHMS285485; NLM/ PMC3170853
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86. Lin S, Shen YH, Zhang ZX, Li HL, Shan L, Liu RH, Xu XK, Zhang WD: Revision of the Structures of 1,5-Dihydroxy-3,8-epoxyvalechlorine, Volvaltrate B, and Valeriotetrate C from Valeriana jatamansi and V. officinalis. J Nat Prod; 2010 Oct 22;73(10):1723-6
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  • Volvaltrate B (6) showed cytotoxic activity against the lung adenocarcinoma (A549), metastatic prostate cancer (PC-3M), colon cancer (HCT-8), and hepatoma (Bel7402) cell lines, with IC50 values of 8.5, 2.0, 3.2, and 6.1 μM, respectively.
  • [MeSH-minor] Colonic Neoplasms. Drug Screening Assays, Antitumor. Humans. Male. Molecular Structure. Nuclear Magnetic Resonance, Biomolecular. Plant Roots / chemistry. Prostatic Neoplasms / drug therapy

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  • (PMID = 20853876.001).
  • [ISSN] 1520-6025
  • [Journal-full-title] Journal of natural products
  • [ISO-abbreviation] J. Nat. Prod.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Drugs, Chinese Herbal; 0 / Iridoids; 0 / valeriotetrate C; 0 / volvaltrate B
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87. Knight D, Peterson AC, Rini BI, Harlin H, Gajewski TF, Stadler WM: The HLA-A2-restricted PSMA peptide LLHETDSAV is poorly immunogenic in patients with metastatic prostate cancer. Prostate; 2009 Feb 1;69(2):142-8
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  • [Title] The HLA-A2-restricted PSMA peptide LLHETDSAV is poorly immunogenic in patients with metastatic prostate cancer.
  • BACKGROUND: Increasing evidence suggests that prostate cancer is visible to the immune system and is potentially responsive to immunotherapeutic interventions.
  • Previous work has identified prostate-specific membrane antigen (PSMA) as a potential antigen for T-cell recognition, and specific PSMA epitopes presented by HLA-A2 have been described.
  • METHODS: HLA-A2(+) patients with castrate-resistant prostate cancer and normal organ function were considered.
  • CONCLUSIONS: Our results suggest that the PSMA peptide LLHETDSAV is poorly immunogenic in humans and that alternative prostate cancer antigens should be pursued.
  • [MeSH-major] Adenocarcinoma / immunology. Antigens, Surface / immunology. Glutamate Carboxypeptidase II / immunology. Peptide Fragments / immunology. Prostatic Neoplasms / immunology

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  • (PMID = 18942640.001).
  • [ISSN] 1097-0045
  • [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, Surface; 0 / Cancer Vaccines; 0 / Epitopes; 0 / HLA-A2 Antigen; 0 / Peptide Fragments; 0 / Recombinant Proteins; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
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88. Hansel DE, Epstein JI: Sarcomatoid carcinoma of the prostate: a study of 42 cases. Am J Surg Pathol; 2006 Oct;30(10):1316-21
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  • [Title] Sarcomatoid carcinoma of the prostate: a study of 42 cases.
  • Sarcomatoid carcinoma of the prostate is a rare type of prostatic cancer.
  • We examined transurethral resection, needle biopsy, and radical prostatectomy specimens from 42 patients with sarcomatoid carcinoma of the prostate, all of which were received in consultation.
  • Prior prostatic adenocarcinoma: The majority of patients (n=21; 66%) had a prior history of acinar adenocarcinoma of the prostate.
  • Of the remaining patients for whom this information was known, 11 patients presented with de novo sarcomatoid carcinoma.
  • The time between the original diagnosis of acinar adenocarcinoma and diagnosis of sarcomatoid carcinoma ranged from 6 months to 16 years (mean 6.8 y).
  • Concurrent adenocarcinoma: The majority of patients demonstrated a concurrent high grade acinar carcinoma of Gleason score 7 (n=3), 8 (n=9), 9 (n=10), and 10 (n=10).
  • A subset of patients contained an admixed ductal adenocarcinoma (n=4), small cell carcinoma (n=3), squamous cell carcinoma (n=3), or other unusual pattern of prostate carcinoma (n=3).
  • In 1 case, the diagnosis was based on immunohistochemical evidence of epithelial differentiation along with the history of prior adenocarcinoma.
  • Of the 12 cases with received immunostains of the sarcomatoid component, 5/7 cases were at least focally positive for cytokeratin, 1/1 case was focally positive for Cam5.2, and 3/6 cases were focally positive for prostate acid phosphatase.
  • The sarcomatoid component did not demonstrate immunoreactivity for prostate-specific antigen in 8 cases.
  • PROGNOSIS: approximately half of all patients developed metastatic disease either at time of presentation or subsequently.
  • No correlation was identified between patient survival and morphologic features, before radiation or hormone therapy, or concurrent high-grade prostate cancer.
  • The epithelial component is typically high-grade acinar adenocarcinoma, yet other aggressive tumor subtypes such as ductal adenocarcinoma and small cell carcinoma may also be seen.
  • Sarcomatoid carcinoma is an aggressive form of prostate cancer, the prognosis of which is dismal regardless of other histologic or clinical findings.
  • [MeSH-major] Carcinosarcoma / secondary. Prostatic Neoplasms / pathology

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  • (PMID = 17001164.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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89. Yang S, Zhong C, Frenkel B, Reddi AH, Roy-Burman P: Diverse biological effect and Smad signaling of bone morphogenetic protein 7 in prostate tumor cells. Cancer Res; 2005 Jul 1;65(13):5769-77
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  • [Title] Diverse biological effect and Smad signaling of bone morphogenetic protein 7 in prostate tumor cells.
  • We found that bone morphogenetic protein (BMP) 7, a member of the BMP family, was strikingly up-regulated during the development of primary prostatic adenocarcinoma in the conditional Pten deletion mouse model.
  • To determine the relevance of this finding to human prostate cancer, we examined the expression of BMPs and BMP receptors (BMPR) as well as the responsiveness to recombinant human BMP7 in a series of human prostate tumor cell lines.
  • All prostatic cell lines tested expressed variable levels of BMP2, BMP4, and BMP7 and at least two of each type I and II BMPRs.
  • BPH-1, a cell line representing benign prostatic epithelial hyperplasia, was growth arrested at G1.
  • In the bone metastasis-derived PC-3 prostate cancer cells, BMP7 induced epithelial-mesenchymal transdifferentiation with classic changes in morphology, motility, invasiveness, and molecular markers.
  • Finally, BMP7 inhibited serum starvation-induced apoptosis in the LNCaP prostate cancer cell line and more remarkably in its bone metastatic variant C4-2B line.
  • Taken together, these findings suggest that BMPs are able to modulate the biological behavior of prostate tumor cells in diverse and cell type-specific manner and point to certain mechanisms by which these secreted signaling molecules may contribute to prostate cancer growth and metastasis.
  • [MeSH-major] Adenocarcinoma / pathology. Bone Morphogenetic Proteins / physiology. DNA-Binding Proteins / physiology. Prostatic Neoplasms / pathology. Trans-Activators / physiology. Transforming Growth Factor beta / physiology

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  • (PMID = 15994952.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA59705
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BMP7 protein, human; 0 / Bone Morphogenetic Protein 7; 0 / Bone Morphogenetic Proteins; 0 / DNA-Binding Proteins; 0 / Recombinant Proteins; 0 / Smad Proteins; 0 / Trans-Activators; 0 / Transforming Growth Factor beta
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90. Pommier P, Chabaud S, Lagrange JL, Richaud P, Lesaunier F, Le Prise E, Wagner JP, Hay MH, Beckendorf V, Suchaud JP, Pabot du Chatelard PM, Bernier V, Voirin N, Perol D, Carrie C: Is there a role for pelvic irradiation in localized prostate adenocarcinoma? Preliminary results of GETUG-01. J Clin Oncol; 2007 Dec 1;25(34):5366-73
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  • [Title] Is there a role for pelvic irradiation in localized prostate adenocarcinoma? Preliminary results of GETUG-01.
  • PURPOSE: To assess the benefit and toxicity and quality-of-life (QOL) outcomes of pelvic nodes irradiation in nonmetastatic prostate carcinoma patients.
  • PATIENTS AND METHODS: Between December 1998 and June 2004, 444 patients with T1b-T3, N0 pNx, M0 prostate carcinoma were randomly assigned to either pelvic and prostate radiotherapy or prostate radiotherapy only.
  • The total dose recommended to the prostate was changed during the course of the study from 66 Gy to 70 Gy.
  • Criteria for progression-free survival (PFS) included biologic prostate-specific antigen recurrences or a local or metastatic evolution.
  • The QOL outcome was recorded with the European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire C30, the International Prostatic Symptom Score, and the Sexual Function Index scales.
  • [MeSH-major] Adenocarcinoma / radiotherapy. Prostatic Neoplasms / radiotherapy

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  • [CommentIn] J Clin Oncol. 2008 Apr 20;26(12):2055-6; author reply 2056-7 [18421061.001]
  • (PMID = 18048817.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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91. Barrisford GW, Sartor O, Richie JP: Solitary adrenal metastatic lesion in a patient with a history of prostate cancer. Clin Genitourin Cancer; 2009 Jan;7(1):64-6
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  • [Title] Solitary adrenal metastatic lesion in a patient with a history of prostate cancer.
  • Prostate cancer is the most commonly diagnosed malignancy among American men.
  • Although prostate cancer-related death approximates only 3%, advanced disease can become widely disseminated.
  • Metastatic disease is often found in a number of common sites.
  • [MeSH-major] Adenocarcinoma / secondary. Adrenal Gland Neoplasms / secondary. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Humans. Male. Prostate-Specific Antigen / blood. Tomography, X-Ray Computed



92. Yeh IT, Reddick RL, Kumar AP: Malignancy arising in seminal vesicles in the transgenic adenocarcinoma of mouse prostate (TRAMP) model. Prostate; 2009 May 15;69(7):755-60
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  • [Title] Malignancy arising in seminal vesicles in the transgenic adenocarcinoma of mouse prostate (TRAMP) model.
  • BACKGROUND: Transgenic adenocarcinoma of mouse prostate (TRAMP) mice, derived by prostate specific expression of SV40 large T antigen using the rat probasin promoter, all develop prostate tumors akin to human prostate cancers.
  • Immunostains (cytokeratin, vimentin, desmin, and MIB-1) and electron microscopy were performed on selected blocks of the genitourinary system and metastatic tumor nodules.
  • In some cases, the stromal cells become large mass lesions that overgrow the prostate.
  • Some metastatic tumors have characteristics similar to the seminal vesicle ES tumor.
  • CONCLUSIONS: Metastatic tumors in TRAMP mice show three patterns:.
  • (1) A definite adenocarcinoma pattern metastatic from the prostate;.
  • [MeSH-major] Adenocarcinoma / pathology. Prostatic Neoplasms / pathology. Seminal Vesicles / pathology

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  • [Copyright] 2009 Wiley-Liss, Inc.
  • (PMID = 19170049.001).
  • [ISSN] 1097-0045
  • [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
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93. Xuan Q, Yang X, Mo L, Huang F, Pang Y, Qin M, Chen Z, He M, Wang Q, Mo ZN: Expression of the serine protease kallikrein 7 and its inhibitor antileukoprotease is decreased in prostate cancer. Arch Pathol Lab Med; 2008 Nov;132(11):1796-801
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  • [Title] Expression of the serine protease kallikrein 7 and its inhibitor antileukoprotease is decreased in prostate cancer.
  • Antileukoprotease overexpression is commonly associated with aggressive, high-risk, or metastatic cancer originating from various organs.
  • OBJECTIVE: To investigate the expression and potential role of hK7 and its inhibitor ALP in prostate cancer.
  • DESIGN: The mRNA expression of KLK7 and ALP transcript in benign prostate epithelial cells and prostate cancers was evaluated by semiquantitative reverse transcription-polymerase chain reaction.
  • We examined hK7 and ALP protein expression by immunohistochemistry in 20 normal prostate tissues, 50 benign prostatic hyperplasia tissues, and 103 prostate cancers.
  • Western blot examination showed protein expression of hK7 and ALP in benign prostate epithelial cells and prostate cancer cell lines.
  • RESULTS: Semiquantitative polymerase chain reaction examination revealed that the mRNA level of KLK7 and ALP was significantly decreased in prostate cancers compared with that in benign prostate epithelial cells (P < .001).
  • Immunohistochemical expression of hK7 was observed in prostate epithelial cells, whereas little or no staining was observed in prostate cancer.
  • Western blot analysis revealed that hK7 and ALP were decreased in malignant prostate epithelium.
  • CONCLUSIONS: Like hK7, ALP is down-regulated in prostate cancers, which begs the question of whether it remains an effective inhibitor of hK7 or whether it is discordant in time or space and is ineffective as an inhibitor of hK7.
  • The function of KLK7 and ALP in prostate cancer should be further studied.
  • [MeSH-major] Adenocarcinoma / metabolism. Kallikreins / metabolism. Prostatic Neoplasms / metabolism. Secretory Leukocyte Peptidase Inhibitor / metabolism
  • [MeSH-minor] Case-Control Studies. Cell Line, Tumor. Down-Regulation. Epithelial Cells / metabolism. Epithelial Cells / pathology. Humans. Male. Prostate / cytology. Prostate / metabolism. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology. RNA, Messenger / metabolism

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  • (PMID = 18976018.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Secretory Leukocyte Peptidase Inhibitor; EC 3.4.21.- / KLK7 protein, human; EC 3.4.21.- / Kallikreins
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94. Chung AC, Zhou S, Liao L, Tien JC, Greenberg NM, Xu J: Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice. Cancer Res; 2007 Jun 15;67(12):5965-75
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  • [Title] Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice.
  • Although the amplified-in-breast cancer 1 (AIB1; SRC-3, ACTR, or NCoA3) was defined as a coactivator for androgen receptor (AR) by in vitro studies, its role in AR-mediated prostate development and prostate cancer remained unexplored.
  • AIB1 deficiency only slightly delayed prostate growth and had no effect on androgen-dependent prostate regeneration, suggesting an unessential role of AIB1 in AR function in the prostate.
  • Surprisingly, when prostate tumorigenesis was induced by the SV40 transgene in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice, AIB1 expression was observed in certain epithelial cells of the prostate intraepithelial neoplasia (PIN) and well-differentiated carcinoma and in almost all cells of the poorly differentiated carcinoma.
  • After AIB1 was genetically inactivated in AIB1-/-/TRAMP mice, the progression of prostate tumorigenesis in most AIB1-/-/TRAMP mice was arrested at the well-differentiated carcinoma stage.
  • Wild-type (WT)/TRAMP mice developed progressive, multifocal, and metastatic prostate tumors and died between 25 and 34 weeks.
  • Our results indicate that induction of AIB1 expression in partially transformed epithelial cells is essential for progression of prostate tumorigenesis into poorly differentiated carcinoma.
  • Inhibition of AIB1 expression or function in the prostate epithelium may be a potential strategy to suppress prostate cancer initiation and progression.