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[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

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(PMID = 15472903.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins

   

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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

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[Copyright] (c) 2006 Wiley-Liss, Inc.

(PMID = 17163422.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Integrin beta3; 0 / RNA, Messenger; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase

   

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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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(PMID = 16885915.001).

[ISSN] 1073-2748

[Journal-full-title] Cancer control : journal of the Moffitt Cancer Center

[ISO-abbreviation] Cancer Control

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 33

   

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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

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(PMID = 15756074.001).

[ISSN] 0042-1138

[Journal-full-title] Urologia internationalis

[ISO-abbreviation] Urol. Int.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

   

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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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[Cites] Endocrinology. 2004 Aug;145(8):3961-70 [15132968.001]

[Cites] Cancer Res. 2007 May 15;67(10):4807-15 [17510410.001]

[Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]

[Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]

[Cites] Nature. 2004 Oct 7;431(7009):707-12 [15361885.001]

[Cites] Am J Respir Cell Mol Biol. 1992 Dec;7(6):574-81 [1449805.001]

[Cites] Hum Pathol. 1998 Sep;29(9):1005-12 [9744319.001]

[Cites] Mol Cancer. 2004 Oct 13;3:29 [15482598.001]

[Cites] Int J Cancer. 2005 Feb 10;113(4):619-28 [15472903.001]

[Cites] Prostate. 2005 Feb 1;62(2):187-99 [15389789.001]

[Cites] J Pathol. 2005 Mar;205(4):522-9 [15685688.001]

[Cites] Cancer Res. 2005 Apr 15;65(8):2990-2 [15833820.001]

[Cites] Cancer Res. 2005 Dec 1;65(23):10946-51 [16322242.001]

[Cites] Carcinogenesis. 2006 Jan;27(1):1-22 [16195239.001]

[Cites] Int J Cancer. 2006 Feb 15;118(4):1022-31 [16108016.001]

[Cites] Oncogene. 2006 Mar 16;25(12):1696-708 [16449977.001]

[Cites] Cell Mol Life Sci. 2006 Feb;63(4):435-48 [16389455.001]

[Cites] Endocr Relat Cancer. 2006 Mar;13(1):197-210 [16601288.001]

[Cites] J Urol. 2006 Aug;176(2):532-7 [16813883.001]

[Cites] Prostate. 2006 Sep 15;66(13):1437-44 [16741920.001]

[Cites] Int J Cancer. 2007 Jan 1;120(1):160-9 [17013895.001]

[Cites] Mol Cancer Ther. 2007 Mar;6(3):967-78 [17363490.001]

[Cites] Cancer Res. 2007 Apr 1;67(7):3153-61 [17409422.001]

[Cites] Lab Invest. 2000 Aug;80(8):1243-50 [10950115.001]

[Cites] Clin Cancer Res. 2000 Dec;6(12):4885-92 [11156248.001]

[Cites] Bioorg Med Chem Lett. 2001 Jul 23;11(14):1911-4 [11459659.001]

[Cites] J Cell Sci. 2001 Nov;114(Pt 21):3865-72 [11719553.001]

[Cites] J Pathol. 2001 Dec;195(5):563-70 [11745692.001]

[Cites] Int J Oncol. 2002 Apr;20(4):681-9 [11894110.001]

[Cites] Clin Cancer Res. 2002 May;8(5):1253-64 [12006546.001]

[Cites] J Immunol Methods. 2002 Jul 1;265(1-2):39-47 [12072177.001]

[Cites] Clin Cancer Res. 2002 Nov;8(11):3438-44 [12429632.001]

[Cites] Clin Cancer Res. 2002 Dec;8(12):3870-6 [12473602.001]

[Cites] J Cancer Res Clin Oncol. 2003 Mar;129(3):165-74 [12712332.001]

[Cites] Cytometry A. 2003 Aug;54(2):89-99 [12879455.001]

[Cites] Nature. 2003 Oct 23;425(6960):851-6 [14520413.001]

[Cites] Br J Cancer. 2004 Jan 26;90(2):449-54 [14735192.001]

[Cites] Pancreas. 2004 May;28(4):401-12 [15097858.001]

[Cites] J Cell Sci. 2004 Jul 15;117(Pt 16):3539-45 [15226377.001]

[Cites] Biochem Biophys Res Commun. 2007 Jun 15;357(4):1084-9 [17466949.001]

[Cites] Cancer. 2007 Jun 1;109(11):2239-47 [17455209.001]

[Cites] Cancer Res. 2007 Jul 15;67(14):6796-805 [17638891.001]

[Cites] Prostate. 2007 Sep 15;67(13):1384-96 [17639507.001]

[Cites] J Urol. 2007 Sep;178(3 Pt 2):S30-5 [17644121.001]

[Cites] Cancer Lett. 2007 Oct 8;255(2):300-6 [17602833.001]

[Cites] Cancer Biol Ther. 2007 May;6(5):763-8 [17592251.001]

[Cites] Ernst Schering Found Symp Proc. 2006;(5):155-79 [17939301.001]

[Cites] J Cell Mol Med. 2007 Sep-Oct;11(5):981-1011 [17979879.001]

[Cites] Mo Med. 2007 Sep-Oct;104(5):408-13; quiz 413-4 [18018527.001]

[Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]

[Cites] Growth Factors. 2007 Dec;25(6):400-16 [18365871.001]

[Cites] Endocr Rev. 2008 Apr;29(2):234-52 [18292464.001]

[Cites] Prostate. 2008 Jun 15;68(9):1007-24 [18398820.001]

[Cites] J Cell Physiol. 2008 Sep;216(3):571-5 [18481259.001]

[Cites] Genome Biol. 2008;9(5):R83 [18492237.001]

[Cites] Cancer Res. 2008 Oct 1;68(19):7905-14 [18829547.001]

[Cites] Proc Natl Acad Sci U S A. 2009 Jan 6;106(1):268-73 [19116269.001]

[Cites] Ageing Res Rev. 2009 Apr;8(2):94-112 [19114129.001]

[Cites] Cancer Genomics Proteomics. 2008 Nov-Dec;5(6):301-10 [19287071.001]

[Cites] Clin Exp Metastasis. 2009;26(5):433-46 [19221883.001]

[Cites] Methods Mol Biol. 2009;568:139-49 [19582424.001]

[Cites] Stem Cells Dev. 2009 Dec;18(10):1515-22 [19260804.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12561-6 [15314219.001]

(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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[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

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(PMID = 16678051.001).

[ISSN] 1078-1439

[Journal-full-title] Urologic oncology

[ISO-abbreviation] Urol. Oncol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen

   

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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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[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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[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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[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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[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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[Cites] Int J Radiat Oncol Biol Phys. 2005 Sep 1;63(1):37-46 [16111570.001]

[Cites] Arch Neurol. 1988 Jul;45(7):741-4 [3390029.001]

[Cites] Surg Neurol. 2003 Dec;60(6):506-14; discussion 514-5 [14670663.001]

[Cites] Cancer. 1987 May 15;59(10):1803-9 [3030528.001]

[Cites] Surg Neurol. 2008 Jun;69(6):641-6; discussion 646 [18262258.001]

[Cites] Cancer. 1999 Dec 1;86(11):2301-11 [10590371.001]

[Cites] Neurosurgery. 1997 Oct;41(4):776-83; discussion 783-5 [9316038.001]

[Cites] J Neurooncol. 2004 Aug-Sep;69(1-3):125-37 [15527085.001]

[Cites] Cancer. 2004 Oct 1;101(7):1639-43 [15468187.001]

[Cites] Am J Med Sci. 1994 Sep;308(3):177-9 [8074136.001]

[Cites] Neurosurgery. 2003 Jun;52(6):1318-26; discussion 1326 [12762877.001]

[Cites] J Urol. 1992 Mar;147(3 Pt 2):935-7 [1311396.001]

[Cites] Cancer. 1996 Oct 15;78(8):1781-8 [8859192.001]

[Cites] Cancer. 2003 Jul 15;98(2):363-8 [12872358.001]

[Cites] Virchows Arch. 2004 Feb;444(2):202-3 [14652753.001]

[Cites] J Urol. 2002 Jun;167(6):2419-22 [11992049.001]

[Cites] Can J Neurol Sci. 2002 Nov;29(4):375-7 [12463494.001]

[Cites] Gynecol Oncol. 2001 May;81(2):196-200 [11330949.001]

(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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[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.

[Cites] Nucleic Acids Res. 1995 Nov 25;23(22):4726-33 [8524667.001]

[Cites] Genes Dev. 1996 Apr 1;10(7):804-15 [8846917.001]

[Cites] J Biol Chem. 1996 Feb 16;271(7):3891-6 [8632009.001]

[Cites] Cancer Res. 1996 Mar 1;56(5):1063-7 [8640762.001]

[Cites] J Biol Chem. 1996 Jul 26;271(30):17974-8 [8663327.001]

[Cites] Mol Cell Biol. 1997 Dec;17(12):7353-61 [9372966.001]

[Cites] Nat Genet. 2001 Mar;27(3):263-70 [11242107.001]

[Cites] Nat Med. 2001 Apr;7(4):444-51 [11283671.001]

[Cites] Prostate. 2001 Jun 15;48(1):54-65 [11391687.001]

[Cites] Mol Cell Biol. 2001 Aug;21(16):5577-90 [11463839.001]

[Cites] J Biol Chem. 2001 Aug 3;276(31):29200-9 [11369759.001]

[Cites] Cell. 2001 Oct 19;107(2):247-58 [11672531.001]

[Cites] Mol Cell. 2001 Oct;8(4):817-28 [11684017.001]

[Cites] Cancer Res. 2002 Jan 15;62(2):528-34 [11809705.001]

[Cites] Cancer Res. 2002 Feb 15;62(4):1008-13 [11861374.001]

[Cites] EMBO J. 2002 Mar 1;21(5):930-41 [11867521.001]

[Cites] Biochem J. 2002 Aug 1;365(Pt 3):561-75 [12006103.001]

[Cites] J Biol Chem. 2004 Feb 20;279(8):7353-8 [14660596.001]

[Cites] Genes Dev. 2004 Apr 15;18(8):912-25 [15107404.001]

[Cites] J Clin Oncol. 2004 Jul 15;22(14):2790-9 [15254046.001]

[Cites] Nature. 1990 Apr 12;344(6267):678-82 [2157987.001]

[Cites] Science. 1991 Jan 18;251(4991):288-92 [1987644.001]

[Cites] Chin Med J (Engl). 1994 Aug;107(8):596-9 [7805444.001]

[Cites] Science. 1995 Aug 25;269(5227):1108-12 [7652557.001]

[Cites] Mol Cell Biol. 1999 Apr;19(4):2936-45 [10082561.001]

[Cites] Br J Cancer. 1999 Mar;79(7-8):1240-8 [10098766.001]

[Cites] Nucleic Acids Res. 1999 Sep 1;27(17):3621-30 [10446255.001]

[Cites] Mol Cell Biol. 2005 Feb;25(4):1325-38 [15684384.001]

[Cites] Clin Cancer Res. 2005 May 1;11(9):3184-90 [15867211.001]

[Cites] Mol Endocrinol. 2006 May;20(5):984-95 [16455820.001]

[Cites] Biochim Biophys Acta. 2006 Aug;1766(1):88-103 [16616425.001]

[Cites] BMC Cancer. 2006;6:158 [16774685.001]

[Cites] Cancer Res. 2007 Jul 15;67(14):6768-76 [17638888.001]

(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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[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

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[Cites] Cancer. 2000 Jun 15;88(12 Suppl):2919-26 [10898335.001]

[Cites] N Engl J Med. 2004 May 27;350(22):2239-46 [15163773.001]

[Cites] JAMA. 1997 May 14;277(18):1452-5 [9145717.001]

[Cites] J Am Board Fam Pract. 2003 Mar-Apr;16(2):95-101 [12665174.001]

[Cites] J Urol. 1995 Aug;154(2 Pt 1):407-13 [7541857.001]

[Cites] Urology. 1996 Mar;47(3):343-6 [8633399.001]

[Cites] N Engl J Med. 1995 Nov 23;333(21):1401-5 [7477122.001]

[Cites] J Clin Oncol. 2003 Jan 15;21(2):383-91 [12525533.001]

[Cites] Urology. 2002 Sep;60(3):469-73; discussion 473-4 [12350486.001]

(PMID = 16238977.001).

[ISSN] 1699-048X

[Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico

[ISO-abbreviation] Clin Transl Oncol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.4.21.77 / Prostate-Specific Antigen

   

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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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[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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[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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[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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[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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[Cites] Nat Cell Biol. 2004 Aug;6(8):784-91 [15247924.001]

[Cites] Biochem Biophys Res Commun. 2004 Jan 16;313(3):552-4 [14697225.001]

[Cites] Int J Cancer. 1978 Mar 15;21(3):274-81 [631930.001]

[Cites] Genes Dev. 2003 Dec 15;17(24):3011-6 [14681208.001]

[Cites] Nat Neurosci. 2004 Feb;7(2):113-7 [14703574.001]

[Cites] Mol Biol Cell. 2004 Mar;15(3):1425-35 [14699070.001]

[Cites] Cancer Res. 2004 Jun 1;64(11):3753-6 [15172979.001]

[Cites] J Clin Oncol. 2004 Jul 15;22(14):2790-9 [15254046.001]

[Cites] Eur Urol. 1996;30(2):201-5 [8875201.001]

[Cites] Carcinogenesis. 1997 Jun;18(6):1215-23 [9214605.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1735-40 [9465086.001]

[Cites] Nat Cell Biol. 2004 Nov;6(11):1048-53 [15516998.001]

[Cites] Cell. 2005 Jan 14;120(1):15-20 [15652477.001]

[Cites] Cell. 2005 Jan 14;120(1):21-4 [15652478.001]

[Cites] Cancer Gene Ther. 2005 Mar;12(3):217-27 [15550938.001]

[Cites] Cancer Sci. 2005 Feb;96(2):111-5 [15723655.001]

[Cites] Cell. 2005 Mar 11;120(5):635-47 [15766527.001]

[Cites] Biochem J. 2005 May 1;387(Pt 3):561-71 [15845026.001]

[Cites] Cancer Res. 2005 May 1;65(9):3509-12 [15867338.001]

[Cites] Nature. 2005 Jun 9;435(7043):839-43 [15944709.001]

[Cites] Curr Opin Struct Biol. 2005 Jun;15(3):331-41 [15925505.001]

[Cites] BMC Cancer. 2005;5:45 [15892885.001]

[Cites] Cell. 2005 Jul 15;122(1):6-7 [16009126.001]

[Cites] J Exp Med. 2005 Jul 18;202(2):261-9 [16009718.001]

[Cites] Nature. 2005 Aug 4;436(7051):740-4 [15973356.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13944-9 [16166262.001]

[Cites] Eur Urol. 2005 Nov;48(5):852-7 [16230228.001]

[Cites] Pathol Int. 2005 Nov;55(11):688-93 [16271080.001]

[Cites] Cancer Gene Ther. 2005 Dec;12(12):926-34 [15956982.001]

[Cites] Cancer Cell. 2005 Nov;8(5):393-406 [16286247.001]

[Cites] Curr Biol. 2005 Dec 6;15(23):2149-55 [16289642.001]

[Cites] Differentiation. 2005 Dec;73(9-10):463-73 [16351690.001]

[Cites] Genes Dev. 2005 Dec 15;19(24):2979-90 [16357216.001]

[Cites] Curr Opin Genet Dev. 2006 Feb;16(1):4-9 [16361094.001]

[Cites] Mol Cancer Ther. 2006 Jan;5(1):179-86 [16432177.001]

[Cites] EMBO J. 2006 Feb 8;25(3):522-32 [16424907.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460.001]

[Cites] Br J Cancer. 2006 Mar 27;94(6):776-80 [16495913.001]

[Cites] Genome Biol. 2006;7(3):210 [16584538.001]

[Cites] Science. 2002 Sep 20;297(5589):2056-60 [12154197.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]

[Cites] Cell. 2001 Jul 13;106(1):23-34 [11461699.001]

[Cites] Science. 2001 Aug 3;293(5531):834-8 [11452083.001]

[Cites] Prostate. 2002 May 1;51(2):98-107 [11948964.001]

[Cites] Cancer Genet Cytogenet. 2002 Jun;135(2):177-81 [12127403.001]

[Cites] Chin Med J (Engl). 2002 Apr;115(4):571-5 [12133301.001]

[Cites] Science. 2002 Sep 13;297(5588):1833-7 [12193640.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16648-53 [12482946.001]

[Cites] Genes Dev. 2003 Feb 15;17(4):438-42 [12600936.001]

[Cites] Urology. 2003 Aug;62(2):378-84 [12893368.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9779-84 [12902540.001]

[Cites] EMBO J. 2004 Oct 13;23(20):4051-60 [15372072.001]

(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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[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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[Title] Estrogen and resveratrol regulate Rac and Cdc42 signaling to the actin cytoskeleton of metastatic breast cancer cells.

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[Cites] Carcinogenesis. 2005 Jan;26(1):1-10 [15217905.001]

[Cites] Curr Biol. 2004 Nov 23;14(22):2052-6 [15556869.001]

[Cites] J Biol Chem. 2005 Mar 4;280(9):7460-8 [15615701.001]

[Cites] Int J Cancer. 2005 May 20;115(1):74-84 [15688415.001]

[Cites] Int J Cancer. 2005 May 20;115(1):36-45 [15688416.001]

[Cites] Neoplasia. 2005 Feb;7(2):128-40 [15802018.001]

[Cites] Oncogene. 2005 May 5;24(20):3274-84 [15735708.001]

[Cites] Free Radic Biol Med. 2005 Jul 1;39(1):118-32 [15925284.001]

[Cites] Mol Endocrinol. 2005 Aug;19(8):1951-9 [15705661.001]

[Cites] Biomed Pharmacother. 2005 Aug;59(7):359-64 [16084059.001]

[Cites] Curr Opin Cell Biol. 2005 Oct;17(5):559-64 [16098726.001]

[Cites] Breast Cancer Res Treat. 2005 Sep;93(2):101-10 [16187229.001]

[Cites] Annu Rev Cell Dev Biol. 2005;21:247-69 [16212495.001]

[Cites] Oncogene. 2005 Nov 24;24(53):7821-9 [16027728.001]

[Cites] Curr Opin Cell Biol. 2006 Feb;18(1):18-25 [16337369.001]

[Cites] Breast Cancer Res. 2005;7(6):R965-74 [16280046.001]

[Cites] Endocrinology. 2006 Mar;147(3):1203-12 [16339197.001]

[Cites] Curr Drug Targets. 2006 Apr;7(4):423-42 [16611030.001]

[Cites] Int J Oncol. 2006 Jul;29(1):217-23 [16773203.001]

[Cites] Biol Reprod. 2006 Jul;75(1):9-16 [16571873.001]

[Cites] Mol Endocrinol. 2006 Aug;20(8):1756-71 [16601072.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):14138-43 [9391166.001]

[Cites] Histochem Cell Biol. 1999 Nov;112(5):341-50 [10603073.001]

[Cites] Hepatology. 2000 Apr;31(4):922-31 [10733549.001]

[Cites] J Cancer Res Clin Oncol. 2001 Apr;127(4):258-64 [11315261.001]

[Cites] Semin Cancer Biol. 2001 Apr;11(2):119-28 [11322831.001]

[Cites] J Cell Sci. 2001 May;114(Pt 10):1801-9 [11329366.001]

[Cites] Int J Oncol. 2001 Jul;19(1):83-8 [11408926.001]

[Cites] Cancer Res. 2001 Oct 15;61(20):7456-63 [11606380.001]

[Cites] Mol Med. 2001 Dec;7(12):816-30 [11844870.001]

[Cites] J Clin Endocrinol Metab. 2002 Mar;87(3):1223-32 [11889192.001]

[Cites] J Biol Chem. 2002 Jul 5;277(27):24753-63 [11948177.001]

[Cites] Free Radic Biol Med. 2002 Aug 1;33(3):387-98 [12126761.001]

[Cites] J Nutr. 2002 Nov;132(11 Suppl):3482S-3489S [12421874.001]

[Cites] Int J Oncol. 2003 Jul;23(1):17-28 [12792772.001]

[Cites] Exp Cell Res. 2003 Jul 1;287(1):47-56 [12799181.001]

[Cites] Science. 2003 Dec 5;302(5651):1704-9 [14657486.001]

[Cites] Int J Cancer. 2004 Mar 20;109(2):167-73 [14750165.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):2076-81 [14764897.001]

[Cites] Breast Cancer Res Treat. 2004 Mar;84(1):13-9 [14999150.001]

[Cites] Breast Cancer Res Treat. 2004 Mar;84(1):43-8 [14999153.001]

[Cites] Breast Cancer Res Treat. 2004 Mar;84(1):49-60 [14999154.001]

[Cites] Oncogene. 2004 Mar 11;23(10):1845-53 [14661062.001]

[Cites] J Cell Sci. 2004 Mar 15;117(Pt 8):1301-12 [15020670.001]

[Cites] Prostate. 2004 May 1;59(2):214-25 [15042621.001]

[Cites] Biochem Soc Trans. 2004 Dec;32(Pt 6):1115-7 [15506983.001]

[Cites] Neurosci Lett. 1999 Apr 2;264(1-3):141-4 [10320034.001]

[Cites] Anticancer Res. 2004 Sep-Oct;24(5A):2783-840 [15517885.001]

[Cites] Clin Exp Metastasis. 2004;21(5):445-51 [15672869.001]

(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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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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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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[Cites] Prostate. 2000 Jan;42(1):18-25 [10579795.001]

[Cites] Pediatr Nephrol. 1993 Feb;7(1):96-104 [8439492.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):3884-9 [10760260.001]

[Cites] Nat Cell Biol. 2000 Oct;2(10):737-44 [11025665.001]

[Cites] Curr Opin Cell Biol. 2001 Oct;13(5):534-40 [11544020.001]

[Cites] Science. 2002 Jun 7;296(5574):1883-6 [11976409.001]

[Cites] Cancer. 2002 Nov 1;95(9):1902-10 [12404284.001]

[Cites] Cell. 1985 Sep;42(2):469-77 [2411423.001]

[Cites] Science. 1987 Jan 23;235(4787):442-7 [2432664.001]

[Cites] Cancer. 1992 Dec 15;70(12):2747-53 [1451050.001]

[Cites] Annu Rev Cell Biol. 1993;9:541-73 [8280471.001]

[Cites] J Invest Dermatol. 1995 Aug;105(2):170-6 [7543547.001]

[Cites] J Cell Physiol. 1995 Dec;165(3):475-83 [7593226.001]

[Cites] Cancer Res. 1996 Jan 1;56(1):190-6 [8548762.001]

[Cites] Int J Cancer. 1996 Feb 20;69(1):9-16 [8600068.001]

[Cites] Br J Cancer. 1996 Apr;73(8):972-8 [8611434.001]

[Cites] Br J Cancer. 1996 Aug;74(3):413-7 [8695357.001]

[Cites] Pathol Int. 1997 Jul;47(7):461-9 [9234385.001]

[Cites] Ann Thorac Surg. 1997 Oct;64(4):1204-11 [9354565.001]

[Cites] Cancer. 1998 Feb 15;82(4):642-50 [9477095.001]

[Cites] Cancer Res. 1998 Mar 1;58(5):1048-51 [9500469.001]

[Cites] Cancer. 1998 Sep 15;83(6):1153-62 [9740080.001]

[Cites] Curr Opin Cell Biol. 1998 Oct;10(5):602-8 [9818170.001]

[Cites] Ann Med. 1999 Feb;31(1):34-45 [10219712.001]

[Cites] Gynecol Oncol. 1999 Jun;73(3):372-82 [10366463.001]

[Cites] Gynecol Oncol. 1999 Oct;75(1):91-8 [10502432.001]

[Cites] Nat Rev Mol Cell Biol. 2007 Mar;8(3):221-33 [17318226.001]

[Cites] Semin Cell Dev Biol. 2008 Feb;19(1):52-60 [17625931.001]

[Cites] Cancer Metastasis Rev. 2008 Dec;27(4):679-90 [18465089.001]

[Cites] Matrix Biol. 2009 Jan;28(1):3-10 [19010413.001]

[Cites] Integr Biol (Camb). 2009 Jun;1(5-6):382-93 [20023745.001]

[Cites] Biochim Biophys Acta. 2010 Jan;1803(1):3-19 [19631700.001]

[Cites] Cell. 2010 Apr 2;141(1):52-67 [20371345.001]

[Cites] Breast Cancer Res Treat. 1999 Dec;58(3):287-93 [10718490.001]

(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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[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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[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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[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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[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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[Cites] J Biol Chem. 2004 Jan 9;279(2):1422-8 [14530270.001]

[Cites] Prostate. 2004 Feb 15;58(3):269-76 [14743466.001]

[Cites] J Cell Biochem. 2004 Feb 15;91(3):483-90 [14755679.001]

[Cites] Clin Cancer Res. 2004 Feb 1;10(3):1032-40 [14871982.001]

[Cites] Trends Mol Med. 2004 Apr;10(4):158-62 [15059606.001]

[Cites] Oncogene. 1993 Aug;8(8):2127-33 [8336939.001]

[Cites] Proc Natl Acad Sci U S A. 1993 Oct 1;90(19):9026-30 [8415648.001]

[Cites] Mol Cell Biol. 1995 May;15(5):2600-11 [7739541.001]

[Cites] Oncogene. 1996 Aug 15;13(4):797-802 [8761301.001]

[Cites] Prostate. 1997 Jul 1;32(2):99-105 [9215397.001]

[Cites] Cancer. 1997 Aug 15;80(4):753-63 [9264360.001]

[Cites] Semin Cancer Biol. 1997 Feb;8(1):11-9 [9299577.001]

[Cites] Mol Cell Biol. 1997 Dec;17(12):7362-74 [9372967.001]

[Cites] Am J Surg Pathol. 1998 Feb;22(2):188-94 [9500219.001]

[Cites] Curr Opin Genet Dev. 1998 Feb;8(1):21-7 [9529601.001]

[Cites] Prostate. 1998 May;35(2):95-101 [9568672.001]

[Cites] J Biol Chem. 1998 Aug 7;273(32):20213-22 [9685369.001]

[Cites] Hum Pathol. 1998 Aug;29(8):778-83 [9712417.001]

[Cites] Genes Dev. 1998 Nov 15;12(22):3499-511 [9832503.001]

[Cites] Eur J Cancer. 1998 Sep;34(10):1575-81 [9893631.001]

[Cites] Prostate. 1999 Jan 1;38(1):40-5 [9973108.001]

[Cites] Prostate. 1999 Feb 15;38(3):175-82 [10068341.001]

[Cites] Mol Cell Biol. 1999 Mar;19(3):1775-83 [10022865.001]

[Cites] Cancer Res. 1999 Feb 15;59(4):803-6 [10029066.001]

[Cites] Breast Cancer Res Treat. 1998;52(1-3):79-98 [10066074.001]

[Cites] Adv Anat Pathol. 2006 Jan;13(1):57-9 [16462155.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2190-5 [16461912.001]

[Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]

[Cites] Mol Cancer. 2006;5:7 [16503970.001]

[Cites] Anat Histol Embryol. 2006 Apr;35(2):125-9 [16542178.001]

[Cites] Mol Endocrinol. 1999 Mar;13(3):376-84 [10076995.001]

[Cites] EMBO J. 1999 Mar 15;18(6):1571-83 [10075928.001]

[Cites] Nature. 1999 Apr 1;398(6726):422-6 [10201372.001]

[Cites] Cancer Res. 1999 May 15;59(10):2297-301 [10344732.001]

[Cites] Int J Cancer. 1999 Jun 21;84(3):225-33 [10371338.001]

[Cites] Endocrinology. 2004 Dec;145(12):5439-47 [15331580.001]

[Cites] Genes Dev. 2004 Nov 15;18(22):2699-711 [15545627.001]

[Cites] Oncogene. 2005 Jan 13;24(3):431-44 [15558026.001]

[Cites] Mol Endocrinol. 2005 Mar;19(3):607-20 [15539430.001]

[Cites] Clin Cancer Res. 2005 Jun 1;11(11):4117-27 [15930347.001]

[Cites] Expert Opin Ther Targets. 2005 Apr;9(2):283-98 [15934916.001]

[Cites] J Cancer Res Clin Oncol. 2005 Jul;131(7):479-85 [15809880.001]

[Cites] J Clin Oncol. 2005 Jun 20;23(18):4215-24 [15961768.001]

[Cites] J Steroid Biochem Mol Biol. 2005 Aug;96(3-4):251-8 [15982869.001]

[Cites] Eur Urol. 2005 Oct;48(4):541-5 [16139417.001]

[Cites] Chem Rev. 2005 Sep;105(9):3352-70 [16159155.001]

[Cites] BMC Cancer. 2005;5:98 [16086840.001]

[Cites] J Cell Biochem. 2005 Dec 1;96(5):906-13 [16163738.001]

[Cites] Oncogene. 2005 Nov 14;24(50):7465-74 [16288293.001]

[Cites] Biochem Biophys Res Commun. 2006 Feb 3;340(1):302-8 [16364255.001]

[Cites] Br J Cancer. 1999 May;80(3-4):546-55 [10408865.001]

[Cites] Prostate. 1999 Sep 1;40(4):256-60 [10420154.001]

[Cites] J Gastroenterol. 1999 Aug;34(4):486-93 [10452682.001]

[Cites] Clin Cancer Res. 1999 Aug;5(8):2082-8 [10473090.001]

[Cites] Clin Cancer Res. 1999 Aug;5(8):2133-9 [10473097.001]

[Cites] Cancer Treat Rev. 2006 Apr;32(2):90-100 [16458434.001]

[Cites] Int J Colorectal Dis. 2006 May;21(4):291-300 [16041507.001]

[Cites] J Surg Oncol. 2006 Aug 1;94(2):155-60 [16847925.001]

[Cites] Cancer Res. 2006 Aug 1;66(15):7783-92 [16885382.001]

[Cites] Endocr Relat Cancer. 2006 Dec;13(4):979-94 [17158750.001]

[Cites] J Natl Cancer Inst. 1999 Nov 3;91(21):1869-76 [10547394.001]

[Cites] Br J Cancer. 1999 Dec;81(7):1174-81 [10584879.001]

[Cites] J Biol Chem. 2000 Apr 21;275(16):12074-9 [10766840.001]

[Cites] Clin Cancer Res. 2000 May;6(5):1891-5 [10815912.001]

[Cites] Mol Pathol. 2000 Feb;53(1):15-8 [10884916.001]

[Cites] Cell Growth Differ. 2000 Jul;11(7):361-72 [10939590.001]

[Cites] Int J Cancer. 2000 Oct 1;88(1):77-81 [10964085.001]

[Cites] Genes Dev. 2000 Dec 15;14(24):3102-14 [11124803.001]

[Cites] Br J Cancer. 2001 Jan;84(2):270-5 [11161387.001]

[Cites] Prostate. 2001 Feb 15;46(3):184-90 [11170146.001]

[Cites] Mol Endocrinol. 2001 May;15(5):797-811 [11328859.001]

[Cites] J Cell Biochem. 2001;81(4):621-38 [11329617.001]

[Cites] Carcinogenesis. 2001 Aug;22(8):1149-54 [11470742.001]

[Cites] Int J Cancer. 2001 Sep 20;95(5):302-6 [11494229.001]

[Cites] J Neurooncol. 2001 Sep;54(2):95-110 [11761437.001]

[Cites] Prostate. 2001 Nov 1;49(3):191-9 [11746264.001]

[Cites] Biochem Biophys Res Commun. 2002 Feb 8;290(5):1368-75 [11820772.001]

[Cites] J Biol Chem. 2002 Mar 8;277(10):8517-23 [11751903.001]

[Cites] Eur J Cancer. 2001 Oct;37 Suppl 7:S119-25 [11887983.001]

[Cites] Clin Cancer Res. 2002 Mar;8(3):775-81 [11895908.001]

[Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]

[Cites] J Biol Chem. 2002 Aug 9;277(32):28733-41 [12048199.001]

[Cites] Gene. 2002 Oct 16;299(1-2):35-55 [12459251.001]

[Cites] Virchows Arch. 2003 Jan;442(1):1-7 [12536308.001]

[Cites] Urology. 2003 Apr;61(4):837 [12670580.001]

[Cites] Mol Cell Biol. 2003 Sep;23(17):6139-49 [12917336.001]

[Cites] Cancer Res. 2003 Aug 15;63(16):4903-13 [12941814.001]

[Cites] Cancer Res. 2003 Nov 1;63(21):7056-61 [14612495.001]

[Cites] Nat Med. 2004 Jan;10(1):33-9 [14702632.001]

(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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[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

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[CommentIn] Cancer. 2007 Nov 1;110(9):1877-9 [17849427.001]

(PMID = 17886253.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Grant] United Kingdom / Medical Research Council / / G0501019

[Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyrrolidines; EC 3.1.3.1 / Alkaline Phosphatase; EC 3.4.21.77 / Prostate-Specific Antigen; V6D7VK2215 / atrasentan

   

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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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[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

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(PMID = 16927303.001).

[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 / Androgens; 0 / Cell Adhesion Molecules

   

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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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[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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[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

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[Cites] Cancer. 1999 Dec 1;86(11):2301-11 [10590371.001]

[Cites] Cancer. 1976 Dec;38(6):2583-7 [1000485.001]

[Cites] Cancer. 1994 Nov 1;74(9):2516-9 [7923009.001]

[Cites] Urology. 1986 Oct;28(4):280-7 [3765236.001]

[Cites] Cancer. 1992 Oct 15;70(8):2149-51 [1394044.001]

[Cites] Cancer. 1984 Dec 15;54(12):3078-84 [6498785.001]

[Cites] Urology. 1996 Nov;48(5):789-93 [8911530.001]

[Cites] Am J Psychiatry. 1996 Aug;153(8):974-84 [8678193.001]

(PMID = 17308872.001).

[ISSN] 0301-1623

[Journal-full-title] International urology and nephrology

[ISO-abbreviation] Int Urol Nephrol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Netherlands

   

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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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[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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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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[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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[Cites] J Endocrinol Invest. 2005;28(11 Suppl International):141-5 [16625864.001]

[Cites] Urology. 2003 Mar;61(3):589-95 [12639653.001]

[Cites] BJU Int. 2007 Jan;99(1):189-95 [17034504.001]

[Cites] Prostate. 1991;19(2):91-8 [1717965.001]

[Cites] Science. 1987 Jan 9;235(4785):177-82 [3798106.001]

[Cites] Hum Pathol. 1994 Jan;25(1):42-6 [7508883.001]

[Cites] Prostate. 1994;24(3):114-8 [7509483.001]

[Cites] Prostate. 1997 May 1;31(2):91-7 [9140121.001]

[Cites] Am J Clin Pathol. 2000 Mar;113(3):383-8 [10705819.001]

[Cites] Am J Clin Pathol. 2001 Aug;116(2):234-9 [11488070.001]

[Cites] Cancer Lett. 2002 Dec 10;187(1-2):1-7 [12359344.001]

[Cites] Hum Pathol. 2005 May;36(5):562-70 [15948124.001]

[Cites] Am J Surg Pathol. 2006 Aug;30(8):980-5 [16861969.001]

[Cites] Cancer. 2007 Feb 1;109(3):477-86 [17186531.001]

[Cites] J Urol. 1997 Jul;158(1):171-4 [9186347.001]

[Cites] Nat Med. 1999 Mar;5(3):280-5 [10086382.001]

[Cites] Urology. 2001 Feb;57(2):291-5 [11182339.001]

[Cites] Am J Clin Pathol. 2002 Mar;117(3):471-7 [11888088.001]

[Cites] Prostate. 2002 Oct 1;53(2):118-23 [12242726.001]

[Cites] Hum Pathol. 2006 Sep;37(9):1137-44 [16938518.001]

(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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[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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[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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[Cites] Genes Dev. 2005 Oct 1;19(19):2265-77 [16204178.001]

[Cites] Invest Urol. 1979 Jul;17(1):16-23 [447482.001]

[Cites] Mol Cell Biol. 2005 Nov;25(22):10052-9 [16260618.001]

[Cites] Cancer Res. 2005 Nov 1;65(21):9789-98 [16267000.001]

[Cites] Nat Genet. 2006 May;38(5):500-1 [16642009.001]

[Cites] Cancer Res. 2006 May 15;66(10):5295-303 [16707455.001]

[Cites] Proc Natl Acad Sci U S A. 1980 Jul;77(7):4113-7 [6933460.001]

[Cites] Hum Mol Genet. 2000 Jun 12;9(10):1495-500 [10888600.001]

[Cites] Neurobiol Dis. 2001 Apr;8(2):266-78 [11300722.001]

[Cites] Breast Cancer Res. 2001;3(3):192-8 [11305954.001]

[Cites] Cancer Res. 2001 Aug 15;61(16):5974-8 [11507037.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13790-5 [11707567.001]

[Cites] Mol Biol Cell. 2002 Jun;13(6):1929-39 [12058060.001]

[Cites] Cancer Cell. 2002 Mar;1(2):203-9 [12086878.001]

[Cites] Int J Cancer. 2002 Jul 10;100(2):181-8 [12115567.001]

[Cites] Nat Rev Mol Cell Biol. 2002 Aug;3(8):586-99 [12154370.001]

[Cites] J Cell Sci. 2002 Nov 1;115(Pt 21):3991-4000 [12356905.001]

[Cites] J Clin Invest. 1981 Aug;68(2):454-60 [6894932.001]

[Cites] Cancer Res. 1984 Aug;44(8):3522-9 [6744277.001]

[Cites] Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3439-43 [7724580.001]

[Cites] Neurology. 1997 Jul;49(1):267-70 [9222206.001]

[Cites] Cancer Res. 1997 Aug 15;57(16):3325-30 [9269988.001]

[Cites] Prostate. 1998 Feb 15;34(3):169-74 [9492844.001]

[Cites] Genes Dev. 1998 Apr 15;12(8):1121-33 [9553042.001]

[Cites] Cancer Res. 1999 Jan 1;59(1):35-43 [9892180.001]

[Cites] Histochem Cell Biol. 2004 Dec;122(6):579-86 [15517334.001]

[Cites] Oncogene. 2005 Mar 10;24(11):1946-57 [15688033.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13479-83 [16157875.001]

[Cites] Cell. 2003 Jul 25;114(2):241-53 [12887925.001]

[Cites] Histochem Cell Biol. 2003 Oct;120(4):277-83 [14574582.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Jan 20;101(3):811-6 [14711987.001]

[Cites] Nat Med. 2004 Feb;10(2):175-81 [14704789.001]

[Cites] Nat Med. 2004 Feb;10(2):182-6 [14704791.001]

[Cites] Neoplasia. 2004 Jan-Feb;6(1):1-6 [15068665.001]

[Cites] J Clin Oncol. 2004 Jul 15;22(14):2790-9 [15254046.001]

[Cites] Science. 2005 Oct 28;310(5748):644-8 [16254181.001]

(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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[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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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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[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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[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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[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

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[Copyright] (c) 2008 American Cancer Society.

(PMID = 18646045.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor

   

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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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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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[Cites] Clin Cancer Res. 2008 Feb 15;14(4):1167-71 [18281551.001]

[Cites] Gut. 2002 Oct;51 Suppl 5:V21-7 [12221036.001]

[Cites] Arch Surg. 1969 Apr;98(4):509-17 [4887290.001]

[Cites] J R Soc Med. 2003 Oct;96(10):505-6 [14519733.001]

[Cites] Ann Intern Med. 1998 Jun 1;128(11):896-9 [9634427.001]

[Cites] Gastrointest Endosc. 2000 Oct;52(4):552-4 [11023581.001]

[Cites] Gut. 1989 Nov;30(11):1588-90 [2599445.001]

[Cites] Colorectal Dis. 2004 Sep;6(5):332-5 [15335366.001]

[Cites] Clin Gastroenterol Hepatol. 2006 Apr;4(4):408-15 [16616343.001]

[Cites] Clin Cancer Res. 2006 May 15;12(10):3209-15 [16707622.001]

[Cites] Cancer. 1982 Mar 1;49(5):971-83 [7059931.001]

[Cites] J Laparoendosc Adv Surg Tech A. 2007 Feb;17(1):140-2 [17362193.001]

[Cites] N Engl J Med. 1987 Jun 11;316(24):1511-4 [3587280.001]

[Cites] Surg Laparosc Endosc. 1998 Feb;8(1):17-20 [9488564.001]

[Cites] Br J Surg. 1990 Mar;77(3):301-2 [2322793.001]

[Cites] Arch Surg. 1981 Sep;116(9):1182-4 [7283716.001]

[Cites] J Pediatr Gastroenterol Nutr. 2004 Aug;39(2):219-20 [15269641.001]

[Cites] Clin Cancer Res. 2003 Aug 1;9(8):3065-72 [12912958.001]

[Cites] Surg Laparosc Endosc Percutan Tech. 2003 Aug;13(4):280-2 [12960794.001]

[Cites] Can J Surg. 1994 Jun;37(3):231-6 [8199943.001]

[Cites] Br J Surg. 1995 Oct;82(10):1311-4 [7489151.001]

[Cites] Dig Dis Sci. 1983 Nov;28(11):1047-51 [6628153.001]

[Cites] Fam Cancer. 2001;1(2):121-5 [14574008.001]

[Cites] Am Surg. 1990 May;56(5):331-3 [2334077.001]

[Cites] Surg Endosc. 2000 Dec;14(12):1185-7 [11148795.001]

[Cites] Physiol Rev. 2009 Jul;89(3):777-98 [19584313.001]

[Cites] J Med Genet. 2005 May;42(5):428-35 [15863673.001]

[Cites] Am J Surg Pathol. 1987 Oct;11(10):743-9 [3661821.001]

[Cites] Hum Mutat. 2005 Oct;26(4):291-7 [16110486.001]

[Cites] Gut. 2007 Oct;56(10):1475-6 [17872577.001]

[Cites] Dis Colon Rectum. 2003 Jan;46(1):48-50 [12544521.001]

[Cites] Gastroenterology. 2000 Dec;119(6):1447-53 [11113065.001]

[Cites] Int J Colorectal Dis. 1994;9(4):177-9 [7876718.001]

(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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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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[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

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[Copyright] 2004 Wiley-Liss, Inc.

(PMID = 15565647.001).

[ISSN] 0730-2312

[Journal-full-title] Journal of cellular biochemistry

[ISO-abbreviation] J. Cell. Biochem.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 110