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1. Kikuchi E, Nakashima J, Ishibashi M, Ohigashi T, Oya M, Nakagawa K, Miyajima A, Murai M: Usefulness of alpha1-antichymotrypsin-PSA complex for predicting bone metastases of prostate cancer. Urology; 2006 Aug;68(2):371-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Usefulness of alpha1-antichymotrypsin-PSA complex for predicting bone metastases of prostate cancer.
  • OBJECTIVES: To determine the usefulness of alpha1-antichymotrypsin-prostate-specific antigen (PSA) complex (PSA-ACT)-based parameters in predicting bone metastasis in patients with prostate cancer.
  • METHODS: PSA-ACT, total PSA, free PSA, their volume-adjusted values, and alkaline phosphatase were evaluated in 220 consecutive patients with newly diagnosed prostate cancer.
  • RESULTS: Bone metastases were detected by bone scan in 27 (12.3%) of the 220 patients.
  • The serum levels of PSA-ACT, total PSA, free PSA, PSA density, PSA adjusted for transition zone volume, PSA-ACT density, PSA-ACT adjusted for transition zone volume, alkaline phosphatase, PSA-ACT/PSA ratio, and Gleason score in patients with bone metastases were each significantly greater than in those without bone metastases.
  • At a sensitivity of 93% (2 patients with bone metastasis missed), unnecessary bone scans would have been avoided in 107 and 102 patients using a PSA-ACT cutoff value of 10 ng/mL and total PSA cutoff value of 11.5 ng/mL, respectively.
  • Multivariate logistic regression analysis demonstrated that PSA-ACT and Gleason score were significant independent predictors of bone metastasis.
  • CONCLUSIONS: PSA-ACT is as useful as total PSA for identifying patients with a low probability of having bone metastasis.
  • PSA-ACT could replace PSA for predicting negative bone scans in a clinical setting in which PSA-ACT is used for monitoring and screening patients for prostate cancer.
  • [MeSH-major] Bone Neoplasms / secondary. Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology. alpha 1-Antichymotrypsin / blood



2. Matsunaga S, Iguchi K, Usui S, Hirano K: Incadronate induces cell detachment and apoptosis in prostatic PC-3 cells. Anticancer Res; 2007 Mar-Apr;27(2):927-32
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  • BACKGROUND: Bisphosphonates are widely used for the treatment and prevention of osteoporosis and are also effective in the treatment of bone metastasis of prostate cancer.
  • Several mechanisms underlying the antitumor effect of bisphosphonates have been proposed, including direct effects on tumor cells, such as induction of apoptosis and inhibition of invasion.
  • [MeSH-minor] Aspartic Acid / analogs & derivatives. Aspartic Acid / pharmacology. Caspase Inhibitors. Cell Adhesion / drug effects. Cell Line, Tumor. Etoposide / pharmacology. Focal Adhesion Protein-Tyrosine Kinases / metabolism. Humans. Male. Mevalonic Acid / pharmacology. Phosphorylation / drug effects. Protease Inhibitors / pharmacology

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  • (PMID = 17465222.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Caspase Inhibitors; 0 / Diphosphonates; 0 / Protease Inhibitors; 0 / benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene; 138330-18-4 / cimadronate; 30KYC7MIAI / Aspartic Acid; 6PLQ3CP4P3 / Etoposide; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; S5UOB36OCZ / Mevalonic Acid
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3. Yates CC, Shepard CR, Stolz DB, Wells A: Co-culturing human prostate carcinoma cells with hepatocytes leads to increased expression of E-cadherin. Br J Cancer; 2007 Apr 23;96(8):1246-52
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  • [Title] Co-culturing human prostate carcinoma cells with hepatocytes leads to increased expression of E-cadherin.
  • Metastasis is a multi-step process wherein tumour cells detach from the primary mass, migrate through barrier matrices, gain access to conduits to disseminate, and subsequently survive and proliferate in an ectopic site.
  • During the initial invasion stage, prostate carcinoma cells undergo epithelial-mesenchymal-like transition with gain of autocrine signalling and loss of E-cadherin, hallmarks that appear to enable invasion and dissemination.
  • However, some metastases express E-cadherin, and we found close connections between prostate carcinoma cells and hepatocytes in a liver microtissue bioreactor.
  • We hypothesise that phenotypic plasticity occurs late in prostate cancer progression at the site of ectopic seeding.
  • Immunofluorescence staining for E-cadherin in co-cultures of hepatocytes and DU-145 prostate cancer cells revealed E-cadherin upregulation at peripheral sites of contact by day 2 of co-culture; E-cadherin expression also increased in PC-3 cells in co-culture.
  • Inhibition of autocrine EGFR signalling increased E-cadherin expression and cell-cell heterotypic adhesion; further, expression of a downregulation-resistant EGFR variant prevented E-cadherin upregulation.
  • These findings were supported by finding E-cadherin and catenins but not activated EGFR in human prostate metastases to the liver.
  • We conclude that the term epithelial-mesenchymal transition only summarises the transient downregulation of E-cadherin for invasion with re-expression of E-cadherin being a physiological consequence of metastatic seeding.
  • [MeSH-minor] Animals. Cell Adhesion. Cell Communication. Cell Line, Tumor. Coculture Techniques. Humans. Male. Rats. Rats, Sprague-Dawley. Receptor, Epidermal Growth Factor / analysis. Receptor, Epidermal Growth Factor / physiology. Signal Transduction

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  • [Cites] J Cell Biol. 2003 Jun 23;161(6):1191-203 [12810698.001]
  • [Cites] BJU Int. 2002 Mar;89(4):400-3 [11872032.001]
  • [Cites] Nat Rev Cancer. 2003 Dec;3(12):921-30 [14737122.001]
  • [Cites] Anticancer Drugs. 2004 Feb;15(2):161-7 [15075673.001]
  • [Cites] Methods Cell Biol. 1976;13:29-83 [177845.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Aug;78(8):4975-9 [6946443.001]
  • [Cites] J Cell Biol. 1991 Aug;114(3):533-43 [1860884.001]
  • [Cites] Cancer Res. 1995 Nov 15;55(22):5195-9 [7585573.001]
  • [Cites] Cancer Res. 1996 Sep 15;56(18):4096-102 [8797572.001]
  • [Cites] J Pathol. 1999 Jan;187(2):155-7 [10365089.001]
  • [Cites] Mol Cancer. 2004 Oct 11;3:28 [15476557.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):9209-16 [15604294.001]
  • [Cites] Hum Pathol. 2004 Dec;35(12):1469-76 [15619205.001]
  • [Cites] Br J Cancer. 2005 Jan 31;92(2):366-75 [15655536.001]
  • [Cites] Ann R Coll Surg Engl. 2005 Jan;87(1):15-20 [15720901.001]
  • [Cites] Cancer Biol Ther. 2005 Apr;4(4):365-70 [15846061.001]
  • [Cites] Endocr Relat Cancer. 2006 Mar;13(1):197-210 [16601288.001]
  • [Cites] Cancer Res. 2006 Dec 1;66(23):11271-8 [17145872.001]
  • [Cites] Adv Cancer Res. 2007;97:225-46 [17419948.001]
  • [Cites] Nat Rev Cancer. 2002 Jun;2(6):442-54 [12189386.001]
  • [Cites] Surgery. 2002 Aug;132(2):141-8 [12219004.001]
  • [Cites] Lab Invest. 2003 Mar;83(3):435-48 [12649344.001]
  • [Cites] Adv Cancer Res. 2000;78:31-101 [10547668.001]
  • [Cites] J Urol. 2000 Mar;163(3):985-92 [10688036.001]
  • [Cites] Hum Pathol. 2001 Jul;32(7):690-7 [11486167.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10356-61 [11526241.001]
  • [Cites] Cancer. 2001 Dec 1;92(11):2786-95 [11753952.001]
  • [Cites] Breast Cancer Res. 2003;5(6):R217-22 [14580257.001]
  • (PMID = 17406365.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cadherins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2360137
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4. Shrivastava V, Christensen R, Poggi MM: Prostate cancer metastatic to the external auditory canals. Clin Genitourin Cancer; 2007 Jun;5(5):341-3
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  • [Title] Prostate cancer metastatic to the external auditory canals.
  • A 58-year-old white man with prostate-specific antigen (PSA) level of 6 ng/mL, a Gleason score of 6 (3+3), and T2a adenocarcinoma of the prostate underwent prostatectomy.
  • The PSA continued to increase, and the patient developed bone-only metastatic disease.
  • Six months later, he presented with bilateral hearing loss and was found to have pathologic and radiographic evidence of metastatic prostate cancer to the external auditory canals.
  • [MeSH-major] Adenocarcinoma / secondary. Ear Canal / pathology. Ear Neoplasms / secondary. Prostatic Neoplasms / pathology
  • [MeSH-minor] Fatal Outcome. Humans. Male. Middle Aged. Prostate-Specific Antigen / blood. Prostatectomy



5. Shih HA, Harisinghani M, Zietman AL, Wolfgang JA, Saksena M, Weissleder R: Mapping of nodal disease in locally advanced prostate cancer: rethinking the clinical target volume for pelvic nodal irradiation based on vascular rather than bony anatomy. Int J Radiat Oncol Biol Phys; 2005 Nov 15;63(4):1262-9
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  • [Title] Mapping of nodal disease in locally advanced prostate cancer: rethinking the clinical target volume for pelvic nodal irradiation based on vascular rather than bony anatomy.
  • We employed a novel magnetic resonance lymphangiographic technique to highlight the likely sites of occult nodal metastasis from prostate cancer.
  • METHODS AND MATERIALS: Eighteen prostate cancer patients with pathologically confirmed node-positive disease had a total of 69 pathologic nodes identifiable by lymphotropic nanoparticle-enhanced MRI and semiquantitative nodal analysis.
  • The position of each of these malignant nodes was mapped to a common template based on its relation to skeletal or vascular anatomy.
  • In contrast, the nodal metastases mapped much more tightly relative to the large pelvic vessels.
  • A proposed pelvic clinical target volume to encompass the region at greatest risk of containing occult nodal metastases would include a 2.0-cm radial expansion volume around the distal common iliac and proximal external and internal iliac vessels that would encompass 94.5% of the pelvic nodes at risk as defined by our node-positive prostate cancer patient cohort.
  • CONCLUSIONS: Nodal metastases from prostate cancer are largely localized along the major pelvic vasculature.
  • [MeSH-major] Lymphatic Irradiation / methods. Lymphatic Metastasis / pathology. Magnetic Resonance Imaging / methods. Prostatic Neoplasms / pathology

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  • [CommentIn] Int J Radiat Oncol Biol Phys. 2006 Dec 1;66(5):1592; author reply 1593 [17126215.001]
  • (PMID = 16253781.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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6. Kabeer MA, Lloyd-Davies E, Maskell G, Hohle R, Mathew J: Metastatic prostate cancer masquerading clinically and radiologically as a primary caecal carcinoma. World J Surg Oncol; 2007;5:2
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  • [Title] Metastatic prostate cancer masquerading clinically and radiologically as a primary caecal carcinoma.
  • BACKGROUND: Prostatic carcinoma is the second most common cause of cancer-related deaths in males in the West.
  • Approximately 20% of patients present with metastatic disease.
  • We describe the case of a patient with metastatic prostate cancer to the bowel presenting clinically and radiologically as a primary caecal cancer.
  • The patient was being treated (Zoladex) for prostatic cancer diagnosed 6 years previously and was known to have bony metastases.
  • Histology showed a poorly differentiated adenocarcinoma which was PSA positive, confirming metastatic prostatic adenocarcinoma to the caecum.
  • CONCLUSION: Metastasis of prostatic carcinoma to the bowel is a very rare occurrence and presents a challenging diagnosis.
  • The diagnosis is supported by immunohistochemistry for PSA.
  • The treatment for metastatic prostate cancer is mainly palliative.
  • [MeSH-major] Adenocarcinoma / secondary. Cecal Neoplasms / secondary. Cecal Neoplasms / therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biopsy, Needle. Chemotherapy, Adjuvant. Colectomy / methods. Diagnosis, Differential. Follow-Up Studies. Gastrointestinal Hemorrhage / diagnosis. Gastrointestinal Hemorrhage / etiology. Humans. Immunohistochemistry. Male. Neoplasm Staging. Prostatectomy / methods. Rectum. Risk Assessment. Tomography, X-Ray Computed. Treatment Outcome



7. Pontes J Jr, Srougi M, Borra PM, Dall' Oglio MF, Ribeiro-Filho LA, Leite KR: E-cadherin and beta-catenin loss of expression related to bone metastasis in prostate cancer. Appl Immunohistochem Mol Morphol; 2010 Mar;18(2):179-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] E-cadherin and beta-catenin loss of expression related to bone metastasis in prostate cancer.
  • A disturbance in epithelial cell adhesion, which leads to a more invasive and metastatic phenotype, is a hallmark of tumor progression.
  • Several immunohistochemical studies have reported a strong correlation between loss of their expression to higher stage and grade in prostate carcinoma, but their influence in metastatic process is not yet known.
  • The aim of this study is to verify the role of adhesion molecules in the progression of prostate cancer (PC), assessing the expression of E-cadherin and beta-catenin in bone metastasis.
  • MATERIALS AND METHODS: Twenty-eight bone metastases of prostate carcinoma were submitted to immunohistochemistry analysis for E-cadherin and beta-catenin expression.
  • In 6 patients, we were able to assess the expression of the adhesion molecules in the primary tumors and their respective metastases.
  • The definition of normal expression for both antibodies was strong and diffuse expression in more than 70% of tumor cells.
  • RESULTS: In bone metastases, there was loss of expression of E-cadherin and beta-catenin in 86% and 82%, respectively.
  • Considering the 6 patients with paired primary and bone metastasis, we found loss of expression for both E-cadherin and beta-catenin in most of the cases.
  • CONCLUSIONS: Comparing primary PC and its metastasis, we showed persistent loss of E-cadherin and beta-catenin expression.
  • This phenomenon may be related to metastatic potential in PC, because we have shown underexpression for E-cadherin and beta-catenin in 86% and 82% of bone metastases.



8. Roma AA, Magi-Galluzzi C, Kral MA, Jin TT, Klein EA, Zhou M: Peritumoral lymphatic invasion is associated with regional lymph node metastases in prostate adenocarcinoma. Mod Pathol; 2006 Mar;19(3):392-8
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  • [Title] Peritumoral lymphatic invasion is associated with regional lymph node metastases in prostate adenocarcinoma.
  • Lymphangiogenesis, detected by antibodies specific for lymphatic endothelial cells, has been associated with regional lymph node metastases and poor prognosis in carcinomas of head and neck, breast and uterine cervix, but remains largely uninvestigated in prostate adenocarcinoma.
  • We evaluated the lymphatic vessel density and lymphatic vessel invasion by prostate cancer cells in the intratumoral, peritumoral and normal prostate tissue compartments in cancer-bearing prostate glands and correlated them with lymph node metastases, Gleason score and other pathological parameters.
  • In all, 26 patients had lymph node dissection, and 14 of them had lymph node metastasis.
  • Lymphatic vessel density in the intratumoral, peritumoral and normal prostate compartments was 0.91+/-0.80, 1.54+/-0.68 and 1.58+/-0.96/mm2, respectively.
  • The intratumoral lymphatic vessel density was significantly lower than that of the peritumoral and normal prostate compartments, and the latter two were not significantly different.
  • The lymphatic vessel density of the three compartments was not significantly different between cases with and without lymph node metastasis.
  • Lymphatic vessel invasion was present in significantly higher percentage of cases with lymph node metastasis (9/14, 62.3%), as compared to those without lymph node metastasis (1/12, 8.3%, P<0.01).
  • The peritumoral lymphatic vessel invasion had a better correlation with the presence of lymph node metastases than intratumoral lymphatic vessel invasion.
  • There is no evidence of lymphangiogenesis in prostate adenocarcinoma.
  • Peritumoral lymphatic vessel invasion correlates with regional lymph node metastases, suggesting that the peritumoral lymphatic vessels are functionally important and identification of lymphatic vessel invasion in this compartment implies a high probability of regional lymph node metastases.
  • [MeSH-minor] Aged. Endothelial Cells / chemistry. Endothelial Cells / pathology. Humans. Immunohistochemistry. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Invasiveness. Prostate / blood supply. Prostate / pathology. Sialoglycoproteins / analysis

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  • (PMID = 16400321.001).
  • [ISSN] 0893-3952
  • [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 / Sialoglycoproteins
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9. Reyes I, Tiwari R, Geliebter J, Reyes N: DNA microarray analysis reveals metastasis-associated genes in rat prostate cancer cell lines. Biomedica; 2007 Jun;27(2):190-203
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  • [Title] DNA microarray analysis reveals metastasis-associated genes in rat prostate cancer cell lines.
  • INTRODUCTION: The molecular and cellular mechanisms involved in prostate cancer progression towards a hormone-independent and highly invasive, metastatic phenotype, are not well understood.
  • Cell lines with different metastatic potential, when analyzed by microarray techniques, offer valuable tools for identifying genes associated with the metastatic phenotype.
  • OBJECTIVES: Gene expression profiles were compared for two rat prostate cancer cell lines with differing metastatic abilities in order to better characterized molecular underpinnings of the prostate cancer metastatic process.
  • MATERIALS AND METHODS: Affymetrix arrays were used to analyze gene expression of two rat prostate cancer cell lines, MAT-LyLu and G.
  • Many of these genes were not previously associated to prostate cancer metastasis.
  • CONCLUSIONS: Many genes with altered expression associated with a metastatic prostate cancer phenotype were identified.
  • Further validation of these genes in human prostate samples will determine their usefulness as biomarkers for early diagnosis of recurrence or metastasis of prostate cancer, as well as potential therapeutic targets for this disease.
  • [MeSH-major] Neoplasm Metastasis / genetics. Oligonucleotide Array Sequence Analysis. Prostatic Neoplasms
  • [MeSH-minor] Animals. Biomarkers / metabolism. Cell Line, Tumor. Gene Expression Profiling. Humans. Male. Molecular Sequence Data. Phenotype. Rats

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  • (PMID = 17713630.001).
  • [ISSN] 0120-4157
  • [Journal-full-title] Biomédica : revista del Instituto Nacional de Salud
  • [ISO-abbreviation] Biomedica
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE7703
  • [Grant] United States / NCI NIH HHS / CA / 1R21 CA 088982
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Colombia
  • [Chemical-registry-number] 0 / Biomarkers
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10. Damodaran D, Kathiresan N, Satheesan B: Oral cavity metastasis: An unusual presentation of carcinoma prostate. Indian J Urol; 2008 Jan;24(1):112-3
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  • [Title] Oral cavity metastasis: An unusual presentation of carcinoma prostate.
  • The oral cavity is a very rare site for metastases and has been described in various cancers, particularly lung, breast, kidney and colon carcinoma.
  • Here a very rare case of a buccal metastasis from prostate carcinoma that was originally evaluated as a primary oral cavity malignancy is presented.
  • Histopathological examination of a biopsy of the lesion revealed papillary adenocarcinoma Grade II, nuclear Grade II, which initiated the evaluation of prostate.
  • On evaluation diagnosis of carcinoma prostate was made which was confirmed by immunohistochemistry for PSA.

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  • [Cites] Int J Cancer. 2005 Sep 20;116(5):740-54 [15849747.001]
  • [Cites] Pathol Int. 1999 Jun;49(6):500-5 [10469392.001]
  • [Cites] J Periodontol. 1999 Apr;70(4):441-4 [10328657.001]
  • [Cites] Br J Oral Maxillofac Surg. 2003 Feb;41(1):3-6 [12576032.001]
  • [Cites] BJU Int. 1999 Dec;84(9):1028-31 [10571628.001]
  • (PMID = 19468372.001).
  • [ISSN] 0970-1591
  • [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/ PMC2684236
  • [Keywords] NOTNLM ; Oral cavity metastasis / prostate cancer / prostate specific antigen immunohistochemistry
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11. Shirakawa H, Kozakai N, Sugiura H, Hara S: [Urinary bladder metastasis of prostate cancer : a case report]. Hinyokika Kiyo; 2010 Feb;56(2):123-5
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  • [Title] [Urinary bladder metastasis of prostate cancer : a case report].
  • The transrectal ultrasonography guided biopsy of the prostate revealed prostate cancer.
  • Computed tomography, magnetic resonance imaging (MRI) and bone scintigraphy showed multiple metastases to his bones and lymph nodes.
  • The MRI incidentally revealed a solitary tumor at the right lateral wall of the urinary bladder.
  • Transurethral resection of the bladder tumor was performed, and histopathological examination showed the bladder tumor composed of not urothelial carcinoma but metastatic adenocarcinoma from prostate cancer.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / secondary. Prostatic Neoplasms / pathology. Urinary Bladder Neoplasms / secondary



12. Pinzone JJ, Hall BM, Thudi NK, Vonau M, Qiang YW, Rosol TJ, Shaughnessy JD Jr: The role of Dickkopf-1 in bone development, homeostasis, and disease. Blood; 2009 Jan 15;113(3):517-25
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  • DKK1 has been implicated in causing erosive arthritis, the osteolytic phenotypes of multiple myeloma and metastatic breast cancer, and osteoblastic metastases of prostate cancer.

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  • [Cites] J Biol Chem. 2008 Jul 18;283(29):20505-22 [18487199.001]
  • [Cites] Mol Cell Biol. 2008 Aug;28(15):4875-82 [18505822.001]
  • [Cites] Int J Cancer. 2008 Oct 1;123(7):1526-35 [18623132.001]
  • [Cites] Prostate. 2008 Sep 15;68(13):1396-404 [18561248.001]
  • [Cites] Calcif Tissue Int. 2008 Jun;82(6):445-53 [18521528.001]
  • [Cites] Blood. 2009 Jul 9;114(2):371-9 [19417213.001]
  • [Cites] J Cell Biochem. 2004 Dec 15;93(6):1210-30 [15486964.001]
  • [Cites] Development. 2005 Jan;132(1):49-60 [15576404.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):1098-103 [15592505.001]
  • [Cites] Annu Rev Immunol. 2005;23:1-21 [15771564.001]
  • [Cites] Dev Cell. 2005 May;8(5):739-50 [15866164.001]
  • [Cites] Dev Cell. 2005 May;8(5):751-64 [15866165.001]
  • [Cites] J Biol Chem. 2005 Jun 3;280(22):21162-8 [15802266.001]
  • [Cites] Mol Cell Biol. 2005 Jun;25(12):4946-55 [15923613.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):26770-5 [15908424.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7554-60 [16140917.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2472-83 [15933061.001]
  • [Cites] Br J Haematol. 2005 Oct;131(1):71-3 [16173965.001]
  • [Cites] J Biol Chem. 2005 Sep 30;280(39):33132-40 [16043491.001]
  • [Cites] J Cell Biochem. 2006 Mar 1;97(4):661-72 [16447163.001]
  • [Cites] Nat Immunol. 2006 Apr;7(4):333-7 [16550195.001]
  • [Cites] J Cell Sci. 2006 Apr 1;119(Pt 7):1283-96 [16522681.001]
  • [Cites] N Engl J Med. 2006 Mar 30;354(13):1362-9 [16571879.001]
  • [Cites] Gene. 2006 May 10;372:62-70 [16574347.001]
  • [Cites] Stem Cells. 2006 Apr;24(4):986-91 [16293576.001]
  • [Cites] J Bone Miner Res. 2006 Jun;21(6):934-45 [16753024.001]
  • [Cites] J Cell Sci. 2006 Jun 15;119(Pt 12):2613-20 [16763196.001]
  • [Cites] Oncogene. 2006 Aug 17;25(36):5027-36 [16568085.001]
  • [Cites] Cell. 2006 Nov 3;127(3):469-80 [17081971.001]
  • [Cites] J Biol Chem. 2006 Dec 15;281(50):38276-84 [17052975.001]
  • [Cites] J Biol Chem. 2007 Jan 5;282(1):526-33 [17085452.001]
  • [Cites] Am J Pathol. 2007 Jan;170(1):160-75 [17200191.001]
  • [Cites] Bone. 2007 Feb;40(2):485-92 [17055793.001]
  • [Cites] Mol Endocrinol. 2007 Feb;21(2):486-98 [17068196.001]
  • [Cites] Nat Med. 2007 Feb;13(2):156-63 [17237793.001]
  • [Cites] Ann N Y Acad Sci. 2006 Dec;1092:385-96 [17308163.001]
  • [Cites] Blood. 2007 Mar 1;109(5):2106-11 [17068150.001]
  • [Cites] Br J Cancer. 2007 Feb 26;96(4):646-53 [17245340.001]
  • [Cites] BMC Musculoskelet Disord. 2007;8:12 [17295923.001]
  • [Cites] Stem Cells. 2007 Mar;25(3):544-52 [17095705.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2517-25 [17363569.001]
  • [Cites] FASEB J. 2007 May;21(7):1410-21 [17283219.001]
  • [Cites] Blood. 2007 May 15;109(10):4470-7 [17255354.001]
  • [Cites] Front Biosci. 2007;12:3068-92 [17485283.001]
  • [Cites] Endocrinology. 2007 Jun;148(6):2635-43 [17395698.001]
  • [Cites] Endocrinology. 2007 Jun;148(6):2630-4 [17395705.001]
  • [Cites] J Cell Physiol. 2007 Sep;212(3):817-26 [17458904.001]
  • [Cites] Nat Rev Cancer. 2007 Aug;7(8):585-98 [17646864.001]
  • [Cites] J Cell Biochem. 2007 Aug 1;101(5):1109-24 [17546602.001]
  • [Cites] PLoS Med. 2007 Jul 31;4(7):e249 [17676991.001]
  • [Cites] Bone. 2007 Sep;41(3):331-9 [17613296.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1587-94 [17515399.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2035-42 [17581613.001]
  • [Cites] Br J Cancer. 2007 Oct 8;97(7):964-70 [17876334.001]
  • [Cites] Br J Haematol. 2007 Nov;139(3):434-8 [17910634.001]
  • [Cites] J Clin Invest. 2007 Nov;117(11):3248-57 [17948129.001]
  • [Cites] Nat Cell Biol. 2007 Nov;9(11):1273-85 [17952062.001]
  • [Cites] Br J Cancer. 2007 Dec 3;97(11):1552-9 [17987039.001]
  • [Cites] Leuk Lymphoma. 2007 Dec;48(12):2323-9 [18067006.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2833-42 [18094333.001]
  • [Cites] Bone. 2008 Apr;42(4):669-80 [18294945.001]
  • [Cites] Endocrinology. 2008 Apr;149(4):1793-801 [18174290.001]
  • [Cites] Cell Stem Cell. 2008 Mar 6;2(3):274-83 [18371452.001]
  • [Cites] Eur J Haematol. 2008 Jun;80(6):490-4 [18331598.001]
  • [Cites] Mol Biol Cell. 2008 Jun;19(6):2588-96 [18400942.001]
  • [Cites] Prostate. 2008 Jul 1;68(10):1116-25 [18461562.001]
  • [Cites] Blood. 2008 Jul 1;112(1):196-207 [18305214.001]
  • [Cites] Int J Cancer. 2008 Sep 1;123(5):1034-42 [18546262.001]
  • [Cites] Blood. 2008 Jul 15;112(2):374-82 [18344425.001]
  • [Cites] Dev Cell. 2008 Jul;15(1):37-48 [18606139.001]
  • [Cites] Science. 2000 Aug 11;289(5481):950-3 [10937998.001]
  • [Cites] Am J Hum Genet. 2001 Mar;68(3):577-89 [11179006.001]
  • [Cites] Nature. 2001 May 17;411(6835):321-5 [11357136.001]
  • [Cites] Dev Cell. 2001 Sep;1(3):423-34 [11702953.001]
  • [Cites] Cell. 2001 Nov 16;107(4):513-23 [11719191.001]
  • [Cites] Am J Hum Genet. 2002 Jan;70(1):11-9 [11741193.001]
  • [Cites] N Engl J Med. 2002 Feb 21;346(8):564-9 [11856795.001]
  • [Cites] EMBO J. 2002 Mar 1;21(5):966-75 [11867524.001]
  • [Cites] J Cell Biol. 2002 Apr 15;157(2):303-14 [11956231.001]
  • [Cites] N Engl J Med. 2002 May 16;346(20):1513-21 [12015390.001]
  • [Cites] Nature. 2002 Jun 6;417(6889):664-7 [12050670.001]
  • [Cites] Dev Biol. 2002 Nov 1;251(1):142-56 [12413904.001]
  • [Cites] J Clin Invest. 2003 Jun;111(11):1771-82 [12782679.001]
  • [Cites] J Bone Miner Res. 2003 Jun;18(6):960-74 [12817748.001]
  • [Cites] N Engl J Med. 2003 Jun 26;348(26):2609-17 [12826635.001]
  • [Cites] Immunol Rev. 2003 Aug;194:140-63 [12846813.001]
  • [Cites] J Biol Chem. 2003 Jul 25;278(30):28067-78 [12740383.001]
  • [Cites] Development. 2003 Sep;130(18):4295-305 [12900447.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):10954-9 [12941866.001]
  • [Cites] N Engl J Med. 2003 Dec 25;349(26):2483-94 [14695408.001]
  • [Cites] Cytokine Growth Factor Rev. 2004 Feb;15(1):49-60 [14746813.001]
  • [Cites] Development. 2004 Jun;131(11):2543-52 [15115753.001]
  • [Cites] Dev Biol. 2004 Aug 1;272(1):39-52 [15242789.001]
  • [Cites] Stem Cells. 2004;22(5):849-60 [15342948.001]
  • [Cites] J Biol Chem. 1996 Oct 18;271(42):26131-7 [8824257.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Jul 18;236(2):502-4 [9240469.001]
  • [Cites] Nature. 1998 Jan 22;391(6665):357-62 [9450748.001]
  • [Cites] Nature. 1999 Apr 1;398(6726):431-6 [10201374.001]
  • [Cites] J Bone Miner Res. 2004 Dec;19(12):2033-40 [15537447.001]
  • (PMID = 18687985.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA101875; United States / NCI NIH HHS / CA / P01 CA055819; United States / NCI NIH HHS / CA / CA101875; United States / NCI NIH HHS / CA / CA55819
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DKK1 protein, human; 0 / Intercellular Signaling Peptides and Proteins
  • [Number-of-references] 100
  • [Other-IDs] NLM/ PMC2628360
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13. Saad F: The role of bisphosphonates in the management of prostate cancer. Curr Oncol Rep; 2006 May;8(3):221-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of bisphosphonates in the management of prostate cancer.
  • Current therapies have extended the survival of patients with prostate cancer.
  • Low bone mineral density (BMD) is prevalent in patients with early-stage prostate cancer, and androgen-deprivation therapy by either pharmaceutical agent (including hormonal) or surgical castration causes significant decreases in BMD.
  • Fractures can result in a loss of independence and have been associated with shorter survival in patients with prostate cancer.
  • Zoledronic acid is the only bisphosphonate that has demonstrated objective and long-term benefits in reducing skeletal morbidity in patients with bone metastases due to prostate cancer, and it has produced long-term reductions in pain levels compared with placebo in this setting.
  • Therefore, bisphosphonates, particularly zoledronic acid, may provide important benefits for preserving bone health during the course of prostate cancer progression.

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  • [Cites] Acta Oncol. 2005;44(3):282-92 [16076701.001]
  • [Cites] Curr Opin Oncol. 2002 Nov;14(6):609-15 [12409650.001]
  • [Cites] J Natl Cancer Inst. 2003 Sep 3;95(17 ):1300-11 [12953084.001]
  • [Cites] J Clin Invest. 1996 Jun 15;97(12):2692-6 [8675678.001]
  • [Cites] J Urol. 2002 Jun;167(6):2361-7; discussion 2367 [11992038.001]
  • [Cites] Drugs Aging. 2003;20(3):175-83 [12578398.001]
  • [Cites] CA Cancer J Clin. 2005 Jan-Feb;55(1):10-30 [15661684.001]
  • [Cites] J Urol. 2000 Jan;163(1):181-6 [10604342.001]
  • [Cites] Cancer. 2004 Mar 1;100(5):892-9 [14983482.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):295-306 [12538482.001]
  • [Cites] J Urol. 1997 Feb;157(2):439-44 [8996327.001]
  • [Cites] Cancer. 1998 Oct 15;83(8):1561-6 [9781950.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Dec;90(12):6410-7 [16189261.001]
  • [Cites] Am J Clin Oncol. 2002 Dec;25(6 Suppl 1):S10-8 [12562046.001]
  • [Cites] Cancer. 2000 Jun 15;88(12 Suppl):2989-94 [10898342.001]
  • [Cites] Br J Cancer. 2003 Jan 27;88(2):195-201 [12610502.001]
  • [Cites] Eur J Surg. 1994 Oct;160(10):535-42 [7849154.001]
  • [Cites] Cochrane Database Syst Rev. 2002;(2):CD002068 [12076438.001]
  • [Cites] Cancer Chemother Pharmacol. 2006 Jan;57(1):46-51 [16001175.001]
  • [Cites] N Engl J Med. 2001 Sep 27;345(13):948-55 [11575286.001]
  • [Cites] J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68 [12359855.001]
  • [Cites] J Urol. 2003 Jun;169(6):2008-12 [12771706.001]
  • [Cites] Cancer Invest. 2002;20 Suppl 2:45-54 [12442349.001]
  • [Cites] Semin Oncol. 2002 Dec;29(6 Suppl 21):19-27 [12584691.001]
  • [Cites] Ann Oncol. 2005 Apr;16(4):579-84 [15734776.001]
  • [Cites] J Natl Cancer Inst. 2005 Jan 5;97(1):59-69 [15632381.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4277-84 [14581438.001]
  • [Cites] Semin Nucl Med. 2001 Jan;31(1):62-8 [11200206.001]
  • [Cites] J Chemother. 2005 Oct;17(5):555-9 [16323446.001]
  • [Cites] Urology. 2002 Sep;60(3 Suppl 1):79-85; discussion 86 [12231056.001]
  • [Cites] J Natl Cancer Inst. 2004 Jun 2;96(11):879-82 [15173273.001]
  • [Cites] J Urol. 2002 Sep;168(3):1005-7 [12187209.001]
  • [Cites] J Urol. 2000 Oct;164(4):1248-53 [10992374.001]
  • [Cites] J Urol. 1989 Jan;141(1):85-7 [2462069.001]
  • [Cites] N Engl J Med. 2005 Jan 13;352(2):154-64 [15647578.001]
  • [Cites] CMAJ. 1998 Sep 22;159(6):685-91 [9780970.001]
  • [Cites] Anticancer Res. 1997 Nov-Dec;17(6D):4717-21 [9494595.001]
  • [Cites] Cancer Metastasis Rev. 2001;20(3-4):333-49 [12085970.001]
  • [Cites] Cancer Treat Rev. 2001 Jun;27(3):165-76 [11417967.001]
  • [Cites] Urology. 2005 Nov;66(5):1054-9 [16286123.001]
  • [Cites] J Neurooncol. 1995;23(2):135-47 [7543940.001]
  • [Cites] Pain. 1997 Jan;69(1-2):1-18 [9060007.001]
  • [Cites] Br J Cancer. 1997;76(7):939-42 [9328156.001]
  • [Cites] BJU Int. 2000 Sep;86(4):449-52 [10971270.001]
  • [Cites] Cancer. 2001 Jun 15;91(12):2238-45 [11413511.001]
  • [Cites] Int Urol Nephrol. 1992;24(2):159-66 [1385586.001]
  • [Cites] J Clin Oncol. 2003 Sep 1;21(17):3335-42 [12947070.001]
  • (PMID = 16618387.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
  • [Number-of-references] 50
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14. Cai T, Salvadori A, Nesi G, Detti B, Tinacci G, Zini E, Bartoletti R: Penile metastasis from a T1b prostate carcinoma. Onkologie; 2007 May;30(5):249-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Penile metastasis from a T1b prostate carcinoma.
  • BACKGROUND: Penile metastasis from incidental prostate carcinoma has not been described to date.
  • CASE REPORT: The case of a 72-year-old man affected by penile metastasis from incidental prostate carcinoma is described.
  • In March 1998, the patient underwent prostate surgery for lower urinary tract symptoms related to benign prostatic obstruction.
  • Histological examination revealed an incidental adenocarcinoma of the prostate.
  • The pre-operative prostate-specific antigen (PSA) value was 3.6 ng/ml.
  • A prostate biopsy in the peripheral prostate lobes was negative.
  • The prostate biopsy was repeated and was still negative.
  • Surgical biopsy showed a metastasis from prostate adenocarcinoma and he underwent partial penectomy.
  • CONCLUSION: We underline the uncertainty of the biological behaviour and optimal management of incidentally identified prostate carcinoma.
  • [MeSH-major] Adenocarcinoma / secondary. Penile Neoplasms / secondary. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / blood. Biopsy. Disease Progression. Humans. Incidental Findings. Male. Neoplasm Staging. Palliative Care. Penis / pathology. Prostate / pathology. Prostate-Specific Antigen / blood. Prostatectomy

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  • (PMID = 17460419.001).
  • [ISSN] 0378-584X
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
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15. Challagundla S, Gokden M, Viswamitra S, Kohli M: Orbital metastasis from prostate cancer: an atypical case of neuroendocrine dedifferentiation during progression from hormone-sensitive to refractory stage. Clin Prostate Cancer; 2005 Sep;4(2):134-7
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  • [Title] Orbital metastasis from prostate cancer: an atypical case of neuroendocrine dedifferentiation during progression from hormone-sensitive to refractory stage.
  • We report a case of orbital metastasis from a neuroendocrine dedifferentiated prostate cancer during progression from hormone-sensitive to hormone refractory stage.
  • A patient receiving androgen deprivation for hormone-sensitive prostate cancer presented with sudden-onset right-sided ptosis and an increasing serum prostate-specific antigen level.
  • Comparison of the metastatic histology with the original pathology confirmed a histologic change to poorly differentiated prostate adenocarcinoma with neuroendocrine features.
  • Because prostate cancer metastasis involves hematogenous and lymphatic routes, we also evaluated expression of the vascular endothelial growth factor (VEGF) and receptors (VEGFR-1, VEGFR-2, and VEGFR-3) in the metastatic deposit by immunohistochemistry.
  • Strong expression of VEGFR-2 and VEGFR-3 restricted to the malignant epithelium was noted.
  • We recommend a second biopsy of atypical prostate metastasis associated with sudden change to aggressive clinical behavior in order to evaluate for dedifferentiation features before planning appropriate treatment interventions especially in patients who are candidates for systemic chemotherapy.
  • [MeSH-major] Carcinoma, Neuroendocrine / secondary. Orbital Neoplasms / secondary. Prostatic Neoplasms / pathology

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  • (PMID = 16197616.001).
  • [ISSN] 1540-0352
  • [Journal-full-title] Clinical prostate cancer
  • [ISO-abbreviation] Clin Prostate Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Synaptophysin; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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16. Ripamonti C, Fagnoni E, Campa T, Seregni E, Maccauro M, Bombardieri E: Incident pain and analgesic consumption decrease after samarium infusion: a pilot study. Support Care Cancer; 2007 Mar;15(3):339-42
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  • OBJECTIVE: The aim of this pilot study was to observe the variations of pain intensity on movement and at rest and the variation of analgesic drug consumption in patients with prostate cancer and painful bone metastases treated with a single dose of 1.0 mCi/kg of samarium-153 (153-Sm) lexidronam.
  • SETTING: The Nuclear Medicine Unit and Pain Therapy and Palliative Care Unit, National Cancer Institute of Milan, Italy.
  • PATIENTS: Thirteen outpatients with hormone refractory prostate cancer and painful multiple bone metastases.
  • INTERVENTIONS: Infusion of a single dose of 1.0 mCi/kg of 153-Sm lexidronam, pain therapy, and the assessment of pain intensity at rest and on movement.
  • MAIN OUTCOME MEASURES: Variation of pain intensity on movement and at rest by means of a verbal scale and the reduction of analgesic drug consumption 4 weeks after infusion of 153-Sm lexidronam.
  • CONCLUSIONS: In patients with bone metastases, pain on movement is a frequent and often difficult clinical problem to treat and the most frequent cause of breakthrough pain.
  • In patients with painful multiple bone metastases due to prostate cancer, the infusion of a single dose of 1.0 mCi/kg of 153-Sm lexidronam may be considered an effective and safe treatment for pain either at rest or during movement.
  • [MeSH-minor] Aged. Analgesics, Opioid / therapeutic use. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Bone Marrow / drug effects. Bone Neoplasms / secondary. Dose-Response Relationship, Drug. Humans. Infusions, Intravenous. Male. Middle Aged. Morphine / therapeutic use. Movement. Pain Measurement. Pilot Projects. Prospective Studies. Prostatic Neoplasms / pathology. Rest. Severity of Illness Index. Treatment Outcome

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  • [Cites] J Cancer Res Clin Oncol. 2005 Jan;131(1):60-6 [15449184.001]
  • [Cites] J Pain Symptom Manage. 1995 Jul;10(5):348-55 [7673767.001]
  • [Cites] J Clin Oncol. 2002 Sep 1;20(17):3719-36 [12202673.001]
  • [Cites] Eur J Cancer. 1997 Sep;33(10 ):1583-91 [9389919.001]
  • [Cites] Pain. 1999 Sep;82(3):263-74 [10488677.001]
  • [Cites] Cancer. 2000 Jun 15;88(12 Suppl):2934-9 [10898337.001]
  • [Cites] Pain. 1992 Aug;50(2):151-5 [1408310.001]
  • [Cites] Pain. 1990 Jun;41(3):273-81 [1697056.001]
  • [Cites] Urology. 2004 May;63(5):940-5 [15134985.001]
  • [Cites] J Nucl Med. 1992 Aug;33(8):1451-8 [1378887.001]
  • [Cites] Pain. 1991 Nov;47(2):129-34; discussion 127-8 [1762805.001]
  • [Cites] Cancer. 2002 Feb 1;94(3):832-9 [11857319.001]
  • [Cites] J Pain Symptom Manage. 2000 Aug;20(2):87-92 [10989246.001]
  • [Cites] Lancet Oncol. 2005 Jun;6(6):392-400 [15925817.001]
  • [Cites] Br J Cancer. 1987 Jan;55(1):61-6 [3814476.001]
  • [Cites] Pain. 1999 May;81(1-2):129-34 [10353500.001]
  • [Cites] Cochrane Database Syst Rev. 2003;(4):CD003347 [14583970.001]
  • [Cites] Pain. 1994 Oct;59(1):141-5 [7531837.001]
  • [Cites] Pain. 1989 May;37(2):203-9 [2748193.001]
  • [Cites] J Clin Oncol. 1998 Apr;16(4):1574-81 [9552068.001]
  • [Cites] J Clin Oncol. 2003 Nov 1;21(21):4042-57 [12963702.001]
  • (PMID = 16967302.001).
  • [ISSN] 0941-4355
  • [Journal-full-title] Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer
  • [ISO-abbreviation] Support Care Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Analgesics, Non-Narcotic; 0 / Analgesics, Opioid; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Organometallic Compounds; 0 / Organophosphorus Compounds; 745X144DZY / samarium Sm-153 lexidronam; 76I7G6D29C / Morphine
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17. Salvati M, Frati A, Russo N, Brogna C, Piccirilli M, D'Andrea G, Occhiogrosso G, Pichierri A, Caroli E: Brain metastasis from prostate cancer. Report of 13 cases and critical analysis of the literature. J Exp Clin Cancer Res; 2005 Jun;24(2):203-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Brain metastasis from prostate cancer. Report of 13 cases and critical analysis of the literature.
  • Brain metastasis from prostate carcinoma occurs very rarely.
  • We describe 13 patients with single brain metastasis from prostatic cancer.
  • Eight patients died for systemic disease after a mean time of 9.2 months with a diagnosis of metastasis.
  • Even if brain metastasis from prostate cancer is often a terminal event with death occurring within few months from diagnosis, we suggest the same protocol (surgery and/or radiosurgery plus postoperative WBRT) usually adopted to treat brain metastasis from other primitive tumours.
  • A non specific neurological symptomatology and a possible normal dosage of serum specific antigen may contribute to a delay in diagnosis.
  • However, considering the rarity of brain metastasis from prostate carcinoma, standard brain MRI follow-up in men with prostatic cancer does not seem to be necessary yet.
  • [MeSH-major] Brain Neoplasms / secondary. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Humans. Male. Middle Aged. Neoplasm Metastasis. Time Factors. Treatment Outcome



18. Kobashi-Katoh R, Tanioka M, Takahashi K, Miyachi Y: Skin metastasis of prostate adenocarcinoma to glans penis showing no correlation with serum prostate-specific antigen level. J Dermatol; 2009 Feb;36(2):106-8
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  • [Title] Skin metastasis of prostate adenocarcinoma to glans penis showing no correlation with serum prostate-specific antigen level.
  • [MeSH-major] Adenocarcinoma / secondary. Biomarkers, Tumor / blood. Penile Neoplasms / secondary. Prostate-Specific Antigen / blood. Prostatic Neoplasms / pathology. Skin Neoplasms / secondary

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  • (PMID = 19284456.001).
  • [ISSN] 1346-8138
  • [Journal-full-title] The Journal of dermatology
  • [ISO-abbreviation] J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
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19. Saeki N, Gu J, Yoshida T, Wu X: Prostate stem cell antigen: a Jekyll and Hyde molecule? Clin Cancer Res; 2010 Jul 15;16(14):3533-8
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  • [Title] Prostate stem cell antigen: a Jekyll and Hyde molecule?
  • Prostate stem cell antigen (PSCA) is a glycosylphosphatidylinositol (GPI)-anchored cell surface protein.
  • Although PSCA is thought to be involved in intracellular signaling, much remains unknown about its physiological function and regulatory mechanism in normal and cancer cells.
  • It is up-regulated in several major cancers including prostate, bladder, and pancreatic cancers.
  • The expression of PSCA is positively correlated with advanced clinical stage and metastasis in prostate cancers and is also associated with malignant progression of premalignant prostate lesions.
  • Therefore, PSCA has been proposed as a biomarker of diagnosis and prognosis, as well as a target of therapy for these cancers.
  • In addition, PSCA has also shown clinical potential in immunotherapy as a prostate-specific antigen, which, when presented by dendritic cells, may elicit strong tumor-specific immunity.
  • In contrast, PSCA is down-regulated in esophageal and gastric cancer and may have a tumor-suppressing function in the gastric epithelium.
  • Recent exciting findings that genetic variations of PSCA conferred increased risks of gastric cancer and bladder cancer have opened up a new avenue of research about the pathological function of PSCA.
  • PSCA seems to be a Jekyll and Hyde molecule that plays differential roles, tumor promoting or suppressing, depending on the cellular context.

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  • [Cites] Protein Sci. 2004 Aug;13(8):2045-58 [15273305.001]
  • [Cites] J Gene Med. 2007 Aug;9(8):715-26 [17595048.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1735-40 [9465086.001]
  • [Cites] Int J Gynecol Pathol. 2005 Jan;24(1):67-72 [15626919.001]
  • [Cites] Clin Cancer Res. 2005 Apr 1;11(7):2591-6 [15814638.001]
  • [Cites] Pancreas. 2005 Aug;31(2):119-25 [16024997.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9495-500 [16230414.001]
  • [Cites] Prostate. 2005 Dec 1;65(4):299-305 [16015594.001]
  • [Cites] BJU Int. 2006 Jun;97(6):1202-7 [16686711.001]
  • [Cites] BJU Int. 2006 Sep;98(3):668-73 [16925770.001]
  • [Cites] Cancer Immunol Immunother. 2006 Dec;55(12):1524-33 [16612599.001]
  • [Cites] Int J Cancer. 2006 Nov 15;119(10):2428-34 [16977630.001]
  • [Cites] Prostate. 2007 May 1;67(6):653-60 [17342746.001]
  • [Cites] Int J Cancer. 2008 Feb 15;122(4):864-70 [17957793.001]
  • [Cites] Prostate. 2008 Feb 1;68(2):139-51 [18044730.001]
  • [Cites] Prostate. 2008 Feb 1;68(2):190-9 [18076024.001]
  • [Cites] Histopathology. 2008 Jan;52(2):167-74 [18184265.001]
  • [Cites] Cancer Res. 2008 Feb 1;68(3):861-9 [18245488.001]
  • [Cites] Lancet. 2008 May 17;371(9625):1710-21 [18486743.001]
  • [Cites] Nat Genet. 2008 Jun;40(6):730-40 [18488030.001]
  • [Cites] Mol Cancer Res. 2008 Jul;6(7):1154-68 [18644980.001]
  • [Cites] Clin Cancer Res. 2008 Nov 15;14(22):7488-96 [19010866.001]
  • [Cites] Nat Rev Cancer. 2008 Dec;8(12):976-90 [19029958.001]
  • [Cites] Protein Eng Des Sel. 2009 Mar;22(3):209-16 [18957406.001]
  • [Cites] ACS Nano. 2009 Mar 24;3(3):502-10 [19243145.001]
  • [Cites] Clin Chem. 2009 Apr;55(4):765-73 [19233911.001]
  • [Cites] Mol Ther. 2009 Jun;17(6):1101-8 [19337234.001]
  • [Cites] Prostate. 2009 Jul 1;69(10):1101-8 [19343734.001]
  • [Cites] Prostate. 2009 Sep 1;69(12):1292-302 [19462463.001]
  • [Cites] Nat Genet. 2009 Sep;41(9):991-5 [19648920.001]
  • [Cites] Nat Rev Cancer. 2009 Dec;9(12):874-85 [19935676.001]
  • [Cites] J Neurosci. 2009 Nov 25;29(47):14847-54 [19940180.001]
  • [Cites] J Surg Oncol. 2010 Feb 1;101(2):145-8 [20039280.001]
  • [Cites] Cancer Treat Rev. 2010 Apr;36(2):131-41 [19954892.001]
  • [Cites] Carcinogenesis. 2010 Apr;31(4):621-4 [20083643.001]
  • [Cites] Int J Cancer. 2010 Nov 1;127(9):2183-9 [20131315.001]
  • [Cites] Mol Imaging. 2007 Mar-Apr;6(2):131-9 [17445507.001]
  • [Cites] J Immunother. 2007 May-Jun;30(4):396-405 [17457214.001]
  • [Cites] Leukemia. 2007 May;21(5):868-76 [17361230.001]
  • [Cites] Genes Chromosomes Cancer. 2000 Jan;27(1):95-103 [10564591.001]
  • [Cites] Oncogene. 2000 Mar 2;19(10):1288-96 [10713670.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Sep 7;275(3):783-8 [10973799.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Feb 27;98(5):2658-63 [11226295.001]
  • [Cites] Cancer Lett. 2001 Jul 10;168(1):37-43 [11368875.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4320-4 [11389052.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4660-5 [11406532.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):401-6 [11752398.001]
  • [Cites] Cell Mol Life Sci. 2001 Dec;58(14):1969-87 [11814051.001]
  • [Cites] Clin Cancer Res. 2002 Jun;8(6):1794-9 [12060619.001]
  • [Cites] Mol Endocrinol. 2002 Oct;16(10):2323-37 [12351697.001]
  • [Cites] Mol Cancer Res. 2002 Dec;1(2):113-21 [12496358.001]
  • [Cites] Int J Cancer. 2003 Mar 1;103(6):768-74 [12516096.001]
  • [Cites] J Urol. 2003 Jun;169(6):2094-100 [12771726.001]
  • [Cites] Anticancer Res. 2003 May-Jun;23(3B):2711-6 [12894563.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2003 Sep;11(3):238-43 [12966350.001]
  • [Cites] Nat Rev Cancer. 2003 Oct;3(10):756-67 [14570040.001]
  • [Cites] J Urol. 2004 Mar;171(3):1117-21 [14767283.001]
  • [Cites] Prostate. 2007 Jul 1;67(10):1121-31 [17492652.001]
  • [Cites] Oncol Rep. 2007 Jul;18(1):161-6 [17549363.001]
  • [Cites] Prostate. 2007 Aug 1;67(11):1143-51 [17503471.001]
  • [Cites] Arch Immunol Ther Exp (Warsz). 2004 Jul-Aug;52(4):255-66 [15467490.001]
  • (PMID = 20501618.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA091846; United States / NCI NIH HHS / CA / R01 CA074880; United States / NCI NIH HHS / CA / U01 CA127615; United States / NCI NIH HHS / CA / CA127615-02; United States / NCI NIH HHS / CA / R01CA74880; United States / NCI NIH HHS / CA / R01 CA131335; United States / NCI NIH HHS / CA / P50CA91846; United States / NCI NIH HHS / CA / R01 CA131335-02; United States / NCI NIH HHS / CA / R01 CA074880-10; United States / NCI NIH HHS / CA / CA091846-090007; United States / NCI NIH HHS / CA / U01 CA127615-02; United States / NCI NIH HHS / CA / R01CA131335; United States / NCI NIH HHS / CA / P50 CA091846-090007; United States / NCI NIH HHS / CA / U01CA127615; United States / NCI NIH HHS / CA / CA074880-10; United States / NCI NIH HHS / CA / R01 CA111922; United States / NCI NIH HHS / CA / CA131335-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Neoplasm Proteins; 0 / PSCA protein, human
  • [Other-IDs] NLM/ NIHMS204237; NLM/ PMC2905486
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20. Messiou C, Cook G, deSouza NM: Imaging metastatic bone disease from carcinoma of the prostate. Br J Cancer; 2009 Oct 20;101(8):1225-32
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  • [Title] Imaging metastatic bone disease from carcinoma of the prostate.
  • Imaging bone metastases from prostate cancer presents several challenges.
  • Bone scintigraphy is the mainstay of lesion detection, but is often not suitable for assessment of treatment response, particularly because of a 'flare' phenomenon after therapy.
  • This article reviews the available imaging modalities for evaluating prostatic bony metastases, and links them to the underlying pathological changes within bone lesions.
  • [MeSH-major] Bone Neoplasms / diagnosis. Bone Neoplasms / secondary. Prostatic Neoplasms / pathology

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  • [Cites] Eur J Nucl Med Mol Imaging. 2008 Oct;35(10):1766-74 [18465129.001]
  • [Cites] Nucl Med Biol. 2008 Aug;35(6):689-95 [18678354.001]
  • [Cites] Eur J Cancer. 2009 Jan;45(2):228-47 [19097774.001]
  • [Cites] Radiology. 2008 Dec;249(3):1017-25 [18849502.001]
  • [Cites] Cancer. 2002 Sep 1;95(5):1028-36 [12209687.001]
  • [Cites] Cancer. 2003 Feb 1;97(3 Suppl):739-47 [12548571.001]
  • [Cites] Cancer. 2003 Feb 1;97(3 Suppl):758-71 [12548573.001]
  • [Cites] Br J Cancer. 2003 Jan 27;88(2):195-201 [12610502.001]
  • [Cites] Acta Radiol. 2004 Feb;45(1):71-4 [15164782.001]
  • [Cites] Radiology. 2004 Aug;232(2):599-605 [15286325.001]
  • [Cites] Lancet Oncol. 2004 Oct;5(10):607-16 [15465464.001]
  • [Cites] Radiology. 1983 Feb;146(2):513-8 [6294738.001]
  • [Cites] Cancer. 1983 Aug 15;52(4):610-4 [6861098.001]
  • [Cites] AJR Am J Roentgenol. 1984 Apr;142(4):773-6 [6230903.001]
  • [Cites] Radiographics. 1991 Mar;11(2):219-32 [2028061.001]
  • [Cites] Mayo Clin Proc. 1994 Jan;69(1):69-79 [7505870.001]
  • [Cites] Radiology. 1996 Jun;199(3):751-6 [8638000.001]
  • [Cites] Cancer. 1996 Oct 1;78(7):1388-94 [8839543.001]
  • [Cites] Invest Radiol. 1997 Jun;32(6):344-50 [9179709.001]
  • [Cites] J Nucl Med. 1998 Jun;39(6):990-5 [9627331.001]
  • [Cites] Clin Cancer Res. 1998 Jul;4(7):1765-72 [9676853.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):948-57 [10071289.001]
  • [Cites] Semin Nucl Med. 2005 Apr;35(2):135-42 [15765376.001]
  • [Cites] Endocrinology. 2005 Apr;146(4):1727-36 [15637291.001]
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3210-6 [15867215.001]
  • [Cites] Prostate. 2005 Oct 1;65(2):178-87 [15948151.001]
  • [Cites] Semin Nucl Med. 2006 Jan;36(1):73-92 [16356797.001]
  • [Cites] J Nucl Med. 2006 Feb;47(2):287-97 [16455635.001]
  • [Cites] Cancer Imaging. 2006;6:135-43 [17015238.001]
  • [Cites] Radiology. 2007 Apr;243(1):204-11 [17392254.001]
  • [Cites] Acta Radiol. 2000 Mar;41(2):178-82 [10741794.001]
  • [Cites] Hum Pathol. 2000 May;31(5):578-83 [10836297.001]
  • [Cites] Cancer. 2000 Jun 15;88(12 Suppl):2989-94 [10898342.001]
  • [Cites] Eur J Nucl Med. 2000 Sep;27(9):1415-9 [11007527.001]
  • [Cites] AJR Am J Roentgenol. 2001 Jun;176(6):1525-30 [11373226.001]
  • [Cites] J Nucl Med. 2002 Feb;43(2):181-6 [11850482.001]
  • [Cites] Urology. 2002 Jun;59(6):913-8 [12031380.001]
  • [Cites] J Clin Oncol. 2007 Aug 1;25(22):3281-7 [17664475.001]
  • [Cites] J Nucl Med. 2008 Dec;49(12):2031-41 [18997047.001]
  • (PMID = 19789531.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
  • [Number-of-references] 39
  • [Other-IDs] NLM/ PMC2768452
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21. Lattouf JB, Saad F: Preservation of bone health in prostate cancer. Curr Opin Support Palliat Care; 2007 Oct;1(3):192-7
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  • [Title] Preservation of bone health in prostate cancer.
  • PURPOSE OF REVIEW: Bone is the most common site of metastasis in prostate cancer.
  • The burden of disease from bone metastasis has repercussions in terms of cost to society, decreased quality of life, and decreased survival.
  • Given the magnitude of bone-related morbidity in advanced prostate cancer, physicians need to be aware of preventive and therapeutic measures, and to be proactive in implementing them.
  • RECENT FINDINGS: Patients with prostate cancer are often osteopenic at baseline.
  • Bisphosphonates reduce androgen-deprivation therapy-related bone loss in prostate cancer patients.
  • Zoledronic acid is the only bisphosphonate proven to decrease skeletal-related events in a randomized controlled trial in patients with metastatic prostate cancer.
  • SUMMARY: Bone mineral density loss and skeletal complications are directly related to androgen-deprivation therapy and metastases in prostate cancer patients.
  • [MeSH-major] Androgen Antagonists / adverse effects. Bone Density / drug effects. Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Palliative Care / methods. Prostatic Neoplasms / pathology



22. Suzuki H, Kamiya N, Yano M, Endo T, Takano M, Kawamura K, Imamoto T, Ichikawa T: [Bone and Men's Health. Bisphosphonate therapy for prostate cancer]. Clin Calcium; 2010 Feb;20(2):258-66
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  • [Title] [Bone and Men's Health. Bisphosphonate therapy for prostate cancer].
  • Recently, prostate cancer is one of the common cancer in Japanese men, with a high incidence of bone metastasis.
  • Bone metastasis is incurable and contributes significantly to disease-specific morbidity and mortality.
  • And more, there are many opportunity to perform androgen deprivation therapy in prostate cancer patients, but worsen osteoporosis and raise a risk of bone fracture.
  • The bisphosphonates are targeted to osteoclasts and are considered to be standard management in the care of bone metastasis patients in combination with chemotherapy and hormone therapy.
  • In this review, we summarized the current understanding and therapy of bone metastasis in prostate cancer in mainly respect to Zoredronic acid use.
  • [MeSH-major] Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Prostatic Neoplasms / drug therapy

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  • (PMID = 20118519.001).
  • [ISSN] 0917-5857
  • [Journal-full-title] Clinical calcium
  • [ISO-abbreviation] Clin Calcium
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
  • [Number-of-references] 22
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23. Dimitroff CJ, Descheny L, Trujillo N, Kim R, Nguyen V, Huang W, Pienta KJ, Kutok JL, Rubin MA: Identification of leukocyte E-selectin ligands, P-selectin glycoprotein ligand-1 and E-selectin ligand-1, on human metastatic prostate tumor cells. Cancer Res; 2005 Jul 1;65(13):5750-60
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  • [Title] Identification of leukocyte E-selectin ligands, P-selectin glycoprotein ligand-1 and E-selectin ligand-1, on human metastatic prostate tumor cells.
  • Prostate tumor cells, which characteristically metastasize to bone, initiate binding interactions with bone marrow endothelium under blood flow conditions through binding interactions with E-selectin.
  • We hypothesized that E-selectin ligands on prostate tumor cells are directly associated with bone-metastatic potential.
  • In this report, we elucidate the identity of E-selectin ligands on human metastatic prostate tumor cells and examine their association with prostate tumor progression and metastasis in vivo.
  • To our surprise, we found that the E-selectin-binding form of P-selectin glycoprotein ligand-1 (PSGL-1) is expressed on the human bone-metastatic prostate tumor MDA PCa 2b cell line.
  • Interestingly, we also found that human prostate tumor cells derived from bone, lymph node, and brain metastases expressed another leukocyte E-selectin ligand, E-selectin ligand-1 (ESL-1).
  • Immunohistochemical analysis of PSGL-1 and ESL-1 in normal prostate tissue and in localized and metastatic prostate tumors revealed that ESL-1 was principally localized to intracellular cell membrane and expressed on all normal and malignant prostate tissue, whereas PSGL-1 was notably detected on the surfaces of bone-metastatic prostate tumor cells.
  • These findings implicate a functional role of PSGL-1 in the bone tropism of prostate tumor cells and establish a new perspective into the molecular mechanism of human prostate tumor metastasis.

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  • [Cites] Cancer Res. 2004 Dec 15;64(24):9209-16 [15604294.001]
  • [Cites] Int J Cancer. 2004 Aug 10;111(1):152-9 [15185357.001]
  • [Cites] J Cell Biol. 2001 Jun 11;153(6):1277-86 [11402070.001]
  • [Cites] Am J Pathol. 2001 Sep;159(3):837-43 [11549576.001]
  • [Cites] Cancer Res. 2002 Mar 15;62(6):1832-7 [11912162.001]
  • [Cites] JAMA. 2002 Apr 3;287(13):1662-70 [11926890.001]
  • [Cites] J Immunol. 2002 Jun 1;168(11):5645-51 [12023362.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):563-72 [12154349.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):584-93 [12154351.001]
  • [Cites] J Clin Invest. 2002 Aug;110(4):559-69 [12189250.001]
  • [Cites] Blood. 2003 Jan 15;101(2):602-10 [12393521.001]
  • [Cites] Clin Cancer Res. 2000 Mar;6(3):1038-45 [10741732.001]
  • [Cites] Hum Pathol. 2000 May;31(5):578-83 [10836297.001]
  • [Cites] Eur J Clin Invest. 2000 Jul;30(7):618-29 [10886302.001]
  • [Cites] N Engl J Med. 2000 Oct 5;343(14):1020-34 [11018170.001]
  • [Cites] Neoplasia. 2004 Jul-Aug;6(4):302-9 [15256052.001]
  • [Cites] FASEB J. 2004 Aug;18(11):1240-2 [15180966.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5261-9 [15289332.001]
  • [Cites] Cancer Res. 2004 Aug 15;64(16):5702-11 [15313910.001]
  • [Cites] Cancer Res. 1984 Aug;44(8):3522-9 [6744277.001]
  • [Cites] J Biol Chem. 1989 Jan 5;264(1):646-53 [2909545.001]
  • [Cites] Cell. 1991 Sep 6;66(5):921-33 [1716182.001]
  • [Cites] J Cell Biol. 1993 Apr;121(2):449-59 [7682218.001]
  • [Cites] Exp Cell Res. 1995 Aug;219(2):562-70 [7543854.001]
  • [Cites] Am J Pathol. 1996 Jan;148(1):165-75 [8546203.001]
  • [Cites] Blood. 1996 Oct 15;88(8):3010-21 [8874199.001]
  • [Cites] J Biol Chem. 1996 Dec 20;271(51):33002-8 [8955145.001]
  • [Cites] DNA Cell Biol. 1996 Dec;15(12):1121-8 [8985126.001]
  • [Cites] J Cell Sci. 1997 Mar;110 ( Pt 6):687-94 [9099943.001]
  • [Cites] Nature. 1997 Oct 30;389(6654):978-81 [9353122.001]
  • [Cites] J Natl Cancer Inst. 1998 Jan 21;90(2):118-23 [9450571.001]
  • [Cites] Clin Cancer Res. 1996 Sep;2(9):1627-36 [9816342.001]
  • [Cites] Cancer Res. 1999 Jan 1;59(1):241-8 [9892213.001]
  • [Cites] Clin Cancer Res. 1997 Dec;3(12 Pt 1):2493-500 [9815652.001]
  • [Cites] Science. 1999 Feb 5;283(5403):845-8 [9933168.001]
  • [Cites] J Clin Pathol. 1998 Nov;51(11):798-802 [10193318.001]
  • [Cites] Cancer Metastasis Rev. 1998-1999;17(4):331-6 [10453276.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3091-6 [15280192.001]
  • [Cites] Cancer. 2003 Feb 1;97(3 Suppl):739-47 [12548571.001]
  • [Cites] J Bone Miner Res. 2003 Feb;18(2):190-4 [12568395.001]
  • [Cites] Urology. 2003 Feb;61(2):277-81 [12597930.001]
  • [Cites] Int J Oncol. 2003 May;22(5):1045-9 [12684670.001]
  • [Cites] J Cell Biochem. 2003 Jun 1;89(3):462-73 [12761880.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2060-7 [12763924.001]
  • [Cites] J Clin Invest. 2003 Oct;112(7):1008-18 [14523038.001]
  • [Cites] J Cell Biochem. 2004 Mar 1;91(4):706-17 [14991762.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):2083-9 [15026347.001]
  • [Cites] Prostate. 2004 May 1;59(2):157-66 [15042616.001]
  • [Cites] Blood. 2004 Apr 15;103(8):2981-9 [15070674.001]
  • [Cites] Blood. 2001 May 15;97(10):3283-91 [11342460.001]
  • (PMID = 15994950.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 1R21 CA102913-02; United States / NCI NIH HHS / CA / CA69568; United States / NIAMS NIH HHS / AR / P30 AR042689; United States / NCI NIH HHS / CA / R21 CA104828; United States / NCI NIH HHS / CA / 1R21 CA104828-01; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / CA06516-37; United States / NCI NIH HHS / CA / P30 CA006516; United States / NIAMS NIH HHS / AR / 5P30 AR042689; United States / NCI NIH HHS / CA / R21 CA102913
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / E-Selectin; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / P-selectin ligand protein; 0 / Receptors, Fibroblast Growth Factor; 0 / Sialoglycoproteins; 0 / cysteine-rich fibroblast growth factor receptor
  • [Other-IDs] NLM/ NIHMS2052; NLM/ PMC1472661
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24. Podgorski I, Linebaugh BE, Sloane BF: Cathepsin K in the bone microenvironment: link between obesity and prostate cancer? Biochem Soc Trans; 2007 Aug;35(Pt 4):701-3
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  • [Title] Cathepsin K in the bone microenvironment: link between obesity and prostate cancer?
  • The skeleton is the most common site of metastasis in patients with advanced prostate cancer.
  • Despite many advances in targeting skeletal metastases, the mechanisms behind the attraction of prostate cancer cells to the bone are not known.
  • Osteoclast cathepsin K, due to its ability to effectively degrade bone matrix collagen I, has been implicated in colonization and growth of prostate tumours in the bone.
  • Identification of new cathepsin K substrates in the bone microenvironment and the recent findings demonstrating its involvement in obesity and inflammation suggest additional roles for this enzyme in skeletal metastases of prostate cancer.
  • [MeSH-minor] Bone Neoplasms / pathology. Bone Neoplasms / secondary. Cathepsin K. Cell Movement / physiology. Humans. Male



25. Russell MR, Jamieson WL, Dolloff NG, Fatatis A: The alpha-receptor for platelet-derived growth factor as a target for antibody-mediated inhibition of skeletal metastases from prostate cancer cells. Oncogene; 2009 Jan 22;28(3):412-21
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  • [Title] The alpha-receptor for platelet-derived growth factor as a target for antibody-mediated inhibition of skeletal metastases from prostate cancer cells.
  • Bone resorption by osteoclasts is thought to promote the proliferation of prostate cancer cells disseminated to the skeleton (Mundy, 2002).
  • Using a mouse model of experimental metastasis, we found that although late-stage metastatic tumors were indeed surrounded by osteoclasts, these cells were spatially unrelated to the small foci of cancer cells in early-stage metastases.
  • This is the first evidence that survival and growth of disseminated prostate cancer cells immediately after their extravasation may not depend on osteoclast involvement.
  • Interestingly, prostate cancer cells expressing the alpha-receptor for platelet-derived growth factor (PDGFRalpha) progress during early-stages of skeletal dissemination, whereas cells expressing lower levels or lacking this receptor fail to survive after extravasation in the bone marrow.
  • However, non-metastatic cells acquire bone-metastatic potential upon ectopic overexpression of PDGFRalpha.
  • Finally, functional blockade of human PDGFRalpha on prostate cancer cells utilizing a novel humanized monoclonal antibody -- soon to undergo phase-II clinical trials -- significantly impairs the establishment of early skeletal metastases.
  • In conclusion, our results strongly implicate PDGFRalpha in prostate cancer bone tropism through its promotion of survival and progression of early-metastatic foci, providing ground for therapeutic strategies aimed at preventing or containing the initial progression of skeletal metastases in patients affected by prostate adenocarcinoma.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Bone Neoplasms / prevention & control. Bone Neoplasms / secondary. Prostatic Neoplasms / pathology. Receptor, Platelet-Derived Growth Factor alpha / antagonists & inhibitors
  • [MeSH-minor] Adolescent. Adult. Animals. Blotting, Western. Bone Marrow / metabolism. Bone Marrow / pathology. Bone and Bones / metabolism. Bone and Bones / pathology. Flow Cytometry. Humans. Immunoenzyme Techniques. Male. Mice. Mice, SCID. Middle Aged. Phosphorylation. Tumor Cells, Cultured. Young Adult

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  • (PMID = 18850002.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM067892
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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26. Hövels AM, Heesakkers RA, Adang EM, Jager GJ, Strum S, Hoogeveen YL, Severens JL, Barentsz JO: The diagnostic accuracy of CT and MRI in the staging of pelvic lymph nodes in patients with prostate cancer: a meta-analysis. Clin Radiol; 2008 Apr;63(4):387-95
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  • [Title] The diagnostic accuracy of CT and MRI in the staging of pelvic lymph nodes in patients with prostate cancer: a meta-analysis.
  • AIM: To compare the diagnostic accuracy of computed tomography (CT) and magnetic resonance imaging (MRI) in the diagnosis of lymph node metastases in prostate cancer.
  • METHODS: After a comprehensive literature search, studies were included that allowed construction of contingency tables for detection of lymph node metastases using CT or MRI.
  • CONCLUSION: CT and MRI demonstrate an equally poor performance in the detection of lymph node metastases from prostate cancer.
  • Reliance on either CT or MRI will misrepresent the patient's true status regarding nodal metastases, and thus misdirect the therapeutic strategies offered to the patient.
  • [MeSH-major] Magnetic Resonance Imaging / standards. Pelvic Neoplasms / diagnosis. Prostatic Neoplasms / pathology. Tomography, X-Ray Computed / standards
  • [MeSH-minor] Humans. Lymph Nodes. Lymphatic Metastasis. Male. Neoplasm Staging. ROC Curve. Sensitivity and Specificity



27. Divoli A, Bloch G, Chittenden S, Malaroda A, O'Sullivan JM, Dearnaley DP, Flux GD: Tumor dosimetry on SPECT (186)Re-HEDP scans: variations in the results from the reconstruction methods used. Cancer Biother Radiopharm; 2007 Feb;22(1):121-4
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  • [Title] Tumor dosimetry on SPECT (186)Re-HEDP scans: variations in the results from the reconstruction methods used.
  • The aim of this work was to estimate tumor-absorbed doses delivered from the administration of fixed activities of (186)Re-HEDP for the treatment of bone metastases from prostate cancer.
  • We concluded that the administration of fixed activity resulted in a range of absorbed doses, and we showed that, despite using the same approach, the choice of the reconstruction algorithm can result in differences higher than 50% in the estimated tumor-absorbed doses.

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  • (PMID = 17627420.001).
  • [ISSN] 1084-9785
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501019; United States / NCI NIH HHS / CA / 1 R21 CA86784-01A1
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radioisotopes; 7440-15-5 / Rhenium; M2F465ROXU / Etidronic Acid
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28. Zafeirakis A: Collagenous and non-collagenous biochemical markers of bone metastases from prostate cancer. Hippokratia; 2010 Jul;14(3):164-9
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  • [Title] Collagenous and non-collagenous biochemical markers of bone metastases from prostate cancer.
  • The importance of the bone microenvironment to the pathophysiology and morbidity associated with prostate cancer bone metastasis is becoming increasingly apparent.
  • This review will discuss the diagnostic and predictive implications of various collagenous and non-collagenous bone markers, along with the novel markers of osteoclastogenesis and other matrix enzymes such as metalloproteinases and growth factors responsible for the complex biochemical mechanisms that upregulate bone resorption/formation during the development of metastasis.
  • Further prospective studies are needed to determine whether any of these markers measured longitudinally in prostate cancer patients without bone scan evidence of skeletal disease will ultimately predict those patients who will develop bone metastases from their malignancy.

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  • (PMID = 20981164.001).
  • [ISSN] 1790-8019
  • [Journal-full-title] Hippokratia
  • [ISO-abbreviation] Hippokratia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Other-IDs] NLM/ PMC2943353
  • [Keywords] NOTNLM ; Prostate cancer / RANKL / bone metastases / bone turnover markers / osteoprotegerin / review / type I collagen
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29. Polascik TJ: Bisphosphonates in oncology: evidence for the prevention of skeletal events in patients with bone metastases. Drug Des Devel Ther; 2009 Sep 21;3:27-40
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  • [Title] Bisphosphonates in oncology: evidence for the prevention of skeletal events in patients with bone metastases.
  • Bone metastases frequently occur in patients with advanced solid tumors, particularly breast and prostate cancers, and nearly all patients with multiple myeloma have some degree of skeletal involvement.
  • The results of a large, randomized phase 3 study comparing zoledronic acid and pamidronate in breast cancer or multiple myeloma patients with osteolytic lesions showed that the incidence of SREs, time to first SRE, and risk of developing a SRE were similar between treatment groups.
  • However, in patients with solid tumors (excluding breast or prostate cancer) metastatic to the bone, only zoledronic acid has demonstrated clinical efficacy.

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  • [Cites] Cancer Treat Rev. 2008 Nov;34(7):629-39 [18579314.001]
  • [Cites] Cancer. 2000 Mar 1;88(5):1082-90 [10699899.001]
  • [Cites] Ann Oncol. 2008 Mar;19(3):420-32 [17906299.001]
  • [Cites] N Engl J Med. 2007 Nov 1;357(18):1799-809 [17878149.001]
  • [Cites] J Clin Oncol. 2007 Jun 10;25(17):2464-72 [17515569.001]
  • [Cites] N Engl J Med. 2007 May 3;356(18):1809-22 [17476007.001]
  • [Cites] Pediatrics. 2007 Mar;119 Suppl 2:S150-62 [17332236.001]
  • [Cites] Cancer Biol Ther. 2006 Sep;5(9):1074-7 [16969118.001]
  • [Cites] Cochrane Database Syst Rev. 2006;(4):CD006250 [17054286.001]
  • [Cites] Clin Cancer Res. 2006 Oct 15;12(20 Pt 2):6243s-6249s [17062708.001]
  • [Cites] Clin Cancer Res. 2006 Oct 15;12(20 Pt 2):6222s-6230s [17062705.001]
  • [Cites] Clin Cancer Res. 2006 Oct 15;12(20 Pt 2):6213s-6216s [17062703.001]
  • [Cites] Oncologist. 2006 Jul-Aug;11(7):841-8 [16880243.001]
  • [Cites] Lancet. 2006 Jun 17;367(9527):2010-8 [16782492.001]
  • [Cites] Clin Ther. 2006 Feb;28(2):151-73 [16678639.001]
  • [Cites] Oncologist. 2006 Mar;11(3):227-33 [16549806.001]
  • [Cites] Cochrane Database Syst Rev. 2005;(3):CD003474 [16034900.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3314-21 [15738536.001]
  • [Cites] Oncology. 2004;67(5-6):390-6 [15713995.001]
  • [Cites] J Natl Cancer Inst. 2005 Jan 5;97(1):59-69 [15632381.001]
  • [Cites] J Intern Med. 1999 Jul;246(1):67-74 [10447227.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):846-54 [10071275.001]
  • [Cites] Eur J Cancer. 1998 Dec;34(13):2021-6 [10070304.001]
  • [Cites] J Exp Clin Cancer Res. 1998 Jun;17(2):213-7 [9700583.001]
  • [Cites] J Clin Oncol. 1998 Jun;16(6):2038-44 [9626201.001]
  • [Cites] Br J Haematol. 1998 Feb;100(2):317-25 [9488619.001]
  • [Cites] J Clin Oncol. 1998 Feb;16(2):593-602 [9469347.001]
  • [Cites] Cancer. 1997 Oct 15;80(8 Suppl):1546-56 [9362421.001]
  • [Cites] N Engl J Med. 1996 Dec 12;335(24):1785-91 [8965890.001]
  • [Cites] N Engl J Med. 1996 Feb 22;334(8):488-93 [8559201.001]
  • [Cites] J Clin Oncol. 1993 Jan;11(1):59-65 [8418243.001]
  • [Cites] Oncologist. 2004;9 Suppl 4:14-27 [15459426.001]
  • [Cites] Cancer. 2004 Jun 15;100(12):2613-21 [15197804.001]
  • [Cites] J Natl Cancer Inst. 2004 Jun 2;96(11):879-82 [15173273.001]
  • [Cites] Br J Cancer. 2004 Mar 22;90(6):1133-7 [15026791.001]
  • [Cites] Cancer. 2004 Jan 1;100(1):36-43 [14692022.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4277-84 [14581438.001]
  • [Cites] J Clin Oncol. 2003 Nov 1;21(21):4042-57 [12963702.001]
  • [Cites] Cancer. 2003 Oct 15;98(8):1735-44 [14534891.001]
  • [Cites] J Natl Cancer Inst. 2003 Sep 3;95(17):1300-11 [12953084.001]
  • [Cites] Ann Oncol. 2003 Sep;14(9):1399-405 [12954579.001]
  • [Cites] J Clin Oncol. 2003 Aug 15;21(16):3150-7 [12915606.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1404-11 [12663734.001]
  • [Cites] J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68 [12359855.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2353-9 [11981007.001]
  • [Cites] Cancer J. 2001 Sep-Oct;7(5):377-87 [11693896.001]
  • [Cites] Br J Haematol. 2001 Jun;113(4):1035-43 [11442499.001]
  • [Cites] J Clin Oncol. 2001 Jan 15;19(2):558-67 [11208851.001]
  • [Cites] Support Cancer Ther. 2007 Jan 1;4(2):92-100 [18632473.001]
  • (PMID = 19920919.001).
  • [ISSN] 1177-8881
  • [Journal-full-title] Drug design, development and therapy
  • [ISO-abbreviation] Drug Des Devel Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2769231
  • [Keywords] NOTNLM ; bisphosphonates / bone metastases / cancer / prevention / skeletal-related events
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30. Gálvez R, Ribera V, González-Escalada JR, Souto A, Cánovas ML, Castro A, Herrero B, de Los Angeles Maqueda M, Castilforte M, Marco-Martínez JJ, Pérez C, Vicente-Fatela L, Md CN, Orduña MJ, Padrol A, Reig E, Carballido J, Cózar JM: Analgesic efficacy of zoledronic acid and its effect on functional status of prostate cancer patients with metastasis. Patient Prefer Adherence; 2008;2:215-24
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  • [Title] Analgesic efficacy of zoledronic acid and its effect on functional status of prostate cancer patients with metastasis.
  • OBJECTIVES: A multi-centered observational study evaluated the efficacy of zoledronic acid for improving pain and mobility, and preventing skeletal-related events (SRE) (fracture, spinal compression, pain-relieving radiotherapy), in patients with prostate cancer and bone metastasis.
  • MATERIALS AND METHODS: Males (n = 218) with prostate cancer and bone metastasis undergoing oncologic therapy received zoledronic acid (4 mg iv/month) for 6 months.
  • Of the 212 patients (97.2%) evaluable for safety, 16% suffered adverse events and 66% expressed satisfaction with the treatment DISCUSSION: Zoledronic acid is effective for reducing pain, improving mobility, and increasing the quality of life in patients with prostate cancer with bone metastasis.
  • Its easy administration and good tolerability make zoledronic acid one of the principal therapeutic tools in the management of patients with pain associated with bone metastasis from prostate cancer.

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  • [Cites] Br J Cancer. 2000 Feb;82(4):858-64 [10732759.001]
  • [Cites] Cancer. 2000 Jan 1;88(1):6-14 [10618600.001]
  • [Cites] Cancer Res. 2000 Jun 1;60(11):2949-54 [10850442.001]
  • [Cites] Cancer. 2000 Jun 15;88(12 Suppl):3015-21 [10898346.001]
  • [Cites] Cancer. 2000 Jun 15;88(12 Suppl):3047-53 [10898350.001]
  • [Cites] Breast Cancer. 2000;7(4):361-9 [11114866.001]
  • [Cites] Cancer Treat Rev. 2001 Jun;27(3):165-76 [11417967.001]
  • [Cites] N Engl J Med. 2001 Sep 27;345(13):948-55 [11575286.001]
  • [Cites] J Urol. 2001 Dec;166(6):2023-31 [11696699.001]
  • [Cites] J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68 [12359855.001]
  • [Cites] Cancer. 2003 Feb 1;97(3 Suppl):758-71 [12548573.001]
  • [Cites] J Natl Cancer Inst. 2004 Jun 2;96(11):879-82 [15173273.001]
  • [Cites] Lancet Oncol. 2004 Oct;5(10):607-16 [15465464.001]
  • [Cites] Oncologist. 2005 Jan;10(1):52-62 [15632252.001]
  • [Cites] Oncology (Williston Park). 1992 Oct;6(10):37-43; discussion 43, 47-50 [1390013.001]
  • [Cites] Oncology (Williston Park). 1991 Aug;5(8):55-60; discussion 60-2, 65 [1834153.001]
  • [Cites] Br J Urol. 1991 Jul;68(1):74-80 [1873694.001]
  • [Cites] Cancer. 1993 Dec 1;72(11 Suppl):3443-52 [8242577.001]
  • [Cites] Cancer. 1993 Feb 1;71(3 Suppl):1131-7 [8428335.001]
  • [Cites] Drug Saf. 1996 Mar;14(3):158-70 [8934578.001]
  • [Cites] Hosp J. 1996;11(2):1-10 [8949010.001]
  • [Cites] J Urol. 1997 Feb;157(2):439-44 [8996327.001]
  • [Cites] Cancer. 1997 Feb 1;79(3):545-50 [9028366.001]
  • [Cites] Semin Urol Oncol. 1997 Feb;15(1):28-32 [9050137.001]
  • [Cites] Cancer. 1997 Oct 15;80(8 Suppl):1652-60 [9362432.001]
  • [Cites] Drug Saf. 1999 Nov;21(5):389-406 [10554053.001]
  • [Cites] Leukemia. 2000 May;14(5):841-4 [10803515.001]
  • (PMID = 19920966.001).
  • [ISSN] 1177-889X
  • [Journal-full-title] Patient preference and adherence
  • [ISO-abbreviation] Patient Prefer Adherence
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2770417
  • [Keywords] NOTNLM ; bone metastasis / pain / prostate cancer / zoledronic acid
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31. Cone LA, Koochek K, Henager HA, Fausel R, Gade-Andavolu R, Potts BE, Jennings LM: Leptomeningeal carcinomatosis in a patient with metastatic prostate cancer: case report and literature review. Surg Neurol; 2006 Apr;65(4):372-5, discussion 375-6
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  • [Title] Leptomeningeal carcinomatosis in a patient with metastatic prostate cancer: case report and literature review.
  • BACKGROUND: Leptomeningeal metastasis is discovered at autopsy in approximately 5% of patients with systemic cancer.
  • Until recently with the introduction of magnetic resonance imaging (MRI), premorbid diagnosis was extremely difficult.
  • Leptomeningeal metastasis in metastatic prostate cancer has been reported in only 14 patients previously.
  • CASE DESCRIPTION: We recently studied such a patient and were able to establish a correct diagnosis based solely on the MRI and the presence of an elevated cerebrospinal fluid (CSF) prostate-specific antigen (PSA).
  • Only 3 previous patients with leptomeningeal prostate metastasis have undergone CSF PSA evaluations.
  • [MeSH-major] Arachnoid / pathology. Carcinoma / secondary. Meningeal Neoplasms / secondary. Pia Mater / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Anti-Inflammatory Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / secondary. Consciousness Disorders / etiology. Diagnostic Errors / prevention & control. Early Diagnosis. Fatal Outcome. Headache / etiology. Humans. Lymph Nodes / pathology. Magnetic Resonance Imaging. Male. Neoplasm Metastasis / drug therapy. Neoplasm Metastasis / pathology. Neoplasm Metastasis / physiopathology. Prostate-Specific Antigen / blood. Prostate-Specific Antigen / cerebrospinal fluid. Tomography, X-Ray Computed. Treatment Failure



32. Lecouvet FE, Simon M, Tombal B, Jamart J, Vande Berg BC, Simoni P: Whole-body MRI (WB-MRI) versus axial skeleton MRI (AS-MRI) to detect and measure bone metastases in prostate cancer (PCa). Eur Radiol; 2010 Dec;20(12):2973-82
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  • [Title] Whole-body MRI (WB-MRI) versus axial skeleton MRI (AS-MRI) to detect and measure bone metastases in prostate cancer (PCa).
  • OBJECTIVE: To compare whole-body MRI (WB-MRI) and axial skeleton MRI (AS-MRI) in detecting and measuring bone metastases in patients with prostate cancer (PCa).
  • METHODS: WB-MRI and AS-MRI examinations were performed in 60 patients with PCa at high risk of metastases.
  • Two radiologists separately categorised the AS-MRI and WB-MRI as negative or positive for metastases, and measured focal metastases using the "Response evaluation criteria in solid tumours" (RECIST) criteria transposed to bone.
  • Inter- and intraobserver agreements in establishing the presence/absence of metastases were calculated.
  • RESULTS: Strong to perfect inter- and intraobserver agreements were found between AS-MRI and WB-MRI in defining the presence/absence of bone metastases.
  • There were no patients with isolated "peripheral" metastases at WB-MRI, missed at AS-MRI.
  • CONCLUSIONS: In our series of PCa patients, AS-MRI and WB-MRI were equivalent in determining the presence/absence of bone metastases and provided similar evaluation of the metastatic burden.
  • [MeSH-major] Bone Neoplasms / diagnosis. Bone Neoplasms / secondary. Bone and Bones / pathology. Magnetic Resonance Imaging / methods. Prostatic Neoplasms / diagnosis. Whole Body Imaging / methods



33. English BC, Baum CE, Adelberg DE, Sissung TM, Kluetz PG, Dahut WL, Price DK, Figg WD: A SNP in CYP2C8 is not associated with the development of bisphosphonate-related osteonecrosis of the jaw in men with castrate-resistant prostate cancer. Ther Clin Risk Manag; 2010;6:579-83
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  • [Title] A SNP in CYP2C8 is not associated with the development of bisphosphonate-related osteonecrosis of the jaw in men with castrate-resistant prostate cancer.
  • A single nucleotide polymorphism (SNP) in CYP2C8 (rs1934951), was previously identified in a genome-wide association study as a risk factor for the development of osteonecrosis of the jaw (ONJ) in patients receiving bisphosphonates (BPs) for multiple myeloma.
  • To determine if the same SNP is also associated with the development of ONJ in men receiving BPs for bone metastases from prostate cancer, we genotyped 100 men with castrate-resistant prostate cancer treated with bisphosphonates for bone metastases, 17 of whom developed ONJ.
  • This intronic SNP in CYP2C8 (rs1934951) does not seem to be a risk factor for the development of bisphosphonate-related ONJ in men with prostate cancer.
  • It is important to note that this is only the second study to investigate the genetics associated with BP-related ONJ and the first to do so in men with prostate cancer.

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  • (PMID = 21151627.001).
  • [ISSN] 1178-203X
  • [Journal-full-title] Therapeutics and clinical risk management
  • [ISO-abbreviation] Ther Clin Risk Manag
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2999510
  • [Keywords] NOTNLM ; CYP2C8 / ONJ / bisphosphonates / polymorphism
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34. Rinnab L, Kufer R, Hautmann RE, Gottfried HW: Use of transrectal ultrasound-guided biopsy in the diagnosis of pelvic malignancies. J Clin Ultrasound; 2006 Nov-Dec;34(9):440-5
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  • [Title] Use of transrectal ultrasound-guided biopsy in the diagnosis of pelvic malignancies.
  • METHODS: Eleven patients with clinical suspecion of advanced malignant pelvic tumor were referred to our institution with a history of unsuccessful CT-guided biopsy, although a target lesion was demonstrated on pelvic CT or MRI.
  • In all patients, the harvested material was of excellent quality and was adequate for definitive pathological diagnosis.
  • Pathological results included 6 nodal metastases from transitional cell carcinoma, 1 case of lymph node metastasis from prostate cancer, 1 paravesical recurrence of cervical cancer, 1 metastasis from cecal cancer, and 2 cases of paravesical metastasis of a gastric cancer.
  • CONCLUSION: TRUS-guided biopsy is a useful technique for the diagnosis of pelvic malignancies.
  • It is faster and less expensive than CT-guided biopsy, and in most cases sufficient material can be harvested for a definitive pathological diagnosis.

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  • [Copyright] Copyright 2006 Wiley Periodicals, Inc.
  • (PMID = 17109402.001).
  • [ISSN] 0091-2751
  • [Journal-full-title] Journal of clinical ultrasound : JCU
  • [ISO-abbreviation] J Clin Ultrasound
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Beheshti M, Vali R, Waldenberger P, Fitz F, Nader M, Hammer J, Loidl W, Pirich C, Fogelman I, Langsteger W: The use of F-18 choline PET in the assessment of bone metastases in prostate cancer: correlation with morphological changes on CT. Mol Imaging Biol; 2009 Nov-Dec;11(6):446-54
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  • [Title] The use of F-18 choline PET in the assessment of bone metastases in prostate cancer: correlation with morphological changes on CT.
  • AIM: F-18 fluor choline-positron emission tomography/computed tomography (FCH-PET/CT) has emerged as a new diagnostic tool for the imaging of prostate cancer.
  • In this study, we have evaluated the potential role of FCH-PET/CT for the assessment of bone metastases in patients with prostate cancer.
  • METHODS: Seventy men with biopsy-proven prostate cancer underwent FCH-PET/CT for preoperative staging or follow-up evaluation.
  • PET imaging consisted of a dynamic PET/CT acquisition of the pelvic region during 8 min (1-min frames) starting 1 min after i.v. injection of 4.07 MBq/kg/bw FCH which was followed immediately by a semi whole body acquisition.
  • Two hundred ten lesions (210/262) were interpreted as bone metastases.
  • The mean standardized uptake values (SUV) in all malignant lesions was 8.1 +/- 3.9.
  • Forty-nine lesions (24%) had no detectable morphological changes on CT-probably due to bone marrow metastases.
  • Fifty-six sclerotic lesions (having a Hounsfield unit (HU) level of more than 825) were interpreted as highly suspicious for metastatic bone disease on CT and/or other imaging modalities such as the bone scan but showed no FCH uptake.
  • The sensitivity, specificity, and accuracy of FCH-PET/CT in detecting bone metastases from prostate cancer was 79%, 97%, and 84%, respectively.
  • CONCLUSION: FCH-PET/CT showed promising results for the early detection of bone metastases in prostate cancer patients.
  • [MeSH-major] Bone Neoplasms / diagnostic imaging. Bone Neoplasms / secondary. Fluorine Radioisotopes. Prostatic Neoplasms / diagnostic imaging. Tomography, X-Ray Computed / methods



36. Zhang X, Ling MT, Wang Q, Lau CK, Leung SC, Lee TK, Cheung AL, Wong YC, Wang X: Identification of a novel inhibitor of differentiation-1 (ID-1) binding partner, caveolin-1, and its role in epithelial-mesenchymal transition and resistance to apoptosis in prostate cancer cells. J Biol Chem; 2007 Nov 16;282(46):33284-94
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  • [Title] Identification of a novel inhibitor of differentiation-1 (ID-1) binding partner, caveolin-1, and its role in epithelial-mesenchymal transition and resistance to apoptosis in prostate cancer cells.
  • Recently, ID-1 (inhibitor of differentiation/DNA binding) is suggested as an oncogene and is reported to promote cell proliferation, invasion, and survival in several types of human cancer cells through multiple signaling pathways.
  • In this study, using a yeast two-hybrid screening technique, we identified a novel Id-1-interacting protein, caveolin-1 (Cav-1), a cell membrane protein, and a positive regulator of cell survival and metastasis in prostate cancer.
  • In addition, we also demonstrated that the physical interaction between Id-1 and Cav-1 played a key role in the epithelial-mesenchymal transition and increased cell migration rate as well as resistance to taxol-induced apoptosis in prostate cancer cells.
  • Our study demonstrates a novel Id-1 binding partner and suggests a molecular mechanism that mediates the function of Id-1 in promoting prostate cancer progression through activation of the Akt pathway leading to cancer cell invasion and resistance to anticancer drug-induced apoptosis.
  • [MeSH-minor] Cell Movement. Drug Resistance, Neoplasm. Humans. Male. Molecular Sequence Data. Neoplasm Invasiveness. Paclitaxel / pharmacology. Protein Binding. Two-Hybrid System Techniques



37. Kawashima H, Tanaka T, Kuratsukuri K, Uchida J, Sugimura K, Tamada S, Nishisaka N, Kumata K, Iwai Y, Ikemoto S, Ezaki K, Nakatani T: Palliative treatment of bone metastases in hormone-refractory prostate cancer: effects of pamidronate on the carboxyterminal telopeptide of type-I collagen level in patients with increasing prostate-specific antigen levels. Urol Int; 2007;78(4):345-50
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  • [Title] Palliative treatment of bone metastases in hormone-refractory prostate cancer: effects of pamidronate on the carboxyterminal telopeptide of type-I collagen level in patients with increasing prostate-specific antigen levels.
  • PURPOSE: Bisphosphonates have been reported to be effective in reducing bone pain and skeletal-related events associated with bone metastases in hormone-refractory prostate cancer (HRPC).
  • However, whether bone resorption is reduced primarily by these particular drugs is difficult to evaluate because patients with HRPC are usually treated with secondary or tertiary hormonal manipulations including second-line antiandrogens, high-dose diethylstilbestrol, or low-dose dexamethasone therapies, some of which may also be effective.
  • Thus, we assessed changes in the level of the carboxyterminal telopeptide of type-I collagen (ICTP), a bone resorption marker, before and after pamidronate administration in HRPC patients with increasing prostate-specific antigen (PSA) levels.
  • PATIENTS AND METHODS: Twenty-one HRPC patients with bone metastases and increasing PSA levels were intravenously treated with pamidronate at a dose of 30 mg either every 2 or every 4 weeks.
  • CONCLUSION: In 67% of the HRPC patients with increasing PSA levels, pamidronate reduced the accelerated turnover of bone metabolism caused by metastases of prostate cancer.
  • [MeSH-major] Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / drug therapy. Collagen Type I / drug effects. Diphosphonates / therapeutic use. Prostate-Specific Antigen / blood. Prostatic Neoplasms / drug therapy



38. Sabbota AL, Kim HR, Zhe X, Fridman R, Bonfil RD, Cher ML: Shedding of RANKL by tumor-associated MT1-MMP activates Src-dependent prostate cancer cell migration. Cancer Res; 2010 Jul 1;70(13):5558-66
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  • [Title] Shedding of RANKL by tumor-associated MT1-MMP activates Src-dependent prostate cancer cell migration.
  • We previously found high expression of MT1-MMP in skeletal metastasis of prostate cancer patients, in a pattern similar to RANKL expression.
  • We also showed that overexpression of MT1-MMP in prostate cancer cells increases tumor growth and osteolysis in an intratibial mouse model of bone metastasis, and that soluble factor(s) shed by tumor-derived MT1-MMP enhance osteoclast differentiation in a RANKL-dependent manner.
  • Recent evidence indicates that the cognate receptor for RANKL, RANK, is expressed in prostate cancer cells, suggesting the presence of an autocrine pathway.
  • In this study, we show that MT1-MMP-expressing LNCaP prostate cancer cells display enhanced migration.
  • Moreover, conditioned medium from LNCaP cells expressing both RANKL and MT1-MMP stimulates the migration of MT1-MMP-deficient C42b prostate cancer cells.
  • These findings indicate that tumor-derived MT1-MMP enhances tumor cell migration through initiation of an autocrine loop requiring ectodomain shedding of membrane-bound RANKL in prostate cancer cells, and that Src is a key downstream mediator of RANKL-induced migration of prostate cancer cells.

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  • [Copyright] Copyright 2010 AACR.
  • [Cites] Clin Cancer Res. 1999 Dec;5(12):4105-10 [10632347.001]
  • [Cites] Scand J Clin Lab Invest. 2009;69(1):151-5 [19058084.001]
  • [Cites] Urology. 2001 Apr;57(4):611-6 [11306358.001]
  • [Cites] J Biol Chem. 2001 May 4;276(18):14665-74 [11278735.001]
  • [Cites] J Clin Invest. 2001 May;107(10):1235-44 [11375413.001]
  • [Cites] J Clin Pathol. 2002 Nov;55(11):877-8 [12401833.001]
  • [Cites] Cancer Metastasis Rev. 2003 Jun-Sep;22(2-3):177-203 [12784996.001]
  • [Cites] Cell. 2003 Jul 11;114(1):33-45 [12859896.001]
  • [Cites] Nature. 2003 Aug 21;424(6951):889-90 [12931168.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):1058-66 [14871838.001]
  • [Cites] Invest Urol. 1979 Jul;17(1):16-23 [447482.001]
  • [Cites] Cell. 1991 Feb 22;64(4):693-702 [1997203.001]
  • [Cites] J Clin Invest. 1992 Oct;90(4):1622-7 [1383278.001]
  • [Cites] Cancer Res. 1994 May 15;54(10):2577-81 [8168083.001]
  • [Cites] Int J Cancer. 1994 May 1;57(3):406-12 [8169003.001]
  • [Cites] J Biol Chem. 1997 Jan 24;272(4):2446-51 [8999957.001]
  • [Cites] J Biol Chem. 1998 Oct 23;273(43):28355-9 [9774460.001]
  • [Cites] Nature. 1999 Jan 28;397(6717):315-23 [9950424.001]
  • [Cites] J Biol Chem. 1999 May 7;274(19):13613-8 [10224132.001]
  • [Cites] Prostate. 1999 Jun 1;39(4):246-61 [10344214.001]
  • [Cites] Cell. 1999 Oct 1;99(1):81-92 [10520996.001]
  • [Cites] J Cell Biol. 2004 Nov 22;167(4):769-81 [15557125.001]
  • [Cites] Curr Opin Genet Dev. 2005 Feb;15(1):87-96 [15661538.001]
  • [Cites] Cancer Lett. 2005 Jun 1;223(1):121-8 [15890244.001]
  • [Cites] Cancer Cell. 2005 May;7(5):485-96 [15894268.001]
  • [Cites] J Biol Chem. 2005 Oct 7;280(40):33992-4002 [16046398.001]
  • [Cites] J Cell Physiol. 2006 Jan;206(1):1-8 [15920734.001]
  • [Cites] J Biol Chem. 2005 Dec 16;280(50):41700-6 [16234249.001]
  • [Cites] Trends Mol Med. 2006 Jan;12(1):17-25 [16356770.001]
  • [Cites] Chem Biol Drug Des. 2006 Jan;67(1):46-57 [16492148.001]
  • [Cites] Nature. 2006 Mar 30;440(7084):692-6 [16572175.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 18;103(29):10889-94 [16832052.001]
  • [Cites] Cancer. 2006 Jul 15;107(2):289-98 [16752412.001]
  • [Cites] J Biol Chem. 2006 Dec 1;281(48):36846-55 [17018528.001]
  • [Cites] Cancer Res. 2009 Feb 15;69(4):1517-26 [19208838.001]
  • [Cites] J Urol. 2009 Aug;182(2):509-15; discussion 515-6 [19524963.001]
  • [Cites] Cancer Res. 2009 Aug 15;69(16):6747-55 [19679556.001]
  • [Cites] Clin Cancer Res. 2009 Dec 1;15(23):7421-8 [19920114.001]
  • [Cites] Cancer Treat Rev. 2010 Apr;36(2):177-84 [20015594.001]
  • [Cites] Bone. 2007 Apr;40(4):981-90 [17196895.001]
  • [Cites] Am J Pathol. 2007 Jun;170(6):2100-11 [17525276.001]
  • [Cites] Prostate. 2008 Jan 1;68(1):92-104 [18008334.001]
  • [Cites] Histol Histopathol. 2008 Jun;23(6):709-15 [18366009.001]
  • [Cites] Cell Res. 2008 Aug;18(8):858-70 [18645583.001]
  • [Cites] Oncogene. 2008 Oct 23;27(49):6365-75 [18679417.001]
  • [Cites] Int J Cancer. 2009 Jan 1;124(1):1-6 [18942061.001]
  • [Cites] Mol Cell. 1999 Dec;4(6):1041-9 [10635328.001]
  • (PMID = 20551048.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA137280-02; United States / NCI NIH HHS / CA / CA137280; United States / NCI NIH HHS / CA / T32-CA009531; United States / NIDDK NIH HHS / DK / DK067687-05; United States / NCI NIH HHS / CA / R01 CA061986; United States / NIDDK NIH HHS / DK / R01 DK067687-05; United States / NCI NIH HHS / CA / R01 CA061986-15; United States / NIDDK NIH HHS / DK / R01 DK067687; United States / NCI NIH HHS / CA / T32 CA009531; United States / NIDDK NIH HHS / DK / DK67687; United States / NCI NIH HHS / CA / R01 CA137280; United States / NCI NIH HHS / CA / CA061986-15; United States / NCI NIH HHS / CA / CA61986
  • [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 / RANK Ligand; 0 / TNFSF11 protein, human; EC 2.7.10.2 / src-Family Kinases; EC 3.4.24.80 / MMP14 protein, human; EC 3.4.24.80 / Matrix Metalloproteinase 14
  • [Other-IDs] NLM/ NIHMS206695; NLM/ PMC2896434
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39. Stanko C, Grandinetti L, Baldassano M, Mahmoodi M, Kantor GR: Epidermotropic metastatic prostate carcinoma presenting as an umbilical nodule-Sister Mary Joseph nodule. Am J Dermatopathol; 2007 Jun;29(3):290-2
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  • [Title] Epidermotropic metastatic prostate carcinoma presenting as an umbilical nodule-Sister Mary Joseph nodule.
  • Carcinoma of the prostate accounts for fewer than 1% of all skin metastases.
  • Cutaneous metastases from prostate carcinoma most often involve the penis, the anterior aspect of the thighs, the suprapubic area, and the perineum, but they also have been reported in the scalp, the chest, the back, and even the face.
  • We report an unusual case of metastatic prostate adenocarcinoma that presented as an umbilical nodule (Sister Mary Joseph nodule) and demonstrated significant epidermotropism histologically.
  • A review of the literature has found only one documented case of prostatic carcinoma metastasizing to the umbilicus, and one other documented case of epidermotropic metastatic prostate carcinoma.
  • [MeSH-major] Adenocarcinoma / secondary. Prostatic Neoplasms / pathology. Skin Neoplasms / secondary. Umbilicus / pathology

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  • (PMID = 17519629.001).
  • [ISSN] 0193-1091
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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40. Subhawong AP, Subhawong TK, Li QK: Fine needle aspiration of metastatic prostate carcinoma simulating a primary adrenal cortical neoplasm: a case report and review of the literature. Diagn Cytopathol; 2010 Feb;38(2):147-53
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  • [Title] Fine needle aspiration of metastatic prostate carcinoma simulating a primary adrenal cortical neoplasm: a case report and review of the literature.
  • Adrenal metastases usually occur in prostate cancer patients with widespread bone and visceral disease.
  • Autopsy studies have shown that adrenal metastases may be found in up to 23% of these patients.
  • However, the finding of an isolated adrenal metastasis without the involvement of other organs in a patient with prostate cancer is exceedingly rare.
  • We report a patient with a history of prostate cancer, status post radiation, and hormonal therapy 4 years before, who presented with a new, single adrenal mass on abdominal imaging studies.
  • The ultrasound-guided FNA cytology of the adrenal mass revealed cytomorphological features that were suggestive of a primary adrenal cortical neoplasm, but overlapped with those of a prostate metastasis.
  • To our knowledge, FNA findings of metastatic prostate cancer simulating an adrenal cortical neoplasm have not been previously reported in the English literature.
  • The purpose of our study is to discuss the differential diagnosis of these entities.
  • The accurate diagnosis is important because of different prognosis and treatment implications for the various diseases.
  • [MeSH-major] Adenocarcinoma / secondary. Adrenal Cortex Neoplasms / secondary. Biopsy, Fine-Needle. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Antineoplastic Agents, Hormonal. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Prostate-Specific Antigen / blood. Radiotherapy. Tomography, X-Ray Computed. Ultrasonography, Interventional

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  • (PMID = 19693937.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 29
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41. Nilsson S, Strang P, Ginman C, Zimmermann R, Edgren M, Nordström B, Ryberg M, Kälkner KM, Westlin JE: Palliation of bone pain in prostate cancer using chemotherapy and strontium-89. A randomized phase II study. J Pain Symptom Manage; 2005 Apr;29(4):352-7
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  • [Title] Palliation of bone pain in prostate cancer using chemotherapy and strontium-89. A randomized phase II study.
  • Strontium-89 is an established alternative for the alleviation of bone pain in prostate cancer.
  • The aim of this randomized phase II study was to assess and compare the analgesic efficacy of strontium-89 and chemotherapy (FEM=5-FU, epirubicin, and mitomycin C) in 35 patients with disseminated, hormone-refractory prostate cancer suffering from persisting bone pain despite analgesic treatment.
  • The effect of FEM on pain is surprising as chemotherapy has generally only limited effect on tumor growth in bone metastases due to prostate cancer.
  • A possible explanation is that FEM has an inhibitory activity on the inflammatory component of metastases.



42. Kamiya N, Suzuki H, Kawamura K, Imamoto T, Ichikawa T: [Bony lesion with prostate cancer]. Clin Calcium; 2008 Apr;18(4):431-7
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  • [Title] [Bony lesion with prostate cancer].
  • Bone metastases of prostate cancer usually have an underlying osteoclastic component.
  • Bone metastasis is incurable and contributes significantly to disease-specific morbidity and mortality.
  • Several key factors have been found to be important in tumor-induced promotion of osteoclast activity.
  • Receptor activator of nuclear factor-kappa B ligand (RANKL) is produced by bone metastasis of prostate cancer, enabling these metastasis to induce osteolysis through osteoclast activation.
  • Matrix metalloproteinases (MMPs) are secreted by prostate cancer cells and promote osteolysis primarily through degradation of bone matrix.
  • In this way, many factors derived from prostate cancer metastases can promote osteolysis, and these factors may serve as therapeutic targets.
  • The new agents are targeted to osteoclasts (i.e.: zoledronic acid, anti-RANKL monoclonal antibody, cathepsin K inhibitor, and anti-PTHrP monoclonal antibody), are considered to be standard management in the care of bone metastasis patients in combination with chemotherapy and hormone therapy.
  • In this review, we summarized the current understanding and therapy of bone metastasis in prostate cancer.
  • [MeSH-major] Bone Neoplasms / secondary. Prostatic Neoplasms / pathology

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  • (PMID = 18379023.001).
  • [ISSN] 0917-5857
  • [Journal-full-title] Clinical calcium
  • [ISO-abbreviation] Clin Calcium
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Azepines; 0 / Diphosphonates; 0 / Enzyme Inhibitors; 0 / Imidazoles; 0 / Parathyroid Hormone-Related Protein; 0 / RANK Ligand; 0 / Sulfones; 0 / TNFSF11 protein, human; 6XC1PAD3KF / zoledronic acid; BL51M8CB8R / relacatib; EC 3.4.- / Cathepsins; EC 3.4.22.38 / CTSK protein, human; EC 3.4.22.38 / Cathepsin K; EC 3.4.24.- / Matrix Metalloproteinases
  • [Number-of-references] 20
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43. Wei JC, Wu MF, Zhang YT, Zhao LP, Lu YP, Ma D: [Effects of vimentin on invasion and metastasis of prostate cancer cell lines PC-3M-1E8 and PC-3M-2B4]. Ai Zheng; 2008 Jan;27(1):30-4
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  • [Title] [Effects of vimentin on invasion and metastasis of prostate cancer cell lines PC-3M-1E8 and PC-3M-2B4].
  • This study was to detect the expression of vimentin in prostate cancer cell lines PC-3M-1E8 and PC-3M-2B4, and evaluate the effects of vimentin on invasion and metastasis of prostate cancer cells.
  • METHODS: Two-dimensional gel electrophoresis (2-DE) followed by matrix-assisted laser desorption/time of flight mass spectrometry (MALDI TOF-MS) were used to detect the expression of vimentin in prostate cancer cell lines PC-3M-1E8 and PC-3M-2B4.
  • Genetic intervention of vimentin gene and in vitro invasion assay were used to investigate the effects of vimentin on the invasion and metastasis of prostate cancer cells.
  • RESULTS: The protein level of vimentin was higher in PC-3M-1E8 cells with high metastatic potential than in PC-3M-2B4 cells with low metastatic potential.
  • CONCLUSION: Vimentin is a promising marker for predicting the invasion and metastasis of prostate cancer cells.
  • [MeSH-minor] Cell Line, Tumor. DNA, Antisense. Electrophoresis, Gel, Two-Dimensional. Genetic Vectors. Humans. Male. Neoplasm Invasiveness. Neoplasm Metastasis. Phosphorylation. Plasmids. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Transfection

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  • (PMID = 18184460.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Antisense; 0 / Vimentin; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src)
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44. Chacon G, Alexandraki I, Palacio C: Collet-sicard syndrome: an uncommon manifestation of metastatic prostate cancer. South Med J; 2006 Aug;99(8):898-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Collet-sicard syndrome: an uncommon manifestation of metastatic prostate cancer.
  • Metastatic spread of prostate adenocarcinoma to the temporal bone is very rare.
  • A case of metastatic prostate adenocarcinoma involving the temporal bone causing Collet-Sicard syndrome is presented.
  • This case highlights an uncommon manifestation of prostate adenocarcinoma causing symptoms referable to the occipital condyle of the temporal bone.
  • Few cases have been reported in the literature of Collet-Sicard syndrome due to metastatic prostate cancer.
  • [MeSH-major] Adenocarcinoma / secondary. Prostatic Neoplasms / pathology. Skull Neoplasms / secondary. Temporal Bone
  • [MeSH-minor] Deglutition Disorders / diagnosis. Deglutition Disorders / etiology. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Syndrome. Tomography, X-Ray Computed



45. Pusulari BB, Akbar RA, Butt M, ul Haq SM: Hypocalcemia with bony metastases in prostate cancer. J Ayub Med Coll Abbottabad; 2008 Jan-Mar;20(1):138-9
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  • [Title] Hypocalcemia with bony metastases in prostate cancer.
  • He was found to have had a hepatomegaly & a large nodular prostate on rectal examination.
  • Investigations revealed a normal full blood count and renal profile, raised alkaline phosphatase and Prostate Specific Antigen (PSA), and low serum Calcium.
  • A bone scan was performed which revealed widespread bony metastases in the axial and appendicular skeleton resulting in a 'superscan', consistent with prostatic metastases.
  • We recommend that calcium levels be checked in all patients with prostate cancer and metastatic bone disease as this may have a bearing on their symptoms and the use of bisphosphonate therapy.
  • [MeSH-major] Bone Neoplasms / diagnosis. Bone Neoplasms / secondary. Calcium / blood. Hypocalcemia / etiology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Alkaline Phosphatase / blood. Fatigue / etiology. Humans. Low Back Pain / etiology. Male. Prostate-Specific Antigen / blood. Risk Factors



46. Shah SH: Reversible, isolated, unilateral hypoglossal nerve palsy due to metastatic prostate cancer. Palliat Med; 2006 Sep;20(6):639-40
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  • [Title] Reversible, isolated, unilateral hypoglossal nerve palsy due to metastatic prostate cancer.
  • [MeSH-major] Hypoglossal Nerve Diseases / etiology. Prostatic Neoplasms. Skull Base Neoplasms / secondary



47. DePuy V, Anstrom KJ, Castel LD, Schulman KA, Weinfurt KP, Saad F: Effects of skeletal morbidities on longitudinal patient-reported outcomes and survival in patients with metastatic prostate cancer. Support Care Cancer; 2007 Jul;15(7):869-76
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  • [Title] Effects of skeletal morbidities on longitudinal patient-reported outcomes and survival in patients with metastatic prostate cancer.
  • GOALS OF WORK: Patients with prostate cancer metastasized to bone frequently experience skeletal morbidities as a result of their disease.
  • MATERIALS AND METHODS: Data are from a clinical trial for the treatment of SREs associated with advanced prostate cancer metastatic to bone.
  • Outcome measures included the Functional Assessment of Cancer Therapy-General (FACT-G) and the Brief Pain Inventory.
  • [MeSH-major] Bone Neoplasms / secondary. Musculoskeletal System / pathology. Prostatic Neoplasms / pathology. Quality of Life. Treatment Outcome
  • [MeSH-minor] Aged. Diphosphonates / therapeutic use. Humans. Imidazoles. Male. Neoplasm Metastasis. Prognosis. Risk Factors. Survival

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  • [Cites] Stat Med. 1992 Jun 30;11(9):1151-70 [1509217.001]
  • [Cites] Urology. 1997 Dec;50(6):920-8 [9426724.001]
  • [Cites] Med Care. 2004 Feb;42(2):164-75 [14734954.001]
  • [Cites] Pain. 1999 Nov;83(2):157-62 [10534586.001]
  • [Cites] J Clin Oncol. 1997 Mar;15(3):974-86 [9060536.001]
  • [Cites] Control Clin Trials. 1999 Oct;20(5):408-22 [10503801.001]
  • [Cites] Ann Acad Med Singapore. 1994 Mar;23(2):129-38 [8080219.001]
  • [Cites] Am J Clin Oncol. 2001 Dec;24(6):591-6 [11801761.001]
  • [Cites] Drugs Aging. 1999 Apr;14(4):241-6 [10319239.001]
  • [Cites] Am J Clin Oncol. 2002 Dec;25(6 Suppl 1):S10-8 [12562046.001]
  • [Cites] J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68 [12359855.001]
  • [Cites] J Clin Oncol. 1993 Mar;11(3):570-9 [8445433.001]
  • [Cites] Ann Oncol. 2005 Apr;16(4):579-84 [15734776.001]
  • [Cites] Ann Intern Med. 1997 Oct 15;127(8 Pt 2):757-63 [9382394.001]
  • [Cites] Qual Life Res. 1999 May;8(3):181-95 [10472150.001]
  • [Cites] J Urol. 2000 Oct;164(4):1248-53 [10992374.001]
  • [Cites] Eval Health Prof. 2005 Jun;28(2):172-91 [15851772.001]
  • [Cites] Cancer. 1995 Mar 1;75(5):1151-61 [7850714.001]
  • [Cites] J Pain Symptom Manage. 1999 Sep;18(3):180-7 [10517039.001]
  • [Cites] J Clin Oncol. 1983 Nov;1(11):710-9 [6668489.001]
  • [Cites] J Pain Symptom Manage. 1998 Sep;16(3):171-8 [9769619.001]
  • [Cites] Qual Life Res. 2002 May;11(3):207-21 [12074259.001]
  • [Cites] N Engl J Med. 1996 Dec 12;335(24):1785-91 [8965890.001]
  • [Cites] Pain. 2001 Nov;94(2):149-58 [11690728.001]
  • [Cites] Drugs Aging. 2001;18(12):899-911 [11888345.001]
  • (PMID = 17262196.001).
  • [ISSN] 0941-4355
  • [Journal-full-title] Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer
  • [ISO-abbreviation] Support Care Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
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48. Abouassaly R, Paciorek A, Ryan CJ, Carroll PR, Klein EA: Predictors of clinical metastasis in prostate cancer patients receiving androgen deprivation therapy: results from CaPSURE. Cancer; 2009 Oct 1;115(19):4470-6
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  • [Title] Predictors of clinical metastasis in prostate cancer patients receiving androgen deprivation therapy: results from CaPSURE.
  • BACKGROUND: Virtually all patients with prostate cancer who receive androgen deprivation therapy (ADT) will ultimately develop evidence of resistance to treatment.
  • The prognosis for patients who develop metastatic castrate-resistant disease is reported to be poor, with overall survival historically estimated to be 24 to 36 months.
  • The goal of the current study was to identify predictors of clinical disease progression in patients with prostate cancer who were receiving ADT.
  • METHODS: Of the 13,740 men with biopsy-proven prostate cancer who were enrolled in the Cancer of the Prostate Strategic Urological Research Endeavor (CaPSURE) database from 1995 to 2007, 4003 men treated with ADT after diagnosis without evidence of metastases at treatment initiation were identified.
  • The primary endpoint was the development of bone metastasis.
  • Clinical and pathologic characteristics were compared between patients who developed metastasis and those who did not using chi-square tests in a Cox proportional hazards regression model.
  • One hundred ninety-one men (4.8%) progressed to metastatic disease at a median of 18 months from the initiation of ADT (range, 1-139 months).
  • On multivariate analyses, risk category (hazards ratio [HR], 2.58; P < .0001), percent of biopsies positive >33% (HR, 3.36; P = .003), age </=65 years at diagnosis (HR, 2.11; P = .001, and prostate-specific antigen velocity on ADT (HR, 1.04; P < .001) were found to be significantly associated with the development of metastatic disease after ADT.
  • This, along with the other prognostic variables established in the current study, may help identify candidates for clinical trials evaluating secondary treatments for patients with castrate-resistant disease.
  • [MeSH-minor] Adult. Age Factors. Aged. Aged, 80 and over. Databases as Topic. Humans. Male. Middle Aged. Neoplasm Metastasis. Prognosis. Risk Assessment

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  • [Copyright] 2009 American Cancer Society.
  • (PMID = 19637339.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal
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49. Yu HB, Han XB, Liang YQ, Liu JG, Wang H: [Expression of osteopontin and survivin in prostate cancer and the clinical significance]. Nan Fang Yi Ke Da Xue Xue Bao; 2010 May;30(5):1141-3
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  • [Title] [Expression of osteopontin and survivin in prostate cancer and the clinical significance].
  • OBJECTIVE: To determine the expression of osteopontin (OPN) and survivin in prostate cancer tissue, and study their correlation and roles in tumor invasion and metastasis.
  • METHODS: The expressions of OPN and survivin in prostate cancer tissue, prostate hyperplasia tissue and normal prostate tissue were determined by RT-PCR and immunohistochemistry.
  • RESULTS: The positive expression rates of OPN mRNA and protein in prostate cancer tissue [76.1% (35/46) and 69.6% (32/46)] were significantly correlated to survivin expression [67.4% (31/46) and 67.4% (31/46)] (P<0.05).
  • The expressions of OPN and survivin were related to the tumor grade and clinical stages (P<0.05).
  • OPN and survivin were not found in prostate hyperplasia and normal prostate tissues.
  • CONCLUSION: OPN and survivin may play important roles in the progression of prostate cancer and can be potential markers for invasion and metastasis of prostate cancer.
  • OPN and survivin might play synergetic roles in prostate carcinogenesis.
  • [MeSH-minor] Adult. Aged. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Metastasis. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 20501415.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / RNA, Messenger; 106441-73-0 / Osteopontin
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50. Mentor-Marcel R, Lamartiniere CA, Eltoum IA, Greenberg NM, Elgavish A: Dietary genistein improves survival and reduces expression of osteopontin in the prostate of transgenic mice with prostatic adenocarcinoma (TRAMP). J Nutr; 2005 May;135(5):989-95
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  • [Title] Dietary genistein improves survival and reduces expression of osteopontin in the prostate of transgenic mice with prostatic adenocarcinoma (TRAMP).
  • Studies in vitro suggest that osteopontin (OPN), an extracellular matrix protein secreted by macrophages infiltrating prostate tumors, and by tumor cells, may have a role in the transition from clinically insignificant tumors to metastatic prostate cancer (PC).
  • Our earlier studies in TRAnsgenic Mouse Prostate adenocarcinoma (TRAMP) mice showed that genistein, an isoflavone found in soybeans, lowered the incidence of advanced PC.
  • The steady-state level of OPN mRNA was evaluated by RT-PCR in a longitudinal study in 74 TRAMP and 32 nontransgenic litter mates (NTM).
  • Administration of 250 and 500 mg genistein/kg AIN-76A improved survival (P = 0.008 and P = 0.005, respectively) and reduced mean weight of prostates with poorly differentiated cancer (PD) (P < 0.001), as well as the mean weight of periaortic lymph nodes (LN), although the latter was not significant.
  • OPN mRNA levels in the dorsolateral prostate and metastasis to LN were significantly correlated (r = 0.643; P = 0.00006).
  • Genistein had a dose-dependent, significant inhibitory effect on OPN transcript levels in prostates displaying advanced prostate cancer (PD; score 6; P = 0.05).
  • Studies are consistent with the possibility that dietary genistein may delay the progression from benign to malignant tumors by inhibiting OPN expression.

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  • (PMID = 15867270.001).
  • [ISSN] 0022-3166
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 84926
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Sialoglycoproteins; 0 / Soybean Proteins; 0 / Spp1 protein, mouse; 106441-73-0 / Osteopontin; DH2M523P0H / Genistein
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51. Shiozawa Y, Havens AM, Jung Y, Ziegler AM, Pedersen EA, Wang J, Wang J, Lu G, Roodman GD, Loberg RD, Pienta KJ, Taichman RS: Annexin II/annexin II receptor axis regulates adhesion, migration, homing, and growth of prostate cancer. J Cell Biochem; 2008 Oct 1;105(2):370-80
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  • [Title] Annexin II/annexin II receptor axis regulates adhesion, migration, homing, and growth of prostate cancer.
  • One of the most life-threatening complications of prostate cancer is skeletal metastasis.
  • In order to develop treatment for metastasis, it is important to understand its molecular mechanisms.
  • Our work in this field has drawn parallels between hematopoietic stem cell and prostate cancer homing to the marrow.
  • In this study, we demonstrate that annexin II and its receptor play a crucial role in establishing metastasis of prostate cancer.
  • Prostate cancer cell lines migrate toward annexin II and the adhesion of prostate cancer to osteoblasts and endothelial cells was inhibited by annexin II.
  • By blocking annexin II or its receptor in animal models, short-term and long-term localization of prostate cancers are limited.
  • Annexin II may also facilitate the growth of prostate cancer in vitro and in vivo by the MAPK pathway.
  • These data strongly suggest that annexin II and its receptor axis plays a central role in prostate cancer metastasis, and that prostate cancer utilize the hematopoietic stem cell homing mechanisms to gain access to the niche.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • [Cites] Oncogene. 2003 Mar 13;22(10):1475-85 [12629510.001]
  • [Cites] J Cell Biochem. 2003 Jun 1;89(3):462-73 [12761880.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):836-41 [14574412.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):841-6 [14574413.001]
  • [Cites] J Urol. 2004 Feb;171(2 Pt 1):916-20 [14713853.001]
  • [Cites] Cancer Treat Res. 2004;118:291-309 [15043197.001]
  • [Cites] Gut. 2004 Jul;53(7):993-1000 [15194650.001]
  • [Cites] Mol Cancer. 2003 Oct 8;2:34 [14613585.001]
  • [Cites] Cell. 2004 Jul 23;118(2):149-61 [15260986.001]
  • [Cites] EMBO J. 1984 Jan;3(1):227-33 [6323166.001]
  • [Cites] Biochemistry. 2000 Mar 7;39(9):2140-8 [10694379.001]
  • [Cites] Biochim Biophys Acta. 2000 Mar 7;1477(1-2):215-30 [10708859.001]
  • [Cites] J Cell Biochem. 2000 Oct 20;80(2):259-65 [11074597.001]
  • [Cites] Blood. 2001 Feb 1;97(3):777-84 [11157497.001]
  • [Cites] J Clin Invest. 2001 May;107(10):1235-44 [11375413.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6331-4 [11522620.001]
  • [Cites] Cancer. 2001 Sep 15;92(6):1419-26 [11745218.001]
  • [Cites] Ann N Y Acad Sci. 2001 Dec;947:143-55; discussion 155-6 [11795262.001]
  • [Cites] Cancer Res. 2002 Mar 15;62(6):1832-7 [11912162.001]
  • [Cites] J Cell Biol. 2002 Jun 10;157(6):1061-9 [12045186.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jan 21;100(2):521-6 [12522268.001]
  • [Cites] J Biol Chem. 2003 Feb 7;278(6):4205-15 [12431980.001]
  • [Cites] Exp Cell Res. 1986 Jan;162(1):183-90 [2933269.001]
  • [Cites] Br J Cancer. 1992 Apr;65(4):498-502 [1314068.001]
  • [Cites] Cancer Res. 1992 Dec 15;52(24):6871-6 [1333884.001]
  • [Cites] J Cell Sci. 1992 Nov;103 ( Pt 3):733-42 [1478969.001]
  • [Cites] Carcinogenesis. 1993 Dec;14(12):2575-9 [8269629.001]
  • [Cites] Biochim Biophys Acta. 1994 Apr 5;1197(1):63-93 [8155692.001]
  • [Cites] J Exp Med. 1994 May 1;179(5):1677-82 [7513014.001]
  • [Cites] J Cell Biol. 1994 Jul;126(2):539-48 [7518469.001]
  • [Cites] J Biol Chem. 1994 Nov 18;269(46):28696-701 [7961821.001]
  • [Cites] Oncol Res. 1994;6(12):561-7 [7787249.001]
  • [Cites] J Natl Cancer Inst. 1998 Jan 21;90(2):118-23 [9450571.001]
  • [Cites] Int J Cancer. 1998 Sep 11;77(6):887-94 [9714059.001]
  • [Cites] N Engl J Med. 1999 Apr 1;340(13):994-1004 [10099141.001]
  • [Cites] J Clin Invest. 1999 Jun;103(11):1605-13 [10359570.001]
  • [Cites] J Bone Miner Res. 2005 Feb;20(2):318-29 [15647826.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2631-9 [15585658.001]
  • [Cites] J Biol Chem. 2005 May 27;280(21):20833-41 [15788416.001]
  • [Cites] Cell. 2005 Jul 1;121(7):1109-21 [15989959.001]
  • [Cites] Cell Signal. 2005 Dec;17(12):1578-92 [16005185.001]
  • [Cites] Endocrinology. 2005 Nov;146(11):4584-96 [16081645.001]
  • [Cites] J Biol Chem. 2005 Oct 28;280(43):36442-51 [16055444.001]
  • [Cites] Neoplasia. 2006 Jan;8(1):69-78 [16533428.001]
  • [Cites] BMC Cancer. 2006;6:195 [16859559.001]
  • [Cites] J Biol Chem. 2006 Oct 13;281(41):30542-50 [16895901.001]
  • [Cites] Clin Cancer Res. 2006 Oct 15;12(20 Pt 2):6243s-6249s [17062708.001]
  • [Cites] Prostate. 2007 Jan 1;67(1):61-73 [17034033.001]
  • [Cites] Blood. 2007 Jul 1;110(1):82-90 [17360942.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9417-24 [17909051.001]
  • [Cites] J Biol Chem. 2008 Feb 15;283(7):4283-94 [18057003.001]
  • [Cites] Neoplasia. 2008 Apr;10(4):371-80 [18392141.001]
  • (PMID = 18636554.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U19 CA113317; United States / NIAMS NIH HHS / AR / P30 AR046024; United States / NCI NIH HHS / CA / P50 CA69568; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / U54 CA163124; United States / NCI NIH HHS / CA / P01 CA093900; United States / NCI NIH HHS / CA / CA93900
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A2; 0 / Receptors, Peptide; 0 / annexin II receptor, human
  • [Other-IDs] NLM/ NIHMS447506; NLM/ PMC3614912
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52. Hegele A, Wahl HG, Varga Z, Sevinc S, Koliva L, Schrader AJ, Hofmann R, Olbert P: Biochemical markers of bone turnover in patients with localized and metastasized prostate cancer. BJU Int; 2007 Feb;99(2):330-4
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  • [Title] Biochemical markers of bone turnover in patients with localized and metastasized prostate cancer.
  • OBJECTIVE: To evaluate and compare the value of several markers of bone turnover in different stages of prostate cancer, as bone metastases are a common feature in this disease, and for assessing bone metastases both bone formation and bone resorption markers are diagnostic.
  • 129 undergoing radical retropubic prostatectomy (RRP) and 25 with bone metastases due to prostate cancer, and 65 with benign urological disorders who served as controls.
  • The controls had the lowest marker levels while patients with bone metastases due to prostate cancer had the highest levels, with significance for ALP, osteocalcin and TRACP5b.
  • Patients with lymph node-positive cancer had significantly high serum levels of TRACP5b and ALP but not for osteocalcin and S-CTX.
  • CONCLUSIONS: Bone turnover markers represent a new diagnostic tool in prostate cancer; the present data show that both bone resorption and bone formation are crucial for detecting bone metastases in prostate cancer.
  • The value of bone turnover markers in high-risk patients should be evaluated in a longitudinal study.
  • [MeSH-major] Biomarkers, Tumor / blood. Bone Neoplasms / secondary. Bone Resorption / diagnosis. Prostatic Neoplasms / blood
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Prospective Studies. Prostate-Specific Antigen / blood



53. Lee SH, Hatakeyama S, Yu SY, Bao X, Ohyama C, Khoo KH, Fukuda MN, Fukuda M: Core3 O-glycan synthase suppresses tumor formation and metastasis of prostate carcinoma PC3 and LNCaP cells through down-regulation of alpha2beta1 integrin complex. J Biol Chem; 2009 Jun 19;284(25):17157-69
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  • [Title] Core3 O-glycan synthase suppresses tumor formation and metastasis of prostate carcinoma PC3 and LNCaP cells through down-regulation of alpha2beta1 integrin complex.
  • Although there are numerous reports of carbohydrates enriched in cancer cells, very few studies have addressed the functions of carbohydrates present in normal cells that decrease in cancer cells.
  • It has been reported that core3 O-glycans are synthesized in normal gastrointestinal cells but are down-regulated in cancer cells.
  • To determine the roles of core3 O-glycans, we transfected PC3 and LNCaP prostate cancer cells with beta3-N-acetylglucosaminyltransferase-6 (core3 synthase) required to synthesize core3 O-glycans.
  • Upon inoculation into the prostate of nude mice, PC3 cells expressing core3 O-glycans produced much smaller tumors without metastasis to the surrounding lymph nodes in contrast to robust tumor formation and metastasis seen in mock-transfected PC3 cells.
  • Similarly LNCaP cells expressing core3 O-glycans barely produced subcutaneous tumors in contrast to robust tumor formation by mock-transfected LNCaP cells.
  • These findings indicate that addition of core3 O-glycans to beta1 and alpha2 integrin subunits in prostate cancer cells suppresses tumor formation and tumor metastasis.

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  • [Cites] J Biol Chem. 1993 Aug 15;268(23):17597-601 [7688727.001]
  • [Cites] Eur J Biochem. 1994 Jun 1;222(2):415-24 [8020479.001]
  • [Cites] Glycobiology. 1995 May;5(3):351-7 [7655172.001]
  • [Cites] Cancer Res. 1996 May 15;56(10):2237-44 [8625291.001]
  • [Cites] Cell. 1997 Jul 25;90(2):315-23 [9244305.001]
  • [Cites] J Biol Chem. 1999 Jan 29;274(5):3215-21 [9915862.001]
  • [Cites] J Biol Chem. 1999 Feb 19;274(8):4504-12 [9988682.001]
  • [Cites] Science. 1999 Aug 13;285(5430):1028-32 [10446041.001]
  • [Cites] J Cell Physiol. 1999 Oct;181(1):33-44 [10457351.001]
  • [Cites] J Biol Chem. 2005 Mar 4;280(9):8332-42 [15615721.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 22;102(12):4572-7 [15755813.001]
  • [Cites] J Exp Med. 2005 Dec 19;202(12):1679-89 [16352740.001]
  • [Cites] Oncogene. 2006 Jun 1;25(23):3267-76 [16418723.001]
  • [Cites] Glycoconj J. 2006 Jul;23(5-6):355-69 [16897178.001]
  • [Cites] J Biol Chem. 2006 Oct 27;281(43):32122-30 [16940045.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19506-11 [18048329.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3095-100 [19218444.001]
  • [Cites] Int J Cancer. 2003 Dec 20;107(6):949-57 [14601054.001]
  • [Cites] J Biol Chem. 2004 May 7;279(19):19747-54 [14998999.001]
  • [Cites] J Cell Sci. 2004 Oct 1;117(Pt 21):5059-69 [15383613.001]
  • [Cites] J Biol Chem. 1975 Nov 10;250(21):8518-23 [811657.001]
  • [Cites] Arch Biochem Biophys. 1976 Nov;177(1):330-3 [999292.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Jun;81(11):3389-93 [6203119.001]
  • [Cites] J Biol Chem. 1984 Sep 10;259(17):10834-40 [6088518.001]
  • [Cites] Cancer Res. 1984 Nov;44(11):5279-85 [6386148.001]
  • [Cites] J Biol Chem. 1986 Aug 15;261(23):10772-7 [3015940.001]
  • [Cites] Cancer Res. 1986 Oct;46(10):5270-5 [2428477.001]
  • [Cites] Science. 1987 May 1;236(4801):582-5 [2953071.001]
  • [Cites] J Biol Chem. 2000 Apr 14;275(15):11106-13 [10753916.001]
  • [Cites] Cell. 2000 Mar 31;101(1):47-56 [10778855.001]
  • [Cites] Neuron. 2000 Jul;27(1):33-44 [10939329.001]
  • [Cites] Endocrinology. 2000 Sep;141(9):3172-82 [10965888.001]
  • [Cites] J Biol Chem. 2006 Nov 3;281(44):33258-67 [16959765.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):3799-804 [17360433.001]
  • [Cites] Nat Immunol. 2007 Apr;8(4):409-18 [17334369.001]
  • [Cites] J Exp Med. 2007 Jun 11;204(6):1417-29 [17517967.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2226-31 [11280791.001]
  • [Cites] J Biol Chem. 2001 Apr 6;276(14):11007-15 [11118434.001]
  • [Cites] J Biol Chem. 2002 Apr 12;277(15):12802-9 [11821425.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10231-3 [12149519.001]
  • [Cites] Cell. 2002 Sep 20;110(6):673-87 [12297042.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16613-8 [12464682.001]
  • [Cites] J Biol Chem. 2003 Mar 14;278(11):9953-61 [12529363.001]
  • [Cites] J Biol Chem. 1987 Dec 5;262(34):16403-11 [2824491.001]
  • [Cites] J Biol Chem. 1988 Oct 15;263(29):15146-50 [2971663.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Oct 1;89(19):9326-330 [1329093.001]
  • [Cites] Cancer Res. 1993 Aug 1;53(15):3632-7 [8101764.001]
  • (PMID = 19395705.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA48737; United States / NCI NIH HHS / CA / P01 CA071932; United States / NCI NIH HHS / CA / P01CA71932; United States / NCI NIH HHS / CA / R01 CA048737; United States / NCI NIH HHS / CA / R01 CA033000; United States / NCI NIH HHS / CA / CA33000; United States / NCI NIH HHS / CA / R37 CA033000
  • [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 / DNA Primers; 0 / Integrin alpha2beta1; 0 / Polysaccharides; 0 / Recombinant Proteins; EC 2.4.1.- / N-Acetylglucosaminyltransferases
  • [Other-IDs] NLM/ PMC2719354
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54. Tepper CG, Gregg JP, Shi XB, Vinall RL, Baron CA, Ryan PE, Desprez PY, Kung HJ, deVere White RW: Profiling of gene expression changes caused by p53 gain-of-function mutant alleles in prostate cancer cells. Prostate; 2005 Dec 1;65(4):375-89
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Profiling of gene expression changes caused by p53 gain-of-function mutant alleles in prostate cancer cells.
  • BACKGROUND: Tumor suppressor p53 mutations are associated with the transition of prostate cancer to metastatic, hormone-refractory disease and stable expression of p53 gain-of-function (p53GOF) alleles support growth of LNCaP in androgen-depleted medium.
  • In this study, we performed gene expression profiling of four LNCaP-p53GOF sublines to test the hypothesis that different p53GOF mutants mediated androgen independence via modulation of a common set of genes.
  • [MeSH-minor] Cell Line, Tumor. Gene Expression Profiling. Humans. Inhibitor of Differentiation Protein 1 / biosynthesis. Inhibitor of Differentiation Protein 1 / genetics. Male. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. RNA Interference. RNA, Neoplasm / chemistry. RNA, Neoplasm / genetics. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16037992.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA93373-01; United States / NCI NIH HHS / CA / R01-CA77662
  • [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 / Inhibitor of Differentiation Protein 1; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering
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55. Clarke NW, Hart CA, Brown MD: Molecular mechanisms of metastasis in prostate cancer. Asian J Androl; 2009 Jan;11(1):57-67
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  • [Title] Molecular mechanisms of metastasis in prostate cancer.
  • Prostate cancer (PCa) preferentially metastasizes to the bone marrow stroma of the axial skeleton.
  • The exact mechanism of PCa metastasis is currently unknown, although considerable progress has been made in determining the key players in this process.
  • In this review, we present the current understanding of the molecular processes driving PCa metastasis to the bone.
  • [MeSH-major] Bone Neoplasms / secondary. Prostatic Neoplasms / pathology
  • [MeSH-minor] Cell Adhesion / physiology. Cell Movement / physiology. Chemokines / physiology. Humans. Lipids / physiology. Male. Neoplasm Metastasis / physiopathology

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  • [Cites] Microsc Res Tech. 1998 Nov 1;43(3):265-75 [9840805.001]
  • [Cites] Mol Pathol. 1998 Aug;51(4):191-200 [9893744.001]
  • [Cites] Science. 1999 Feb 5;283(5403):845-8 [9933168.001]
  • [Cites] Br J Cancer. 1999 Apr;79(11-12):1879-83 [10206308.001]
  • [Cites] Hum Pathol. 1999 Apr;30(4):458-66 [10208469.001]
  • [Cites] Urology. 1999 May;53(5):1063-9 [10223507.001]
  • [Cites] Endocr Rev. 1999 Jun;20(3):345-57 [10368775.001]
  • [Cites] Eur J Immunol. 1999 Jun;29(6):1823-31 [10382744.001]
  • [Cites] Endocrinology. 1999 Oct;140(10):4451-8 [10499498.001]
  • [Cites] Nat Rev Cancer. 2005 Jan;5(1):21-8 [15630412.001]
  • [Cites] Br J Cancer. 2005 Feb 14;92(3):503-12 [15668715.001]
  • [Cites] Br J Cancer. 2006 Mar 27;94(6):842-53 [16523199.001]
  • [Cites] Cancer Res. 1992 May 15;52(10):2916-22 [1581909.001]
  • [Cites] Cancer Res. 1992 Sep 15;52(18):5104-9 [1516067.001]
  • [Cites] Cancer Res. 1992 Oct 15;52(20):5770-4 [1394201.001]
  • [Cites] Cancer Metastasis Rev. 1992 Nov;11(3-4):353-75 [1423822.001]
  • [Cites] Eur Urol. 1993;24(2):286-90 [8375452.001]
  • [Cites] Cancer Res. 1993 Oct 1;53(19):4493-8 [7691397.001]
  • [Cites] J Biol Chem. 1993 Oct 25;268(30):22883-94 [8226797.001]
  • [Cites] J Clin Invest. 1993 Dec;92(6):3017-22 [8254056.001]
  • [Cites] Biochim Biophys Acta. 1994 May 27;1198(1):11-26 [8199193.001]
  • [Cites] J Cell Biol. 1994 Jun;125(6):1341-52 [8207062.001]
  • [Cites] Cancer Res. 1994 Jul 15;54(14):3929-33 [7518346.001]
  • [Cites] J Endocrinol. 1994 Sep;142(3):407-15 [7525824.001]
  • [Cites] J Cell Biochem Suppl. 1994;19:232-7 [7823596.001]
  • [Cites] Clin Orthop Relat Res. 1995 Mar;(312):19-33 [7634602.001]
  • [Cites] Clin Exp Metastasis. 1995 Nov;13(6):481-91 [7586806.001]
  • [Cites] Nat Med. 1995 Sep;1(9):944-9 [7585222.001]
  • [Cites] Lancet. 1995 Dec 9;346(8989):1528-30 [7491049.001]
  • [Cites] Cancer Metastasis Rev. 1995 Sep;14(3):219-28 [8548870.001]
  • [Cites] Am J Pathol. 1996 May;148(5):1375-80 [8623909.001]
  • [Cites] Cancer Res. 1996 Feb 15;56(4):663-8 [8630991.001]
  • [Cites] J Urol. 1996 Aug;156(2 Pt 1):526-31 [8683730.001]
  • [Cites] Urology. 1996 Aug;48(2):317-25 [8753751.001]
  • [Cites] BJU Int. 1999 Dec;84(9):1032-4 [10571629.001]
  • [Cites] BJU Int. 2000 Jan;85(1):65-9 [10619948.001]
  • [Cites] Br J Cancer. 2000 Aug;83(3):360-5 [10917552.001]
  • [Cites] Science. 2000 Sep 1;289(5484):1504-8 [10968780.001]
  • [Cites] Clin Cancer Res. 2000 Sep;6(9):3530-5 [10999740.001]
  • [Cites] J Clin Invest. 2000 Dec;106(11):1331-9 [11104786.001]
  • [Cites] Nature. 2001 Mar 1;410(6824):50-6 [11242036.001]
  • [Cites] J Natl Cancer Inst. 2001 Jul 18;93(14):1062-74 [11459867.001]
  • [Cites] Urology. 2001 Nov;58(5):815-20 [11711374.001]
  • [Cites] Lancet Oncol. 2001 Jan;2(1):18-26 [11905614.001]
  • [Cites] Cancer Res. 2002 Mar 15;62(6):1832-7 [11912162.001]
  • [Cites] Br J Cancer. 2002 Apr 8;86(7):1136-42 [11953862.001]
  • [Cites] Cancer Res. 2002 May 1;62(9):2708-14 [11980672.001]
  • [Cites] Urology. 2002 Aug;60(2):270-5 [12137825.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):563-72 [12154349.001]
  • [Cites] Nat Rev Cancer. 2002 Sep;2(9):657-72 [12209155.001]
  • [Cites] Differentiation. 2002 Oct;70(8):385-96 [12366376.001]
  • [Cites] Cancer Lett. 2003 Jan 28;189(2):117-28 [12490304.001]
  • [Cites] Cancer. 2003 Feb 1;97(3 Suppl):779-84 [12548575.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3126-35 [12515720.001]
  • [Cites] BJU Int. 2003 May;91(7):716-20 [12699491.001]
  • [Cites] J Cell Biochem. 2003 Jun 1;89(3):462-73 [12761880.001]
  • [Cites] FEBS Lett. 2003 Aug 28;550(1-3):79-83 [12935890.001]
  • [Cites] Nature. 2003 Sep 18;425(6955):307-11 [13679920.001]
  • [Cites] Oncogene. 2003 Nov 6;22(50):8093-101 [14603250.001]
  • [Cites] J Urol. 2003 Dec;170(6 Pt 2):S65-7; discussion S67-8 [14610413.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2002;5(1):59-62 [15195132.001]
  • [Cites] Int J Cancer. 2004 Sep 20;111(5):783-91 [15252851.001]
  • [Cites] Eur Urol. 2004 Sep;46(3):389-401; discussion 401-2 [15306113.001]
  • [Cites] J Urol. 1968 Jan;99(1):87-96 [4170154.001]
  • [Cites] Nature. 1976 Oct 7;263(5577):507-8 [972697.001]
  • [Cites] Cancer. 1983 Mar 1;51(5):918-24 [6681595.001]
  • [Cites] Cancer Res. 1986 Jan;46(1):1-7 [2998604.001]
  • [Cites] Br J Urol. 1985 Dec;57(6):721-3 [4084733.001]
  • [Cites] Science. 1991 Mar 22;251(5000):1451-5 [2006419.001]
  • [Cites] J Cell Biol. 1991 Apr;113(1):173-85 [2007622.001]
  • [Cites] Cell. 1991 Jul 12;66(1):107-19 [2070412.001]
  • [Cites] Br J Urol. 1991 Jul;68(1):74-80 [1873694.001]
  • [Cites] Br J Urol. 1992 Jan;69(1):64-70 [1737255.001]
  • [Cites] FASEB J. 1992 Apr;6(7):2456-66 [1563597.001]
  • [Cites] J Exp Med. 1997 Jan 6;185(1):111-20 [8996247.001]
  • [Cites] Eur J Cancer. 1997 Feb;33(2):263-71 [9135498.001]
  • [Cites] Clin Exp Metastasis. 1997 May;15(3):218-27 [9174123.001]
  • [Cites] Int J Cancer. 1997 Aug 22;74(4):374-7 [9291424.001]
  • [Cites] Ophthal Plast Reconstr Surg. 1997 Dec;13(4):227-38 [9430298.001]
  • [Cites] J Natl Cancer Inst. 1998 Jan 21;90(2):118-23 [9450571.001]
  • [Cites] Prostate. 1998 Feb 15;34(3):203-13 [9492849.001]
  • [Cites] Endocr Rev. 1998 Feb;19(1):18-54 [9494779.001]
  • [Cites] Clin Exp Metastasis. 1998 Jan;16(1):21-9 [9502074.001]
  • [Cites] Nature. 1998 Mar 12;392(6672):190-3 [9515965.001]
  • [Cites] Prostate. 1998 May 15;35(3):185-92 [9582087.001]
  • [Cites] Cancer Res. 1998 Jun 15;58(12):2520-3 [9635571.001]
  • [Cites] J Exp Med. 1998 Aug 3;188(3):539-48 [9687531.001]
  • [Cites] Urology. 1998 Aug;52(2):261-6; discussion 266-7 [9697792.001]
  • (PMID = 19050684.001).
  • [ISSN] 1008-682X
  • [Journal-full-title] Asian journal of andrology
  • [ISO-abbreviation] Asian J. Androl.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500966
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Chemokines; 0 / Lipids
  • [Number-of-references] 93
  • [Other-IDs] NLM/ PMC3735202
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56. Zhang XM, Shen Y, Xianyu ZQ: [Serum proteomic study of prostate cancer with bone metastasis]. Zhonghua Nan Ke Xue; 2010 Aug;16(8):721-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Serum proteomic study of prostate cancer with bone metastasis].
  • OBJECTIVE: To screen serum biomarker candidates in prostate cancer with bone metastasis by two-dimensional gel electrophoresis (2-DGE) and mass spectrometry.
  • METHODS: Serum samples were obtained from 5 prostate cancer patients with bone metastasis, and another 5 without it.
  • The differentially expressed protein spots in the serum of those with bone metastases were identified by peptide-fingerprinting with matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS).
  • RESULTS: Compared with the serum samples from those without bone metastasis, 10 protein spot-features were found to be significantly increased and 5 significantly decreased, and the 3 identified proteins, Zn-alpha2-glycoprotein (ZAG), haptoglobin and apolipoprotein C-III, were all increased in the bone-metastasis group.
  • The identified proteins involved in the formation and progression of prostate cancer bone metastasis might be applied as biomarkers for bone metastasis from prostate cancer.
  • [MeSH-major] Bone Neoplasms / blood. Bone Neoplasms / secondary. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology. Proteome / analysis
  • [MeSH-minor] Aged. Aged, 80 and over. Case-Control Studies. Electrophoresis, Gel, Two-Dimensional. Humans. Male. Middle Aged. Neoplasm Metastasis. Proteomics



57. Hong JH, Ahn KS, Bae E, Jeon SS, Choi HY: The effects of curcumin on the invasiveness of prostate cancer in vitro and in vivo. Prostate Cancer Prostatic Dis; 2006;9(2):147-52
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  • [Title] The effects of curcumin on the invasiveness of prostate cancer in vitro and in vivo.
  • Curcumin has become a focus of interest with regard to its antitumor effects in prostate cancer; however, the effects of this agent on invasion and metastasis remain less well understood.
  • Matrix metalloproteinases (MMPs) are important prerequisite for tumor invasion and metastasis.
  • In this study, we evaluated the effects of curcumin on prostate cancer cells (DU-145) invasion in both in vitro and in vivo.
  • Curcumin treatment resulted not only in a significant reduction in the expression of MMP-2 and MMP-9, but also effected the inhibition of invasive ability in vitro.
  • Curcumin was shown to induce a marked reduction of tumor volume, MMP-2, and MMP-9 activity in the tumor-bearing site.
  • The metastatic nodules in vivo were significantly fewer in the curcumin-treated group than untreated group.
  • Curcumin appears to constitute a potential agent for the prevention of cancer progression, or at least of the initial phase of metastasis, in prostate cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Curcumin / pharmacology. Neoplasm Invasiveness / pathology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Animals. Biomarkers, Tumor / analysis. Caspase 3. Caspases / analysis. Caspases / metabolism. Cell Proliferation / drug effects. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. In Vitro Techniques. Male. Matrix Metalloproteinase 2 / analysis. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / analysis. Matrix Metalloproteinase 9 / metabolism. Mice. Neoplasms, Experimental. Probability. Sensitivity and Specificity. Statistics, Nonparametric. Transplantation, Heterologous. Tumor Cells, Cultured / cytology. Tumor Cells, Cultured / drug effects

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  • (PMID = 16389264.001).
  • [ISSN] 1365-7852
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; IT942ZTH98 / Curcumin
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58. Turvey SE, Swart E, Denis MC, Mahmood U, Benoist C, Weissleder R, Mathis D: Noninvasive imaging of pancreatic inflammation and its reversal in type 1 diabetes. J Clin Invest; 2005 Sep;115(9):2454-61
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  • Importantly, an essentially identical MNP-MRI strategy has previously been used with great success to image lymph node metastases in prostate cancer patients.

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  • [Cites] Annu Rev Immunol. 2001;19:131-61 [11244033.001]
  • [Cites] J Endocrinol Invest. 1999 Feb;22(2):151-8 [10195385.001]
  • [Cites] Lancet. 2001 Jul 21;358(9277):221-9 [11476858.001]
  • [Cites] Diabetes. 2001 Oct;50(10):2231-6 [11574403.001]
  • [Cites] Nat Immunol. 2001 Dec;2(12):1117-25 [11713466.001]
  • [Cites] N Engl J Med. 2002 May 30;346(22):1685-91 [12037147.001]
  • [Cites] N Engl J Med. 2002 May 30;346(22):1692-8 [12037148.001]
  • [Cites] Radiology. 2003 Jan;226(1):214-20 [12511693.001]
  • [Cites] Nat Rev Immunol. 2003 Feb;3(2):123-32 [12563296.001]
  • [Cites] Nat Med. 2003 Jun;9(6):713-25 [12778170.001]
  • [Cites] N Engl J Med. 2003 Jun 19;348(25):2491-9 [12815134.001]
  • [Cites] Autoimmun Rev. 2002 May;1(3):139-45 [12849007.001]
  • [Cites] Nat Med. 2003 Sep;9(9):1202-8 [12937416.001]
  • [Cites] Tissue Antigens. 2003 Nov;62(5):359-77 [14617043.001]
  • [Cites] Diabetes. 2004 Jan;53(1):250-64 [14693724.001]
  • [Cites] Nat Med. 2000 Mar;6(3):351-5 [10700241.001]
  • [Cites] Curr Diab Rep. 2004 Apr;4(2):87-94 [15035967.001]
  • [Cites] Endocrinol Metab Clin North Am. 2004 Mar;33(1):113-33, ix-x [15053898.001]
  • [Cites] Diabetes. 2004 Jun;53(6):1459-66 [15161749.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12634-9 [15304647.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1985;407(4):359-67 [2413613.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1986;410(1):17-21 [3097948.001]
  • [Cites] Am J Pathol. 1987 Aug;128(2):210-5 [3618725.001]
  • [Cites] N Engl J Med. 1988 Mar 17;318(11):663-70 [3125434.001]
  • [Cites] Diabetes. 1988 Oct;37(10):1444-8 [2458291.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Oct;86(20):8000-4 [2510155.001]
  • [Cites] Science. 1990 Jul 20;249(4966):293-5 [2115690.001]
  • [Cites] Transplantation. 1990 Oct;50(4):537-44 [2219269.001]
  • [Cites] Diabetologia. 1992 Dec;35(12):1118-24 [1478363.001]
  • [Cites] Immunopharmacology. 1993 May-Jun;25(3):229-38 [8354639.001]
  • [Cites] Cell. 1993 Sep 24;74(6):1089-100 [8402882.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jan 4;91(1):123-7 [8278351.001]
  • [Cites] Histol Histopathol. 1993 Oct;8(4):751-9 [8305825.001]
  • [Cites] Endocr Rev. 1994 Aug;15(4):516-42 [7988484.001]
  • [Cites] Cell. 1996 May 3;85(3):291-7 [8616883.001]
  • [Cites] J Immunol. 1997 Mar 15;158(6):2947-54 [9058834.001]
  • [Cites] Horm Metab Res. 1997 Oct;29(10):510-5 [9405979.001]
  • [Cites] Autoimmunity. 1998;27(2):65-77 [9583738.001]
  • [Cites] Endocrinology. 1998 Aug;139(8):3534-41 [9681505.001]
  • [Cites] Eur J Immunol. 1999 Jan;29(1):245-55 [9933106.001]
  • [Cites] Diabetes. 2001 Jun;50(6):1269-73 [11375326.001]
  • (PMID = 16110329.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R24 CA092782; United States / NCI NIH HHS / CA / R24 CA92782
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Immunoglobulin G; 8N3DW7272P / Cyclophosphamide
  • [Other-IDs] NLM/ PMC1187933
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59. Khan R, Maheshwari V, Harris SH, Alam K: Prostatic adenocarcinoma metastasizing to the parietal bones. Indian J Pathol Microbiol; 2007 Oct;50(4):759-61
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  • Prostate cancer metastasis to the axial skeleton occurs at high frequency in patients with advanced disease causing significant morbidity and mortality.
  • Apart from bone, brain is also a common site of metastasis but the involvement of the parietal bones is extremely unusual.
  • Parietal bone metastasis from prostatic adenocarcinoma was the initial presentation seen in our patient.
  • The report is intended to alert the reader of this rare site of metastasis from the prostate.
  • [MeSH-major] Adenocarcinoma / secondary. Parietal Bone / pathology. Prostatic Neoplasms / pathology. Skull Neoplasms / secondary

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  • (PMID = 18306543.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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60. Tomlins SA, Mehra R, Rhodes DR, Cao X, Wang L, Dhanasekaran SM, Kalyana-Sundaram S, Wei JT, Rubin MA, Pienta KJ, Shah RB, Chinnaiyan AM: Integrative molecular concept modeling of prostate cancer progression. Nat Genet; 2007 Jan;39(1):41-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integrative molecular concept modeling of prostate cancer progression.
  • Despite efforts to profile prostate cancer, the genetic alterations and biological processes that correlate with the observed histological progression are unclear.
  • Using laser-capture microdissection to isolate 101 cell populations, we have profiled prostate cancer progression from benign epithelium to metastatic disease.
  • Of note, relative to low-grade prostate cancer (Gleason pattern 3), high-grade cancer (Gleason pattern 4) shows an attenuated androgen signaling signature, similar to metastatic prostate cancer, which may reflect dedifferentiation and explain the clinical association of grade with prognosis.
  • Taken together, these data show that analyzing gene expression signatures in the context of a compendium of molecular concepts is useful in understanding cancer biology.
  • [MeSH-minor] Androgens / metabolism. Disease Progression. Humans. Male. Neoplasm Metastasis. Prostatic Hyperplasia / genetics. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial Neoplasia / genetics. Prostatic Intraepithelial Neoplasia / pathology. Signal Transduction. Systems Integration

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  • (PMID = 17173048.001).
  • [ISSN] 1061-4036
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE6099
  • [Grant] United States / NCI NIH HHS / CA / 5P30 CA46592; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / R01 CA102872; United States / NIDA NIH HHS / DA / U54 DA021519-01A1; United States / NCI NIH HHS / CA / UO1 CA111275-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens
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61. Saleem M, Adhami VM, Ahmad N, Gupta S, Mukhtar H: Prognostic significance of metastasis-associated protein S100A4 (Mts1) in prostate cancer progression and chemoprevention regimens in an autochthonous mouse model. Clin Cancer Res; 2005 Jan 1;11(1):147-53
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  • [Title] Prognostic significance of metastasis-associated protein S100A4 (Mts1) in prostate cancer progression and chemoprevention regimens in an autochthonous mouse model.
  • PURPOSE: We recently showed that metastasis-promoting Mts1 gene (S100A4) and protein is overexpressed during progression of prostate cancer in humans.
  • The purpose of this study was to assess the expression of S100A4 during autochthonous prostate cancer progression in transgenic adenocarcinoma of the mouse prostate (TRAMP) model.
  • Because oral consumption of green tea polyphenols (GTP) has been shown to inhibit metastasis and prostate cancer in TRAMP, we further assessed the significance of S100A4 during chemoprevention regimen.
  • RESULTS: With the progression of age and prostate cancer growth in TRAMP mice, an increase in the expression of S100A4 at mRNA and protein level in dorsolateral prostate, but not in nontransgenic mice, occurred.
  • GTP feeding to TRAMP mice resulted in marked inhibition of prostate cancer progression, which was associated with reduction of S100A4 and restoration of E-cadherin.
  • CONCLUSIONS: S100A4 represents a promising marker for prostate cancer progression and could be employed as a biomarker in chemoprevention regimens.
  • [MeSH-minor] Administration, Oral. Age Factors. Animals. Biomarkers / metabolism. Blotting, Western. Cadherins / metabolism. Cell Line, Tumor. DNA, Complementary / metabolism. Densitometry. Disease Progression. Flavonoids / chemistry. Guanosine Triphosphate / metabolism. Immunohistochemistry. Male. Mice. Mice, Inbred C57BL. Phenols / chemistry. Polymerase Chain Reaction. Polyphenols. RNA / metabolism. RNA, Messenger / metabolism. Tea. Time Factors. Transgenes

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  • [ErratumIn] Clin Cancer Res. 2005 Feb 1;11(3):1353
  • (PMID = 15671539.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P50DK 65303; United States / NCI NIH HHS / CA / R01 CA 101039; United States / NCI NIH HHS / CA / R01 CA 78809
  • [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 / Biomarkers; 0 / Cadherins; 0 / DNA, Complementary; 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; 0 / RNA, Messenger; 0 / S100 Proteins; 0 / S100a4 protein, mouse; 0 / Tea; 63231-63-0 / RNA; 86-01-1 / Guanosine Triphosphate
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62. Axanova L, Morré DJ, Morré DM: Growth of LNCaP cells in monoculture and coculture with osteoblasts and response to tNOX inhibitors. Cancer Lett; 2005 Jul 8;225(1):35-40
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  • An in vitro coculture model of prostate cancer cells (LNCaP) with human osteoblasts (hFOB) was utilized to define the efficacy of the tNOX inhibitors EGCg, capsaicin, Capsibiol-T and phenoxodiol against bone metastasis of prostate cancer alone and in combination with Taxol and cisplatin.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Bone Neoplasms / prevention & control. Bone Neoplasms / secondary. Cell Survival. Cisplatin / pharmacology. Humans. Isoflavones / pharmacology. Male. Paclitaxel / pharmacology. Tumor Cells, Cultured

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  • (PMID = 15922855.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NCCIH NIH HHS / AT / P50 AT0047
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Antioxidants; 0 / Capsibiol-T; 0 / Isoflavones; 0 / Plant Extracts; 8R1V1STN48 / Catechin; 995FT1W541 / phenoxodiol; BQM438CTEL / epigallocatechin gallate; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin; S07O44R1ZM / Capsaicin
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63. Kitagawa Y, Konaka H, Mizokami A, Namiki M: [Clinical implications of bisphosphonate for bone metastases of prostate cancer]. Nihon Rinsho; 2007 Nov 28;65 Suppl 9:356-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical implications of bisphosphonate for bone metastases of prostate cancer].
  • [MeSH-major] Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / secondary. Diphosphonates / therapeutic use. Prostatic Neoplasms / pathology

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  • (PMID = 18161131.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / RANK Ligand
  • [Number-of-references] 12
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64. Briganti A, Blute ML, Eastham JH, Graefen M, Heidenreich A, Karnes JR, Montorsi F, Studer UE: Pelvic lymph node dissection in prostate cancer. Eur Urol; 2009 Jun;55(6):1251-65
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  • [Title] Pelvic lymph node dissection in prostate cancer.
  • CONTEXT: Pelvic lymph node dissection (PLND) is considered the most reliable procedure for the detection of lymph node metastases in prostate cancer (PCa); however, the therapeutic benefit of PLND in PCa management is currently under debate.
  • Keywords included prostate cancer, pelvic lymph node dissection, radical prostatectomy, imaging, and complications.
  • Extended PLND (ePLND; ie, removal of obturator, external iliac, hypogastric with or without presacral and common iliac nodes) significantly improves the detection of lymph node metastases compared with limited PLND (lPLND; ie, removal of obturator with or without external iliac nodes), which is associated with poor staging accuracy.
  • Because not all patients with PCa are at the same risk of harbouring nodal metastases, several nomograms and tables have been developed and validated to identify candidates for PLND.
  • According to these prediction models, a staging PLND might be omitted in low-risk PCa patients because of the low rate of lymph node metastases found, even after extended dissections (<8%).
  • Indeed, patients with low-volume nodal metastases experience excellent survival rates, regardless of adjuvant treatment.
  • Patients with low-volume nodal metastases have a good long-term prognosis; to what extent this prognosis is the result of a positive impact of PLND on PCa outcomes is still to be determined.
  • [MeSH-major] Lymph Node Excision / methods. Lymph Nodes / pathology. Lymph Nodes / surgery. Neoplasm Staging / methods. Prostatectomy / methods. Prostatic Neoplasms / pathology
  • [MeSH-minor] Biopsy, Needle. Humans. Immunohistochemistry. Lymphatic Metastasis. Male. Neoplasm Invasiveness / pathology. Pelvis. Predictive Value of Tests. Prognosis. Risk Assessment. Survival Analysis



65. Venkitaraman R, Cook GJ, Dearnaley DP, Parker CC, Huddart RA, Khoo V, Eeles R, Horwich A, Sohaib SA: Does magnetic resonance imaging of the spine have a role in the staging of prostate cancer? Clin Oncol (R Coll Radiol); 2009 Feb;21(1):39-42
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  • [Title] Does magnetic resonance imaging of the spine have a role in the staging of prostate cancer?
  • AIMS: Magnetic resonance imaging (MRI) is an effective method for evaluating the spine in patients with a high risk of metastatic disease.
  • The aim of this study was to compare MRI spine with radionuclide bone scan in detecting spinal metastases for staging prostate cancer patients.
  • MATERIALS AND METHODS: A cohort of 99 patients with locally advanced prostate cancer at high risk of skeletal metastasis (prostate-specific antigen>10 ng/ml, composite Gleason score>or=8) or equivocal findings on bone scan were included in the retrospective study, and their MRI spine and bone scans were analysed.
  • RESULTS: Ten patients were detected to have definite spinal metastasis by bone scan, whereas 12 patients had definite skeletal metastasis by MRI spine.
  • Compared with the 'gold standard', derived from clinical and radiological follow-up, the sensitivities for radionuclide bone scan and that for MRI spine for detecting skeletal metastasis were 71.4 and 85.7%, respectively (P=0.023), whereas the specificities were 96.5 and 97.7%, respectively (P=0.95).
  • Of the 34 individual metastatic lesions in the spine, 15 were concordantly positive on both scans, whereas five lesions were positive only by bone scan and 11 positive only by MRI.
  • The addition of MRI spine in the staging for prostate cancer resulted in a change of stage and management plan in seven (7%) patients.
  • CONCLUSION: MRI spine has comparable specificity and slightly better sensitivity than bone scan to detect spinal metastasis from prostate cancer.
  • [MeSH-major] Magnetic Resonance Imaging. Prostatic Neoplasms / pathology. Spinal Neoplasms / diagnosis. Spinal Neoplasms / secondary. Spine / pathology

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  • (PMID = 18993040.001).
  • [ISSN] 0936-6555
  • [Journal-full-title] Clinical oncology (Royal College of Radiologists (Great Britain))
  • [ISO-abbreviation] Clin Oncol (R Coll Radiol)
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / 10588; United Kingdom / Medical Research Council / / G0501019
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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66. Yonou H, Ochiai A, Ashimine S, Maeda H, Horiguchi Y, Yoshioka K, Ogawa Y, Hatano T, Tachibana M: The bisphosphonate YM529 inhibits osteoblastic bone tumor proliferation of prostate cancer. Prostate; 2007 Jun 15;67(9):999-1009
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The bisphosphonate YM529 inhibits osteoblastic bone tumor proliferation of prostate cancer.
  • BACKGROUND: In men, prostate cancer frequently metastasizes to the bones, where it forms osteoblastic lesions with an osteolytic element that cause pain.
  • However, the role of osteoclastogenesis in bone metastasis of human prostate cancer is unknown.
  • Bisphosphonates are already known to be beneficical for treating osteolytic bone metastases, so we employed a model of osteoblastic bone tumor of human prostate cancer to investigate whether a new bisphosphonate (YM529: minodronate) could inhibit both the formation of bone tumors and the progression of established osteoblastic tumors.
  • METHODS: Human prostate cancer cells (LNCaP) were injected into adult human bone implants in nonobese diabetic/severe combined immunodeficient mice, after which osteoblastic bone tumors developed.
  • YM529 (1 microg/day) was administered subcutaneously every day for 2 weeks, starting either immediately or 2 weeks after implantation of the tumor cells, and the mice were sacrificed at 4 weeks after implantation.
  • The bone tumors were examined histologically and the number of tartrate-resistant acid phosphatase-stained osteoclasts in each tumor focus was counted.
  • CONCLUSIONS: YM529 reduced the tumor burden in bone by inhibiting both the formation of new lesions and the progression of existing tumors, suggesting that osteoclasts are involved in the formation of bone tumors by prostate cancer.
  • Treatment with this bisphosphonate may potentially be beneficial for patients with bone metastases of prostate cancer.
  • [MeSH-major] Bone Neoplasms / prevention & control. Bone Neoplasms / secondary. Diphosphonates / pharmacology. Imidazoles / pharmacology. Osteoblasts / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Animals. Humans. Male. Mice. Mice, Nude. Neoplasm Transplantation / pathology. Transplantation, Heterologous



67. Compérat E, Azzouzi AR, Chartier-Kastler E, Ménégaux F, Capron F, Richard F, Charlotte F: Late recurrence of a prostatic adenocarcinoma as a solitary splenic metastasis. Urol Int; 2007;78(1):86-8
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  • [Title] Late recurrence of a prostatic adenocarcinoma as a solitary splenic metastasis.
  • Splenic metastases of solid tumors are exceptional.
  • We report the first case of an isolated splenic metastasis from prostate carcinoma, 5 years after radical prostatectomy.
  • The splenic tumor was revealed by a pain and progressive increase in the serum prostate-specific antigen (PSA) level.
  • This case suggests that splenic metastasis might be the result of the growth of an early blood-borne micrometastasis within the spleen after a period of clinical latency.
  • [MeSH-major] Adenocarcinoma / secondary. Neoplasm Recurrence, Local / diagnosis. Prostatic Neoplasms / pathology. Splenic Neoplasms / secondary
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Diagnosis, Differential. Follow-Up Studies. Humans. Male. Prostatectomy. Radiation-Sensitizing Agents. Splenectomy. Taxoids / therapeutic use. Tomography, X-Ray Computed

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  • (PMID = 17192740.001).
  • [ISSN] 0042-1138
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Radiation-Sensitizing Agents; 0 / Taxoids; 15H5577CQD / docetaxel
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68. Klepzig M, Jonas D, Oremek GM: Procollagen type 1 amino-terminal propeptide: a marker for bone metastases in prostate carcinoma. Anticancer Res; 2009 Feb;29(2):671-3
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  • [Title] Procollagen type 1 amino-terminal propeptide: a marker for bone metastases in prostate carcinoma.
  • BACKGROUND: The objective of this study was to assess the utility of the bone formation marker procollagen type 1 amino-terminal propeptide (P1NP) in indicating bone metastases in patients with prostate carcinoma.
  • Alkaline phosphatase (AP) and prostate-specific antigen (PSA) were measured as a comparison.
  • The patients were divided into three groups, 32 patients with benign prostate hyperplasia (BPH), 38 patients with prostate carcinoma and 30 patients with prostate carcinoma with bone metastases.
  • RESULTS: PINP concentrations were elevated in about 87% of the patients with confirmed bone metastases, the P1NP levels were significantly (p < or = 0.001) higher (median: 194.7 ng/ml) than in the patients without bone involvement (median: 38.0 ng/ml) and the BPH patients (median: 42.2 ng/ml), who both presented P1NP levels within the normal range.
  • CONCLUSION: P1NP is a reliable predictor of the presence or absence of bone metastases in prostate carcinoma.
  • [MeSH-major] Biomarkers, Tumor / blood. Bone Neoplasms / blood. Bone Neoplasms / secondary. Peptide Fragments / blood. Procollagen / blood. Prostatic Neoplasms / blood
  • [MeSH-minor] Aged. Humans. Male. Prostate-Specific Antigen / blood. Prostatic Hyperplasia / blood

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  • (PMID = 19331219.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Peptide Fragments; 0 / Procollagen; 0 / procollagen type I carboxy terminal peptide; EC 3.4.21.77 / Prostate-Specific Antigen
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69. Pinto F, Brescia A, Sacco E, Volpe A, Gardi M, Gulino G, Bassi P: Disseminated intravascular coagulation secondary to metastatic prostate cancer: case report and review of the literature. Arch Ital Urol Androl; 2009 Dec;81(4):212-4
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  • [Title] Disseminated intravascular coagulation secondary to metastatic prostate cancer: case report and review of the literature.
  • Disseminated intravascular coagulation (DIC) is the most frequent coagulation disorder associated with metastatic prostate cancer.
  • We report a case of a 60-year-old white man who was admitted in our department with ecchymoses and haematuria secondary to a DIC associated with metastatic prostate cancer.

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  • (PMID = 20608143.001).
  • [ISSN] 1124-3562
  • [Journal-full-title] Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica
  • [ISO-abbreviation] Arch Ital Urol Androl
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Anilides; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide; EFY6W0M8TG / Leuprolide
  • [Number-of-references] 27
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70. Selimoglu H, Duran C, Saraydaroglu O, Guclu M, Kiyici S, Ersoy C, Eren MA, Tuncel E, Imamoglu S: Prostate cancer metastasis to thyroid gland. Tumori; 2007 May-Jun;93(3):292-5
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  • [Title] Prostate cancer metastasis to thyroid gland.
  • Metastases to the thyroid gland are rarely encountered in clinical practice.
  • Prostate cancer is one of the most frequent malignancies in men.
  • It generally has a favorable course, and autopsy series have shown occult prostate cancer in many subjects, especially in aged males.
  • However, prostate cancer sometimes exhibits an aggressive behavior and cases with a poor prognosis have been reported.
  • Occasional reports of metastasis from prostate cancer to the thyroid gland have been documented.
  • We describe the case of a 73-year-old patient presenting with thyroid metastasis from long-standing prostate cancer.
  • [MeSH-major] Adenocarcinoma / secondary. Prostatic Neoplasms / pathology. Thyroid Neoplasms / secondary
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Humans. Male. Neoplasm Proteins / analysis. Prostate-Specific Antigen / analysis



71. Nohara T, Kawashima A, Takahashi T, Kitamura M, Akai H, Oka T, Mano M: [Prostate cancer metastasized to thyroid cartilage: a case report]. Nihon Hinyokika Gakkai Zasshi; 2005 Nov;96(7):697-700
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  • [Title] [Prostate cancer metastasized to thyroid cartilage: a case report].
  • A 75-year-old male was diagnosed as prostate cancer (serum PSA: 4,772 ng/ml, Gleason score: 4 + 4 = 8) with multiple bone metastases.
  • And he noticed a painless mass of the frontal neck a month before the diagnosis.
  • Computed tomography of the neck showed a tumor in the thyroid cartilage.
  • Biopsy of the neck tumor revealed metastasis of prostate cancer by positive PSA staining.
  • Metastasis of malignant tumor to cartilaginous tissue is extremely rare because there are usually no vessels in it.
  • Only 4 cases of the metastasis of prostate cancer to the thyroid cartilage have been reported.
  • It was thought that tiny bone marrows were formed in the ossified cartilage and it caused hematogenous metastasis.
  • [MeSH-major] Adenocarcinoma / secondary. Bone Neoplasms / secondary. Neoplastic Cells, Circulating / pathology. Prostatic Neoplasms / pathology. Thyroid Cartilage / pathology



72. Venkitaraman R, Cook GJ, Dearnaley DP, Parker CC, Khoo V, Eeles R, Huddart RA, Horwich A, Sohaib SA: Whole-body magnetic resonance imaging in the detection of skeletal metastases in patients with prostate cancer. J Med Imaging Radiat Oncol; 2009 Jun;53(3):241-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Whole-body magnetic resonance imaging in the detection of skeletal metastases in patients with prostate cancer.
  • Whole-body MRI is an effective method for evaluating the entire skeletal system in patients with metastatic disease.
  • This study aimed to compare whole-body MRI and radionuclide bone scintigraph in the detection of skeletal metastases in patients with prostate cancer.
  • Patients with prostate cancer at high risk of skeletal metastasis with (i) prostate-specific antigen of > or =50 ng/mL;.
  • (ii) composite Gleason score of > or =8 with prostate-specific antigen of >20 ng/mL; or (iii) node-positive disease were enrolled in this prospective study before systemic treatment was initiated.
  • Seven patients had bone metastases on bone scans, while seven patients had skeletal metastases by whole-body MRI, with concordant findings only in four patients.
  • Bone scans detected more rib metastases, while MRI identified more metastatic lesions in the spine.
  • Whole-body MRI and radionuclide bone scintigraphy have similar specificity and sensitivity and may be used as complementary investigations to detect skeletal metastases from prostate cancer.
  • [MeSH-major] Algorithms. Bone Neoplasms / diagnosis. Bone Neoplasms / secondary. Image Interpretation, Computer-Assisted / methods. Magnetic Resonance Imaging / methods. Prostatic Neoplasms / diagnosis. Whole Body Imaging / methods
  • [MeSH-minor] Aged. Aged, 80 and over. Humans. Image Enhancement / methods. Lymphatic Metastasis. Male. Middle Aged. Reproducibility of Results. Sensitivity and Specificity

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  • (PMID = 19624290.001).
  • [ISSN] 1754-9485
  • [Journal-full-title] Journal of medical imaging and radiation oncology
  • [ISO-abbreviation] J Med Imaging Radiat Oncol
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / 10588; United Kingdom / Medical Research Council / / G0501019; United Kingdom / Cancer Research UK / / C46/A2131
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
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73. Spahn M, Kneitz S, Scholz CJ, Stenger N, Rüdiger T, Ströbel P, Riedmiller H, Kneitz B: Expression of microRNA-221 is progressively reduced in aggressive prostate cancer and metastasis and predicts clinical recurrence. Int J Cancer; 2010 Jul 15;127(2):394-403
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  • [Title] Expression of microRNA-221 is progressively reduced in aggressive prostate cancer and metastasis and predicts clinical recurrence.
  • Emerging evidence shows that microRNAs (miR) are involved in the pathogenesis of a variety of cancers, including prostate carcinoma (PCa).
  • Little information is available regarding miR expression levels in lymph node metastasis of prostate cancer or the potential of miRs as prognostic markers in this disease.
  • Therefore, we analyzed the global expression of miRs in benign, hyperplastic prostate tissue (BPH), primary PCa of a high risk group of PCa patients, and corresponding metastatic tissues by microarray analysis.
  • Consistent with the proposal that some miRs are oncomirs, we found aberrant expression of several miRs, including the downregulation of miR-221, in PCa metastasis.
  • In a large study cohort, the prostate-specific oncomir miR-221 was progressively downregulated in aggressive forms of PCa.
  • Kaplan-Meier estimates and Cox proportional hazard models showed that miR-221 downregulation was linked to tumor progression and recurrence in a high risk prostate cancer cohort.
  • Our results showed that progressive miR-221 downregulation hallmarks metastasis and presents a novel prognostic marker in high risk PCa.
  • [MeSH-major] Biomarkers, Tumor / genetics. MicroRNAs / physiology. Neoplasm Recurrence, Local / diagnosis. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Cohort Studies. Computational Biology. Disease Progression. Humans. Lymphatic Metastasis. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prostatic Hyperplasia / genetics. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19585579.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MIRN221 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger
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74. Kosari F, Munz JM, Savci-Heijink CD, Spiro C, Klee EW, Kube DM, Tillmans L, Slezak J, Karnes RJ, Cheville JC, Vasmatzis G: Identification of prognostic biomarkers for prostate cancer. Clin Cancer Res; 2008 Mar 15;14(6):1734-43
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  • [Title] Identification of prognostic biomarkers for prostate cancer.
  • PURPOSE: This paper describes a process for the identification of genes that can report on the aggressiveness of prostate tumors and thereby add to the information provided by current pathologic analysis.
  • MATERIALS AND METHODS: Expression profiling data from over 100 laser capture microdissection derived samples from nonneoplastic epithelium; Gleason patterns 3, 4, and 5 and node metastasis prostate cancer were used to identify genes at abnormally high levels in only some tumors.
  • Selected genes were validated in a case-control study in which cases (systemic progression within 5 years) and controls (no systemic progression at 7 years of follow-up) were matched for all clinical and pathologic criteria from time of prostatectomy (n = 175).
  • RESULTS: A number of candidate variably overexpressed genes selected for their association with aggressive prostate cancer phenotype were evaluated in the case control study.
  • CONCLUSIONS: The process described here identified genes that add information not available from current clinical measures and can improve the prognosis of prostate cancer.
  • [MeSH-major] Biomarkers, Tumor / genetics. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Antigens, Neoplasm / genetics. Automatic Data Processing. Case-Control Studies. Cluster Analysis. DNA Topoisomerases, Type II / genetics. DNA-Binding Proteins / genetics. Follow-Up Studies. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Male. Neoplasm Invasiveness. Oligonucleotide Array Sequence Analysis. Prognosis. Prostatectomy. Receptors, Somatostatin / genetics

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  • (PMID = 18347174.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Receptors, Somatostatin; 0 / somatostatin receptor type 1; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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75. Chua CW, Chiu YT, Yuen HF, Chan KW, Man K, Wang X, Ling MT, Wong YC: Suppression of androgen-independent prostate cancer cell aggressiveness by FTY720: validating Runx2 as a potential antimetastatic drug screening platform. Clin Cancer Res; 2009 Jul 1;15(13):4322-35
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  • [Title] Suppression of androgen-independent prostate cancer cell aggressiveness by FTY720: validating Runx2 as a potential antimetastatic drug screening platform.
  • PURPOSE: Previously, FTY720 was found to possess potent anticancer effects on various types of cancer.
  • In the present study, we aimed to first verify the role of Runx2 in prostate cancer progression and metastasis, and, subsequently, assessed if FTY720 could modulate Runx2 expression, thus interfering downstream events regulated by this protein.
  • EXPERIMENTAL DESIGN: First, the association between Runx2 and prostate cancer progression was assessed using localized prostate cancer specimens and mechanistic investigation of Runx2-induced cancer aggressiveness was then carried out.
  • Last, the involvement of Runx2 in FTY720-induced anticancer effects was evaluated by modulating Runx2 expression in various prostate cancer cell lines.
  • RESULTS: Runx2 nuclear expression was found to be up-regulated in prostate cancer and its expression could be used as a predictor of metastasis in prostate cancer.
  • Further mechanistic studies indicated that Runx2 accelerated prostate cancer aggressiveness through promotion of cadherin switching, invasion toward collagen I, and Akt activation.
  • CONCLUSION: This study provided a novel mechanism for the anticancer effect of FTY720 on advanced prostate cancer, thus highlighting the therapeutic potential of this drug in treating this disease.
  • [MeSH-major] Core Binding Factor Alpha 1 Subunit / physiology. Drug Screening Assays, Antitumor / methods. Propylene Glycols / therapeutic use. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Sphingosine / analogs & derivatives
  • [MeSH-minor] Aged. Aged, 80 and over. Androgens / pharmacology. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Case-Control Studies. Down-Regulation / drug effects. Down-Regulation / genetics. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Fingolimod Hydrochloride. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Metastasis. Tumor Cells, Cultured

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  • (PMID = 19509141.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 1 Subunit; 0 / Propylene Glycols; 0 / RUNX2 protein, human; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine
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76. Fujii M, Abe K, Hayashi K, Kosuda S, Yano F, Watanabe S, Katagiri S, Ka WJ, Tominaga S: Honda sign and variants in patients suspected of having a sacral insufficiency fracture. Clin Nucl Med; 2005 Mar;30(3):165-9
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  • PURPOSE: The purpose of this study was to reassess whether the Honda sign (HS) and its variants on bone scans can be used to differentiate an insufficiency fracture (IF) of the sacrum from a metastasis and to evaluate extrapelvic tracer accumulation in patients suspected of having a sacral IF.
  • RESULTS: Twenty-four of the patients had a sacral IF and 1 had a sacral metastasis from prostate cancer and another from lung cancer.
  • One of the 2 patients with metastasis exhibited the HS and the other exhibited a variant.
  • The most common site was the pubic bone (50%, 12 of 24), and the second most common site was the spine (46%, 11 of 24), where the accumulation was the result of a compression fracture or degenerative joint disease of the spine.
  • CONCLUSIONS: A "Honda sign or variation" with evidence of fractures elsewhere or no evidence of other metastatic disease should be strong evidence for a sacral insufficiency fracture.
  • The likelihood of having a solitary metastasis to the sacrum is small.
  • [MeSH-major] Sacrum / injuries. Sacrum / radionuclide imaging. Spinal Fractures / radionuclide imaging. Spinal Neoplasms / radionuclide imaging. Spinal Neoplasms / secondary. Technetium Tc 99m Medronate
  • [MeSH-minor] Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Radiopharmaceuticals / pharmacokinetics. Reproducibility of Results. Retrospective Studies. Sensitivity and Specificity

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  • (PMID = 15722819.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; X89XV46R07 / Technetium Tc 99m Medronate
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77. Hövels AM, Heesakkers RA, Adang EM, Barentsz JO, Jager GJ, Severens JL: Cost-effectiveness of MR lymphography for the detection of lymph node metastases in patients with prostate cancer. Radiology; 2009 Sep;252(3):729-36
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  • [Title] Cost-effectiveness of MR lymphography for the detection of lymph node metastases in patients with prostate cancer.
  • PURPOSE: To apply a decision analytic model to determine whether the addition of magnetic resonance (MR) lymphography to the diagnostic workup of patients with intermediate or high probability of lymph node metastases is cost effective from a health care perspective.
  • Probabilistic sensitivity analysis showed that in 63% of simulations, MR lymphography was cost saving and resulted in better patient outcome for patients with prostate cancer and intermediate or high probability of lymph node metastases.
  • CONCLUSION: MR lymphography is an efficient strategy in the detection of lymph node metastases of prostate cancer when compared with the PLND strategy.
  • [MeSH-major] Lymphatic Metastasis / pathology. Magnetic Resonance Imaging / economics. Prostatic Neoplasms / pathology

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  • (PMID = 19717752.001).
  • [ISSN] 1527-1315
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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78. Ananias HJ, van den Heuvel MC, Helfrich W, de Jong IJ: Expression of the gastrin-releasing peptide receptor, the prostate stem cell antigen and the prostate-specific membrane antigen in lymph node and bone metastases of prostate cancer. Prostate; 2009 Jul 1;69(10):1101-8
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  • [Title] Expression of the gastrin-releasing peptide receptor, the prostate stem cell antigen and the prostate-specific membrane antigen in lymph node and bone metastases of prostate cancer.
  • OBJECTIVE: Cell membrane antigens like the gastrin-releasing peptide receptor (GRPR), the prostate stem cell antigen (PSCA), and the prostate-specific membrane antigen (PSMA), expressed in prostate cancer, are attractive targets for new therapeutic and diagnostic applications.
  • Therefore, we investigated in this study whether these antigens are expressed in metastasized prostate cancer.
  • METHODS: Formalin-fixed, paraffin-embedded specimens of 15 patients with uni- or bilateral lymph node metastases of prostate cancer (totaling 21 cases) and 17 patient-cases of bone metastases were processed for immunohistochemistry with anti-GRPR, anti-PSCA, and anti-PSMA antibodies.
  • RESULTS: GRPR staining in lymph node metastases was seen in 85.7% of cases (18 of 21 cases), PSCA in 95.2% (20/21), and PSMA in 100% (21/21).
  • GRPR in bone metastases was seen in 52.9% of cases (9/17), PSCA in 94.1% (16/17), and PSMA in 100% (17/17).
  • CONCLUSION: We have shown for the first time that GRPR is expressed in the vast majority of lymph node metastases and in 52.9% of bone metastases of prostate cancer.
  • PSCA and PSMA are both highly expressed in lymph node and bone metastases.
  • Although PSCA and PSMA are mostly expressed in prostate cancer metastases, GRPR offers an interesting alternative target as it can be targeted relatively easy with peptide-based (radio)pharmaceuticals.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Antigens, Surface / biosynthesis. Bone Neoplasms / metabolism. Bone Neoplasms / secondary. Glutamate Carboxypeptidase II / biosynthesis. Membrane Glycoproteins / biosynthesis. Neoplasm Proteins / biosynthesis. Prostatic Neoplasms / metabolism. Receptors, Bombesin / biosynthesis
  • [MeSH-minor] Biomarkers, Tumor / biosynthesis. GPI-Linked Proteins. Gene Expression Regulation, Neoplastic / physiology. Humans. Lymph Nodes / metabolism. Lymph Nodes / pathology. Lymphatic Metastasis. Male. Retrospective Studies

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19343734.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antigens, Surface; 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / PSCA protein, human; 0 / Receptors, Bombesin; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
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79. Zhao P, Luo R, Wu J, Xie F, Li H, Xiao X, Fu L, Zhu X, Liu R, Zhu Y, Liang Z, Huang W: E10A, an adenovirus carrying human endostatin gene, in combination with docetaxel treatment inhibits prostate cancer growth and metastases. J Cell Mol Med; 2010 Jan;14(1-2):381-91
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  • [Title] E10A, an adenovirus carrying human endostatin gene, in combination with docetaxel treatment inhibits prostate cancer growth and metastases.
  • We assessed whether the combination of E10A with docetaxel would enhance antiangiogenic activities and inhibit prostate cancer growth and metastases.
  • Combination use of conditioned medium from prostate cancer cells infected by E10A and docetaxel exerted synergistic inhibition of HUVECs proliferation, migration and tube formation, compared with either agent alone.
  • In prostate cancer s.c. xenograft models, combined therapy resulted in significant tumor growth inhibition and survival improvement.
  • The antitumoral effect was tightly correlated with a remarkable decrease in tumor cell proliferation, microvessel, especially immature vasculature and significant increase in apoptosis induction.
  • Systemic administration of E10A and docetaxel also effectively inhibited orthotopic growth and metastases of prostate cancer and achieved better in vivo antiangiogenic effects than either agent alone.
  • Our data indicate that E10A in combination with docetaxel exert enhanced antiangiogenic activities and inhibit prostate cancer growth and metastases.
  • Therefore, this approach may be an effective treatment for advanced prostate cancer and deserves more extensive investigation.
  • [MeSH-minor] Adenoviridae / genetics. Animals. Apoptosis. Cell Line, Tumor. Cell Proliferation. Combined Modality Therapy. Genetic Vectors. Human Umbilical Vein Endothelial Cells. Humans. Male. Mice. Mice, Nude. Neoplasm Metastasis / therapy. Xenograft Model Antitumor Assays

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  • [Cites] J Clin Oncol. 2002 Sep 15;20(18):3792-803 [12228199.001]
  • [Cites] Cancer Res. 2002 Oct 15;62(20):5720-6 [12384530.001]
  • [Cites] FASEB J. 2002 Nov;16(13):1802-4 [12354694.001]
  • [Cites] Mol Cancer Ther. 2002 Nov;1(13):1191-200 [12479700.001]
  • [Cites] Int J Cancer. 2003 Mar 10;104(1):121-9 [12532428.001]
  • [Cites] Clin Cancer Res. 2003 Oct 1;9(12):4619-26 [14555538.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8890-8 [14695206.001]
  • [Cites] Cancer Cell. 2004 Jan;5(1):13-7 [14749122.001]
  • [Cites] Nat Rev Cancer. 2004 Jun;4(6):423-36 [15170445.001]
  • [Cites] World J Gastroenterol. 2004 Jul 1;10(13):1867-71 [15222025.001]
  • [Cites] Pharmacol Rev. 1989 Jun;41(2):93-141 [2692037.001]
  • [Cites] J Natl Cancer Inst. 1992 Jun 17;84(12):951-7 [1378502.001]
  • [Cites] Cell. 1997 Jan 24;88(2):277-85 [9008168.001]
  • [Cites] Cancer Res. 1997 Sep 1;57(17):3847-51 [9288798.001]
  • [Cites] Nature. 1998 Jul 16;394(6690):287-91 [9685160.001]
  • [Cites] Clin Cancer Res. 1996 Nov;2(11):1843-9 [9816139.001]
  • [Cites] APMIS. 2004 Jul-Aug;112(7-8):496-507 [15563312.001]
  • [Cites] J Biol Chem. 2002 Aug 2;277(31):27872-9 [12029087.001]
  • [Cites] Cancer Res. 2002 Feb 1;62(3):789-95 [11830534.001]
  • [Cites] Nat Med. 2001 Sep;7(9):987-9 [11533692.001]
  • [Cites] Nature. 2000 Sep 14;407(6801):249-57 [11001068.001]
  • [Cites] Prostate. 2000 Sep 15;45(1):72-9 [10960845.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4802-7 [10758166.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):553-63 [15607960.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Gene Ther. 2008 Feb;15(4):247-56 [18097470.001]
  • [Cites] Cancer Biol Ther. 2007 May;6(5):648-53 [17426445.001]
  • [Cites] J Cell Mol Med. 2007 May-Jun;11(3):374-82 [17635633.001]
  • [Cites] Adv Cancer Res. 2007;97:203-24 [17419947.001]
  • [Cites] Hum Gene Ther. 2007 Mar;18(3):207-21 [17346097.001]
  • [Cites] Clin Cancer Res. 2006 Aug 1;12(15):4702-13 [16899621.001]
  • [Cites] Hepatology. 2005 Apr;41(4):879-86 [15739185.001]
  • [Cites] Lancet Oncol. 2005 Apr;6(4):229-39 [15811618.001]
  • [Cites] Clin Cancer Res. 2005 Jun 1;11(11):4217-24 [15930360.001]
  • [Cites] Clin Exp Metastasis. 2005;22(1):31-8 [16132576.001]
  • [Cites] Nat Rev Cancer. 2005 Sep;5(9):735-43 [16079909.001]
  • [Cites] CA Cancer J Clin. 2005 Sep-Oct;55(5):300-18; quiz 323-5 [16166075.001]
  • [Cites] Mol Ther. 2005 Dec;12(6):1091-100 [16169279.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):11044-50 [16322254.001]
  • [Cites] J Cell Mol Med. 2005 Oct-Dec;9(4):777-94 [16364190.001]
  • [Cites] Int J Cancer. 2006 Apr 15;118(8):2064-71 [16287067.001]
  • [Cites] Lancet Oncol. 2006 Mar;7(3):199 [16538782.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):4319-28 [16618757.001]
  • [Cites] Gastroenterology. 2006 Apr;130(4):1301-10 [16618420.001]
  • [Cites] Science. 2006 May 26;312(5777):1171-5 [16728631.001]
  • (PMID = 26065034.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Endostatins; 0 / Taxoids; 15H5577CQD / docetaxel
  • [Other-IDs] NLM/ PMC3837610
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80. Maeda T, Tateishi U, Komiyama M, Fujimoto H, Watanabe S, Terauchi T, Moriyama N, Arai Y, Sugimura K, Kakizoe T: Distant metastasis of prostate cancer: early detection of recurrent tumor with dual-phase carbon-11 choline positron emission tomography/computed tomography in two cases. Jpn J Clin Oncol; 2006 Sep;36(9):598-601
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  • [Title] Distant metastasis of prostate cancer: early detection of recurrent tumor with dual-phase carbon-11 choline positron emission tomography/computed tomography in two cases.
  • Several types of recurrence may be detected by radiologic assessment after treatment in patients with prostate cancer.
  • However, early detection of distant metastasis using positron emission tomography has so far never been published.
  • We report two patients who underwent hormone therapy or surgical resection for prostate cancer.
  • They developed distant metastases which were detected on whole body [C-11] choline positron emission tomography/computed tomography with significant elevation of serum PSA level.
  • In one patient, recurrent tumor of the supraclavicular node (6 mm) diminished in size after subsequent hormone therapy.
  • Surgical resection of recurrent tumor of the lung (12 mm) was performed in the other patient, the pathology of which confirmed the metastatic adenocarcinoma derived from the prostate.
  • The recurrent tumor can be correctly detected by dual-phase whole body [C-11] choline positron emission tomography/computed tomography.
  • [MeSH-major] Adenocarcinoma / secondary. Lung Neoplasms / radionuclide imaging. Lymph Nodes / pathology. Lymphatic Metastasis / radionuclide imaging. Pelvic Neoplasms / radionuclide imaging. Positron-Emission Tomography. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Antineoplastic Agents, Hormonal / therapeutic use. Carbon Radioisotopes. Choline. Early Diagnosis. Humans. Male. Prostate-Specific Antigen / blood. Tomography, X-Ray Computed

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  • (PMID = 16844733.001).
  • [ISSN] 0368-2811
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Carbon Radioisotopes; EC 3.4.21.77 / Prostate-Specific Antigen; N91BDP6H0X / Choline
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81. Kim HS, Sung W, Lee S, Chang SG, Park YK: Lymphatic vessel densities of lymph node-negative prostate adenocarcinoma in Korea. Pathol Res Pract; 2009;205(4):249-54
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  • [Title] Lymphatic vessel densities of lymph node-negative prostate adenocarcinoma in Korea.
  • Although lymphatic vessel density (LVD) is associated with regional lymph node (LN) metastasis in prostate adenocarcinoma, no study is available that examines whether the LVD is correlated with prognostic factors other than LN metastasis in LN-negative prostate adenocarcinoma.
  • The aim of our study was to analyze intratumoral (IT), peritumoral (PT), and nontumoral (NT) LVDs, and to determine if there is a correlation between the LVD and the clinicopathological parameters in the Korean LN-negative prostate adenocarcinoma patients.
  • The IT-LVD was significantly lower in patients with larger tumor volume (P=0.029) and higher preoperative prostate-specific antigen level (P=0.008).
  • Our results suggest that IT- and PT-LVDs may increase in LN-negative prostate adenocarcinoma as a result of lymphangiogenesis, but IT lymphatics may decrease due to mechanical compression and destruction caused by proliferating tumor cells.
  • In addition, IT-LVD may be used as a prognostic factor in LN-negative prostate adenocarcinoma.
  • [MeSH-minor] Aged. Humans. Immunohistochemistry. Korea. Lymph Nodes / pathology. Male. Middle Aged. Prognosis. Prostate-Specific Antigen / blood

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  • (PMID = 19058917.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
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82. Slavine NV, Antich PP: Practical method for radioactivity distribution analysis in small-animal PET cancer studies. Appl Radiat Isot; 2008 Dec;66(12):1861-9
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  • [Title] Practical method for radioactivity distribution analysis in small-animal PET cancer studies.
  • We demonstrate reconstruction results for the amount of radioactivity within the scanned mouse in a sample study of osteolytic and osteoblastic bone metastasis from prostate cancer xenografts.
  • Our method uses high-resolution images to determine the volume of organ or tumor and the amount of their radioactivity has the possibility of saving time, effort and the necessity to sacrifice animals.
  • This method has utility for prognosis and quantitative analysis in small-animal cancer studies, and will enhance the assessment of characteristics of tumor growth, identifying metastases, and potentially determining the effectiveness of cancer treatment.

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  • [Cites] J Nucl Med. 2006 Jan;47(1):113-21 [16391195.001]
  • [Cites] Med Phys. 2006 Jan;33(1):61-8 [16485410.001]
  • [Cites] J Nucl Med. 2006 Mar;47(3):393-403 [16513607.001]
  • [Cites] J Nucl Med. 2006 Jul;47(7):1181-6 [16818953.001]
  • [Cites] Phys Med Biol. 2006 Aug 7;51(15):R541-78 [16861768.001]
  • [Cites] Clin Cancer Res. 2006 Oct 15;12(20 Pt 2):6213s-6216s [17062703.001]
  • [Cites] Phys Med Biol. 2008 Feb 7;53(3):719-36 [18199911.001]
  • [Cites] Clin Cancer Res. 2008 Mar 1;14(5):1377-85 [18316558.001]
  • [Cites] J Nucl Med. 2004 Sep;45(9):1519-27 [15347719.001]
  • [Cites] J Nucl Med. 2008 Mar;49(3):347-53 [18287260.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1655-64 [15084698.001]
  • [Cites] J Nucl Med. 2004 Feb;45(2):192-201 [14960635.001]
  • [Cites] J Cell Biochem. 2004 Feb 15;91(3):528-39 [14755683.001]
  • [Cites] Clin Exp Metastasis. 2003;20(2):171-80 [12705638.001]
  • [Cites] J Nucl Med. 2003 Mar;44(3):341-6 [12620998.001]
  • [Cites] IEEE Trans Med Imaging. 2001 Aug;20(8):804-14 [11513031.001]
  • [Cites] Comput Med Imaging Graph. 2001 Mar-Apr;25(2):105-11 [11137786.001]
  • [Cites] Nucl Med Biol. 2000 Oct;27(7):643-6 [11091106.001]
  • [Cites] J Nucl Med. 2000 Oct;41(10):1664-72 [11037996.001]
  • [Cites] J Clin Pharmacol. 2000 Jul;40(7):770-80 [10883419.001]
  • [Cites] Prostate. 2000 Jun 1;43(4):263-71 [10861745.001]
  • [Cites] J Immunol. 2004 Jun 15;172(12):7694-702 [15187152.001]
  • [Cites] AJR Am J Roentgenol. 2004 Oct;183(4):1127-32 [15385319.001]
  • [Cites] Phys Med Biol. 1984 Nov;29(11):1421-31 [6334321.001]
  • [Cites] J Nucl Med. 1988 Sep;29(9):1603-4 [3261788.001]
  • [Cites] Phys Med Biol. 1992 May;37(5):1065-76 [1608996.001]
  • [Cites] J Nucl Med. 1995 Oct;36(10):1836-9 [7562051.001]
  • [Cites] Prostate. 1997 Jun 1;31(4):264-81 [9180937.001]
  • [Cites] Int J Cancer. 1998 Sep 11;77(6):887-94 [9714059.001]
  • [Cites] Cancer Res. 2005 Feb 1;65(3):967-71 [15705897.001]
  • [Cites] Clin Cancer Res. 2005 Jun 1;11(11):4022-8 [15930336.001]
  • [Cites] Cancer Biother Radiopharm. 2005 Jun;20(3):310-5 [15989476.001]
  • [Cites] Appl Radiat Isot. 2005 Sep;63(3):343-51 [15955705.001]
  • [Cites] Invest New Drugs. 2005 Oct;23(5):429-36 [16133794.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7554-60 [16140917.001]
  • [Cites] J Nucl Med. 2005 Oct;46(10):1707-18 [16204722.001]
  • (PMID = 18667322.001).
  • [ISSN] 1872-9800
  • [Journal-full-title] Applied radiation and isotopes : including data, instrumentation and methods for use in agriculture, industry and medicine
  • [ISO-abbreviation] Appl Radiat Isot
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U24 CA126608; None / None / / U24 CA126608-02; United States / NCI NIH HHS / CA / U24 CA126608-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
  • [Other-IDs] NLM/ NIHMS77452; NLM/ PMC2644068
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83. Williams SA, Singh P, Isaacs JT, Denmeade SR: Does PSA play a role as a promoting agent during the initiation and/or progression of prostate cancer? Prostate; 2007 Feb 15;67(3):312-29
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does PSA play a role as a promoting agent during the initiation and/or progression of prostate cancer?
  • Prostate cancer cells, like normal prostate epithelial cells, produce high levels of the differentiation marker and serine protease prostate-specific antigen (PSA).
  • PSA is used extensively as a biomarker to screen for prostate cancer, to detect recurrence following local therapies, and to follow response to systemic therapies for metastatic disease.
  • While much is known about PSA's role as a biomarker, only a relatively few studies address the role played by PSA in the pathobiology of prostate cancer.
  • Autopsy studies have documented that not only do prostate cancer cells maintain production of high amounts of PSA but they also maintain the enzymatic machinery required to process PSA to an enzymatically active form.
  • A variety studies performed over the last 10 years have hinted at a role for PSA in growth, progression, and metastases of prostate cancer.
  • A fuller understanding of PSA's functional role in prostate cancer biology, however, has been hampered by the lack of appropriate models and tools.
  • Instead, by reviewing what is known about the genetics, biochemistry, and biology of PSA in normal and malignant prostate tissue, insights may be gained into the role PSA may be playing in the pathobiology of prostate cancer that can connect measurement of this biomarker to an understanding of the underlying etiology and progression of the disease.
  • [MeSH-major] Neoplasms, Hormone-Dependent / enzymology. Prostate-Specific Antigen / metabolism. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Animals. Bone Neoplasms / metabolism. Bone Neoplasms / secondary. Enzyme Activation. Humans. Male. Middle Aged. Models, Molecular



84. Lamoureux F, Ory B, Battaglia S, Pilet P, Heymann MF, Gouin F, Duteille F, Heymann D, Redini F: Relevance of a new rat model of osteoblastic metastases from prostate carcinoma for preclinical studies using zoledronic acid. Int J Cancer; 2008 Feb 15;122(4):751-60
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  • [Title] Relevance of a new rat model of osteoblastic metastases from prostate carcinoma for preclinical studies using zoledronic acid.
  • Animal models that mimic osteoblastic metastases associated with prostate carcinoma are required to improve the therapeutic options in humans.
  • Rat AT6-1 prostate tumor cells were characterized in vitro at the transcriptional (bone and epithelial markers) and functional (induction of mineralized nodules) levels.
  • The tumor itself is associated with bone formation as revealed by SEM analysis and polarized light microscopy.
  • ZOL prevents the development of such osteoblastic lesions, related to a direct inhibitory effect on tumor cell proliferation independent of caspase 3 activation, but associated with cell cycle arrest.
  • A new rat model of osteoblastic bone metastases was validated in immunocompetent rats and used to show the relevance of using ZOL in such lesions, as this compound shows bifunctional effects on both bone remodelling and tumor cell proliferation.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Bone Marrow Cells / drug effects. Bone Remodeling / drug effects. Cell Cycle / drug effects. Cell Proliferation / drug effects. Humans. Male. Mice. Mice, Inbred C3H. Osteoblasts / drug effects. Osteoblasts / metabolism. Osteogenesis / drug effects. Rats. Rats, Sprague-Dawley. Tumor Cells, Cultured / drug effects

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17960623.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
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85. Lerner I, Baraz L, Pikarsky E, Meirovitz A, Edovitsky E, Peretz T, Vlodavsky I, Elkin M: Function of heparanase in prostate tumorigenesis: potential for therapy. Clin Cancer Res; 2008 Feb 1;14(3):668-76
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  • [Title] Function of heparanase in prostate tumorigenesis: potential for therapy.
  • Whereas the role of heparanase in sustaining the pathology of human cancer is well documented, its association with prostate carcinoma remains uncertain.
  • Our research was undertaken to elucidate the significance of heparanase in prostate tumorigenesis and bone metastasis.
  • EXPERIMENTAL DESIGN: We applied immunohistochemical analysis of tissue microarray, in vitro adhesion and invasion assays, as well as mouse models of intraosseous growth and spontaneous metastasis of prostate cancer, monitored by whole-body bioluminescent imaging.
  • RESULTS: We report a highly statistically significant (P < 0.0001) prevalence of heparanase overexpression in prostate carcinomas versus noncancerous tissue, as well as strong correlation between tumor grade and the extent of heparanase expression.
  • We observed >5-fold increase in the metastatic potential of PC-3 prostate carcinoma cells engineered to overexpress heparanase.
  • Notably, overexpression of a secreted form of the enzyme also led to a dramatic increase in intraosseous prostate tumor growth.
  • Local in vivo silencing of heparanase resulted in a 4-fold inhibition of prostate tumor growth, representing the first successful application of anticancer therapy based on heparanase small interfering RNA and validating the potential of heparanase as a target for prostate cancer treatment.
  • CONCLUSIONS: Heparanase directly contributes to prostate tumor growth in bone and its ability to metastasize to distant organs.
  • Thus, anti-heparanase strategy may become an important modality in the treatment of prostate cancer patients, particularly those with bone metastases.
  • [MeSH-minor] Biopsy. Bone Neoplasms / enzymology. Bone Neoplasms / pathology. Bone Neoplasms / secondary. Cell Adhesion. Cell Division. Cell Line, Tumor. Cloning, Molecular. Collagen. Drug Combinations. Gene Expression Regulation, Neoplastic. Humans. Laminin. Male. Neoplasm Invasiveness. Oligonucleotide Array Sequence Analysis. Prostate / enzymology. Proteoglycans. Reference Values. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 18212251.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106456-01
  • [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 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
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86. Shiraishi J, Li Q, Appelbaum D, Pu Y, Doi K: Development of a computer-aided diagnostic scheme for detection of interval changes in successive whole-body bone scans. Med Phys; 2007 Jan;34(1):25-36
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  • [Title] Development of a computer-aided diagnostic scheme for detection of interval changes in successive whole-body bone scans.
  • It is a well-established imaging modality for the diagnosis of osseous metastasis and for monitoring osseous tumor response to chemotherapy and radiation therapy.
  • Although the sensitivity of bone scan examinations for detection of bone abnormalities has been considered to be relatively high, it is time consuming to identify multiple lesions such as bone metastases of prostate and breast cancers.
  • Therefore, we developed a new computer-aided diagnostic (CAD) scheme for the detection of interval changes in successive whole-body bone scans by use of a temporal subtraction image which was obtained with a nonlinear image-warping technique.

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  • (PMID = 17278486.001).
  • [ISSN] 0094-2405
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA62625; United States / NCI NIH HHS / CA / CA98119
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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87. Varghese S, Rabkin SD, Nielsen PG, Wang W, Martuza RL: Systemic oncolytic herpes virus therapy of poorly immunogenic prostate cancer metastatic to lung. Clin Cancer Res; 2006 May 1;12(9):2919-27
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  • [Title] Systemic oncolytic herpes virus therapy of poorly immunogenic prostate cancer metastatic to lung.
  • PURPOSE: Our goal was to evaluate whether systemic administration of NV1042, an interleukin-12 (IL-12)-expressing oncolytic herpes simplex virus, and its noncytokine parental vector NV1023 are effective against preexisting metastatic prostate cancer in an immunocompetent mice model.
  • EXPERIMENTAL DESIGN: Metastatic TRAMP-C2 lung tumors established in C57Bl/6 or nude mice were treated on day 21 with four i.v. administrations of NV1042 or NV1023 and sacrificed on day 42 to assess virus efficacy and the potential mechanism of efficacy.
  • However, NV1042 was further effective compared with NV1023 in controlling the growth of lung tumors (as determined by mean surface tumor nodule number, lung weights, and surface tumor burden) and in extending survival.
  • NV1042-treated mice exhibited a transient increase of serum IL-12 1 day posttreatment, whereas IL-12 levels in tumor bearing lungs persisted a further 2 days at least.
  • The IL-12-mediated enhancement observed with NV1042 in the syngeneic model was abrogated in athymic mice treated in a similar manner, thus indicating a role for T cells in the augmented efficacy of NV1042 virus.
  • CONCLUSIONS: Systemic administration of the IL-12-expressing NV1042 virus is more effective than its noncytokine parent, NV1023, against preestablished metastatic lung tumors.
  • Given the clinical safety profile of NV1020, the parental vector of NV1023, and NV1042's enhanced efficacy and ability to activate the host immune system, NV1042 merits clinical consideration for treating metastatic prostate cancers.
  • [MeSH-major] Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Oncolytic Virotherapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Animals. Cell Line, Tumor. Male. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Organ Size / drug effects

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  • (PMID = 16675589.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA102139
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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88. Walz J, Chun FK, Klein EA, Reuther A, Saad F, Graefen M, Huland H, Karakiewicz PI: Nomogram predicting the probability of early recurrence after radical prostatectomy for prostate cancer. J Urol; 2009 Feb;181(2):601-7; discussion 607-8
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  • [Title] Nomogram predicting the probability of early recurrence after radical prostatectomy for prostate cancer.
  • PURPOSE: We developed a nomogram predicting the probability of early biochemical recurrence after radical prostatectomy because early recurrence predisposes to distant metastasis and prostate cancer related mortality.
  • MATERIALS AND METHODS: From January 1992 to December 2005, 2,911 patients underwent radical prostatectomy for localized prostate cancer.
  • Age, prostate specific antigen, pathological Gleason sum, surgical margin, extracapsular extension, seminal vesicle invasion and lymph node invasion were considered.
  • [MeSH-major] Neoplasm Recurrence, Local / pathology. Nomograms. Prostatectomy / methods. Prostatic Neoplasms / pathology. Prostatic Neoplasms / surgery
  • [MeSH-minor] Age Factors. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Predictive Value of Tests. Probability. Prognosis. Proportional Hazards Models. Retrospective Studies. Risk Assessment. Sensitivity and Specificity. Survival Analysis. Time Factors