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1. Hofer MD, Fecko A, Shen R, Setlur SR, Pienta KG, Tomlins SA, Chinnaiyan AM, Rubin MA: Expression of the platelet-derived growth factor receptor in prostate cancer and treatment implications with tyrosine kinase inhibitors. Neoplasia; 2004 Sep-Oct;6(5):503-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of the platelet-derived growth factor receptor in prostate cancer and treatment implications with tyrosine kinase inhibitors.
  • The platelet-derived growth factor receptor (PDGFR) is a receptor tyrosine kinase overexpressed in a subset of solid tumors and therefore is the target of drugs inhibiting this function such as imatinib mesylate (Gleevec).
  • Thus far, drug therapy has played a limited role in the treatment of localized prostate cancer (PCa).
  • This study characterizes PDGFR-beta expression in a wide spectrum of PCa samples to provide empirical data as part of a rational treatment strategy.
  • A survey of five published prostate expression array studies, including 100 clinically localized PCa, did not identify tumors with increased PDGFR-beta expression level.
  • Protein expression of PDGFR-beta, as determined by immunohistochemistry, revealed 5% of clinically localized PCa and 16% of metastatic PCa cases to show moderate or strong expression.
  • To develop a strategy to detect patients most likely to profit from Gleevec treatment, we analyzed cDNA expression array data from 10,000 transcripts for PDGFR-beta expression and divided tumors in groups based on PDGFR-beta expression level.
  • Performing a supervised analysis to identify potential comarkers of PDGFR-beta in PCa, we identified a set of genes whose expression was associated with PDGFR-beta status including early growth response 1 (Egr1), an upstream effector of PDGF (4.2-fold upregulation), alpha-methylacyl-CoA racemase, as well as v-Maf and neuroblastoma suppressor of tumorigenicity (both with a 2.2-fold downregulation).

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  • [Cites] Nat Med. 1998 Jul;4(7):844-7 [9662379.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1052-6 [11287975.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Cancer Res. 2001 Aug 1;61(15):5692-6 [11479199.001]
  • [Cites] Cancer Res. 2001 Aug 15;61(16):5974-8 [11507037.001]
  • [Cites] Nature. 2001 Aug 23;412(6849):822-6 [11518967.001]
  • [Cites] Lancet. 2001 Oct 27;358(9291):1421-3 [11705489.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15149-54 [11742071.001]
  • [Cites] Mol Carcinog. 2002 Jan;33(1):25-35 [11807955.001]
  • [Cites] JAMA. 2002 Apr 3;287(13):1662-70 [11926890.001]
  • [Cites] Am J Pathol. 2002 Jun;160(6):2169-80 [12057920.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):203-9 [12086878.001]
  • [Cites] Am J Surg Pathol. 2002 Jul;26(7):926-31 [12131161.001]
  • [Cites] Cancer Res. 2002 Aug 1;62(15):4427-33 [12154050.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):472-80 [12181401.001]
  • [Cites] Am J Pathol. 2002 Sep;161(3):841-8 [12213712.001]
  • [Cites] Urology. 2002 Sep;60(3 Suppl 1):115-21; discussion 122 [12231066.001]
  • [Cites] J Biol Chem. 2002 Oct 4;277(40):37929-35 [12151388.001]
  • [Cites] Clin Cancer Res. 2002 Oct;8(10):3034-8 [12374669.001]
  • [Cites] Nature. 2002 Oct 10;419(6907):624-9 [12374981.001]
  • [Cites] Am J Pathol. 2002 Nov;161(5):1743-8 [12414521.001]
  • [Cites] CA Cancer J Clin. 2003 Jan-Feb;53(1):5-26 [12568441.001]
  • [Cites] EMBO J. 1992 Nov;11(11):3911-9 [1396585.001]
  • [Cites] EMBO J. 1993 Jun;12(6):2257-64 [7685273.001]
  • [Cites] Adv Second Messenger Phosphoprotein Res. 1993;28:187-94 [8398402.001]
  • [Cites] Oncogene. 1994 Feb;9(2):651-60 [8290276.001]
  • [Cites] Nature. 1994 Aug 18;370(6490):527-32 [8052307.001]
  • [Cites] Curr Biol. 1994 May 1;4(5):385-93 [7922352.001]
  • [Cites] Mol Cell Biol. 1994 Oct;14(10):6715-26 [7935391.001]
  • [Cites] J Biol Chem. 1994 Dec 23;269(51):32023-6 [7798193.001]
  • [Cites] Prostate. 1996 Nov;29(5):282-6 [8899000.001]
  • [Cites] Science. 1997 Jul 11;277(5323):242-5 [9211853.001]
  • [Cites] Nat Genet. 1998 Apr;18(4):385-8 [9537425.001]
  • [Cites] Cancer Res. 1998 Jun 1;58(11):2461-8 [9622090.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] Am J Pathol. 1999 Oct;155(4):1271-9 [10514409.001]
  • [Cites] Semin Urol Oncol. 1999 Nov;17(4):222-72 [10632123.001]
  • [Cites] Br J Cancer. 2000 Mar;82(6):1123-30 [10735494.001]
  • [Cites] J Natl Cancer Inst. 2000 Jun 7;92(11):937-9 [10841830.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] Clin Cancer Res. 2001 Apr;7(4):800-5 [11309325.001]
  • (PMID = 15548358.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA090381; United States / NCI NIH HHS / CA / CA 97063; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / P50CA90381; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / R01 CA097063
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Platelet-Derived Growth Factor; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Other-IDs] NLM/ PMC1531653
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2. Friedrich RE, Blake FA: Avascular mandibular osteonecrosis in association with bisphosphonate therapy: a report on four patients. Anticancer Res; 2007 Jul-Aug;27(4A):1841-5
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  • [Title] Avascular mandibular osteonecrosis in association with bisphosphonate therapy: a report on four patients.
  • These drugs are used for the treatment of multiple myeloma, bone resorption in the case of metastatic malignant diseases, tumor-associated hypercalcaemia, and in the treatment of osteoporosis.
  • These osteonecroses did not react adequately to local treatment and systemic therapy with antibiotics.
  • One patient suffered from non-Hodgkin's lymphoma, one from breast cancer, one from prostate cancer and one from sarcoidosis.
  • DISCUSSION: Bisphosphonates are considered an established standard in the treatment of multiple myeloma and bone metastases.
  • Over the past few years, a rapidly increasing number of reports have been published describing patients with a history of bisphosphonate therapy in whom therapy-resistant osteonecrosis of jaw bones occurred either after dental extractions or spontaneously.
  • Since then, bisphosphonate therapy has come under scrutiny as a cause of osteonecrosis.
  • However, the multiplicity of drugs prescribed for the treatment of cancer requires caution when determining a cause-and-action effect.
  • Since patients with malignant diseases receive cytostatic therapy and a range of other drugs, including bisphosphonates, enhancement of the side-effects may be presumed.
  • The case report of an osteonecrosis of the jaw following multi-drug therapy for sarcoidosis adds a further and non-cancerous condition to the newly described entity of bisphosphonate-associated jaw necrosis.
  • CONCLUSION: The probable association of the therapeutic use of bisphosphonates and the development of jaw necrosis has to be studied in further investigations.
  • Patients who will undergo bisphosphonate therapy should receive a careful dental check-up prior to drug application.
  • Moreover, established jaw lesions must be diagnosed precisely in order to exclude metastatic disease.
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Breast Neoplasms / drug therapy. Female. Humans. Lymphoma, Non-Hodgkin / drug therapy. Male. Middle Aged. Prostatic Neoplasms / drug therapy. Sarcoidosis / drug therapy

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  • (PMID = 17649782.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bone Density Conservation Agents; 0 / Diphosphonates
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3. Bouchet LG, Bolch WE, Goddu SM, Howell RW, Rao DV: Considerations in the selection of radiopharmaceuticals for palliation of bone pain from metastatic osseous lesions. J Nucl Med; 2000 Apr;41(4):682-7
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  • [Title] Considerations in the selection of radiopharmaceuticals for palliation of bone pain from metastatic osseous lesions.
  • Bone pain is a common complication for terminal patients with bone metastases from prostate, lung, breast, and other malignancies.
  • A multidisciplinary approach in treating bone pain is generally required, 1 which includes a combination of analgesic drug therapy, radiation therapy, hormonal therapy, and chemotherapy.
  • Over the years, treatment of bone pain using bone-seeking radiopharmaceuticals has been explored extensively.
  • Bone-marrow toxicity as a consequence of chronic irradiation by the energetic , particles is a general problem associated with this form of treatment.
  • It is therefore desirable to identify radiochemicals that minimize the dose to the bone marrow and at the same time deliver therapeutic doses to the bone.
  • The relative dosimetric advantage of a given radiopharmaceutical compared with a reference radiochemical was quantitated as a dosimetric relative advantage factor (RAF).
  • CONCLUSION: These results suggest that low-energy electron emitters such as 117mSn and 33P are more likely to deliver a therapeutic dose to the bone while sparing the bone marrow than are energetic beta emitters such as 32p and 89Sr.
  • Therefore, radiochemicals tagged with low-energy electron or beta emitters are the radiopharmaceuticals of choice for treatment of painful metastatic disease in bone.
  • [MeSH-major] Bone Neoplasms / radiotherapy. Bone Neoplasms / secondary. Palliative Care. Radiopharmaceuticals / therapeutic use
  • [MeSH-minor] Bone Marrow / radiation effects. Humans. Pain, Intractable. Phosphorus Radioisotopes / therapeutic use. Radioisotopes / therapeutic use. Radiotherapy Dosage. Tin / therapeutic use

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  • [CommentIn] J Nucl Med. 2000 Apr;41(4):688-91 [10768570.001]
  • (PMID = 10768569.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-32877
  • [Publication-type] Journal Article; 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 / Phosphorus Radioisotopes; 0 / Radioisotopes; 0 / Radiopharmaceuticals; 7440-31-5 / Tin
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4. Eastham JA: Bone health in men receiving androgen deprivation therapy for prostate cancer. J Urol; 2007 Jan;177(1):17-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone health in men receiving androgen deprivation therapy for prostate cancer.
  • PURPOSE: Patients with recurrent or metastatic prostate cancer generally receive androgen deprivation therapy, which can result in significant loss of bone mineral density.
  • We explored androgen deprivation therapy related bone loss in prostate cancer, current treatments and emerging therapies.
  • MATERIALS AND METHODS: Literature published on the pathogenesis and management of androgen deprivation therapy related bone loss was compiled and interpreted.
  • Recent drug therapy findings were reviewed, including treatment guidelines.
  • RESULTS: Men with prostate cancer often present with bone loss and the initiation of androgen deprivation therapy can trigger further rapid decreases.
  • Early detection of osteoporosis through androgen deprivation therapy screening and prompt initiation of therapy are critical to prevent continued decreases.
  • Pharmacological therapy with oral and intravenous bisphosphonates has been demonstrated to prevent or decrease the bone loss associated with androgen deprivation therapy.
  • Only zoledronic acid has been shown to increase bone mineral density above baseline and provide long-term benefit by decreasing the incidence of fracture and other skeletal related events in men with bone metastases.
  • CONCLUSIONS: Androgen deprivation therapy associated bone loss adversely affects bone health, patient quality of life and survival in men with prostate cancer.
  • Increased awareness of this issue, identification of risk factors, lifestyle modification and initiation of bisphosphonate therapy can improve outcomes.
  • Education of patients and physicians regarding the importance of screening, prevention and treatment is essential.
  • [MeSH-major] Androgen Antagonists / adverse effects. Bone Diseases / chemically induced. Orchiectomy / adverse effects. Prostatic Neoplasms / therapy
  • [MeSH-minor] Algorithms. Diphosphonates / therapeutic use. Humans. Male

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  • (PMID = 17161994.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Diphosphonates
  • [Number-of-references] 50
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5. Enmon RM Jr, O'Connor KC, Lacks DJ, Schwartz DK, Dotson RS: Dynamics of spheroid self-assembly in liquid-overlay culture of DU 145 human prostate cancer cells. Biotechnol Bioeng; 2001 Mar 20;72(6):579-91
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  • [Title] Dynamics of spheroid self-assembly in liquid-overlay culture of DU 145 human prostate cancer cells.
  • The in vitro self-assembly of multicellular spheroids generates highly organized structures in which the three-dimensional structure and differentiated function frequently mimic that of in vivo tissues.
  • This has led to their use in such diverse applications as tissue regeneration and drug therapy.
  • Using Smoluchowski-like rate equations, herein we present a model of the self-aggregation of DU 145 human prostate carcinoma cells in liquid-overlay culture to elucidate some of the physical parameters affecting homotypic aggregation in attachment-dependent cells.
  • The adhesion probability increases with spheroid size so that spheroid-spheroid adhesions are a minimum of 2.5 times more likely than those of cell-cell, possibly due to the upregulation of extracellular matrix proteins and cell-adhesion molecules.
  • The radius of influence is at least 1.5 to 3 times greater than expected for spherical geometry as a result of ellipsoidal shape and possible chemotactic or Fröhlich interactions.
  • Brownian-type behavior was noted for spheroids larger than 30 microm in diameter, but smaller aggregates were more motile by as much as a factor of 10 for single cells.
  • The model may improve spheroid fidelity for existing applications of spheroids and form the basis of a simple assay for quantitatively evaluating cellular metastatic potential as well as therapies that seek to alter this potential.
  • [MeSH-minor] Cell Aggregation / physiology. Cell Culture Techniques / methods. Computer Simulation. Humans. Male. Tumor Cells, Cultured

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  • [Copyright] Copyright 2001 John Wiley & Sons, Inc.
  • (PMID = 11460249.001).
  • [ISSN] 0006-3592
  • [Journal-full-title] Biotechnology and bioengineering
  • [ISO-abbreviation] Biotechnol. Bioeng.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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6. Leav I, Plescia J, Goel HL, Li J, Jiang Z, Cohen RJ, Languino LR, Altieri DC: Cytoprotective mitochondrial chaperone TRAP-1 as a novel molecular target in localized and metastatic prostate cancer. Am J Pathol; 2010 Jan;176(1):393-401
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  • [Title] Cytoprotective mitochondrial chaperone TRAP-1 as a novel molecular target in localized and metastatic prostate cancer.
  • Molecular chaperones of the heat shock protein-90 (Hsp90) family promote cell survival, but the molecular requirements of this pathway in tumor progression are not understood.
  • Here, we show that a mitochondria-localized Hsp90 chaperone, tumor necrosis factor receptor-associated protein-1 (TRAP-1), is abundantly and ubiquitously expressed in human high-grade prostatic intraepithelial neoplasia, Gleason grades 3 through 5 prostatic adenocarcinomas, and metastatic prostate cancer, but largely undetectable in normal prostate or benign prostatic hyperplasia in vivo.
  • Prostate lesions formed in genetic models of the disease, including the transgenic adenocarcinoma of the mouse prostate and mice carrying prostate-specific deletion of the phosphatase tensin homolog tumor suppressor (Pten(pc-/-)), also exhibit high levels of TRAP-1.
  • Expression of TRAP-1 in nontransformed prostatic epithelial BPH-1 cells inhibited cell death, whereas silencing of TRAP-1 in androgen-independent PC3 or DU145 prostate cancer cells by small interfering RNA enhanced apoptosis.
  • Targeting TRAP-1 with a novel class of mitochondria-directed Hsp90 inhibitors, ie, Gamitrinibs, caused rapid and complete killing of androgen-dependent or -independent prostate cancer, but not BPH-1 cells, whereas reintroduction of TRAP-1 in BPH-1 cells conferred sensitivity to Gamitrinib-induced cell death.
  • These data identify TRAP-1 as a novel mitochondrial survival factor differentially expressed in localized and metastatic prostate cancer compared with normal prostate.
  • Targeting this pathway with Gamitrinibs could be explored as novel molecular therapy in patients with advanced prostate cancer.

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  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):584-93 [12154351.001]
  • [Cites] Science. 2001 Apr 27;292(5517):727-30 [11326099.001]
  • [Cites] Prostate. 2003 May 15;55(3):219-37 [12692788.001]
  • [Cites] Nature. 2003 Sep 25;425(6956):407-10 [14508491.001]
  • [Cites] Cancer Cell. 2003 Sep;4(3):209-21 [14522255.001]
  • [Cites] Nat Med. 2004 Jun;10(6):594-601 [15156201.001]
  • [Cites] Science. 2004 Jul 30;305(5684):626-9 [15286356.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1488-90 [15470210.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]
  • [Cites] Cancer Res. 1994 May 15;54(10):2577-81 [8168083.001]
  • [Cites] Nature. 2005 Mar 31;434(7033):652-8 [15800626.001]
  • [Cites] Nature. 2005 Mar 31;434(7033):658-62 [15800627.001]
  • [Cites] Nat Rev Cancer. 2005 Oct;5(10):761-72 [16175177.001]
  • [Cites] Oncology. 2005;69(4):273-82 [16282706.001]
  • [Cites] J Natl Cancer Inst. 2006 Nov 1;98(21):1521-7 [17077354.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):256-69 [17384581.001]
  • [Cites] Arch Pathol Lab Med. 2007 Jul;131(7):1103-9 [17616999.001]
  • [Cites] J Biol Chem. 2007 Jul 13;282(28):20553-60 [17513296.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2351-61 [17786228.001]
  • [Cites] J Urol. 2007 Nov;178(5):1846-54 [17868738.001]
  • [Cites] Cell. 2007 Oct 19;131(2):257-70 [17956728.001]
  • [Cites] Stress. 2007 Nov;10(4):342-50 [17853063.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] FASEB J. 2008 Sep;22(9):3264-75 [18524868.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20882-7 [19088204.001]
  • [Cites] J Clin Invest. 2009 Mar;119(3):454-64 [19229106.001]
  • [Cites] Mol Cell. 2009 Mar 13;33(5):627-38 [19285945.001]
  • [Cites] PLoS Biol. 2007 Jul;5(7):e172 [17579517.001]
  • [Cites] FEBS Lett. 2002 Feb 13;512(1-3):1-7 [11852041.001]
  • [Cites] J Biol Chem. 2000 Feb 4;275(5):3305-12 [10652318.001]
  • [Cites] Cancer Cell. 2003 Mar;3(3):213-7 [12676580.001]
  • (PMID = 19948822.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA078810; United States / NCI NIH HHS / CA / R01 CA089720; United States / NCI NIH HHS / CA / CA118005; United States / NCI NIH HHS / CA / R01 CA109874-05; United States / NCI NIH HHS / CA / CA78810; United States / NCI NIH HHS / CA / CA109874-05; United States / NCI NIH HHS / CA / R01 CA109874; United States / NCI NIH HHS / CA / R01 CA089720-05; United States / NCI NIH HHS / CA / CA90917; United States / NCI NIH HHS / CA / CA089720-05; United States / NCI NIH HHS / CA / CA109874; United States / NCI NIH HHS / CA / CA89720; United States / NCI NIH HHS / CA / R56 CA089720; United States / NCI NIH HHS / CA / R01 CA118005; United States / NCI NIH HHS / CA / R01 CA090917
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HSP90 Heat-Shock Proteins; 0 / Molecular Chaperones; 0 / TRAP-1 protein, mouse; 0 / TRAP1 protein, human
  • [Other-IDs] NLM/ PMC2797899
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7. Drake CG: Immunotherapy for metastatic prostate cancer. Urol Oncol; 2008 Jul-Aug;26(4):438-44
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  • [Title] Immunotherapy for metastatic prostate cancer.
  • Chemotherapy with docetaxel is the standard treatment for men with metastatic prostate cancer, and results in statistically significant improvements in survival, as well as in quality of life.
  • More significantly, with the onset of early, PSA-based detection of prostate cancer and closer follow-up, many men present with metastatic disease that remains asymptomatic.
  • For such patients, the side effects of chemotherapy would compromise their current performance status and, thus, a nontoxic, early treatment option that could improve overall survival would be highly desirable.
  • Immunotherapy represents one such approach; a number of clinical trials have suggested a survival benefit for immunotherapy in metastatic prostate cancer and confirmed that these agents are generally well-tolerated.
  • As is the case for chemotherapy, it is doubtful that maximal survival benefit will be achieved with single-agent immunotherapy; experimental treatments in which mechanistically distinct immunotherapy approaches are combined, as well as approaches in which immunotherapy is combined with chemotherapy or hormonal therapy are currently under investigation.
  • This review will discuss the mechanisms of action of several immunotherapy approaches for metastatic prostate cancer, focusing on active immunotherapy as opposed to administration of anti-tumor antibodies.
  • [MeSH-major] Immunotherapy / methods. Prostatic Neoplasms / therapy
  • [MeSH-minor] Dendritic Cells / immunology. Granulocyte-Macrophage Colony-Stimulating Factor / genetics. Humans. Male. Neoplasm Metastasis

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  • (PMID = 18593624.001).
  • [ISSN] 1078-1439
  • [Journal-full-title] Urologic oncology
  • [ISO-abbreviation] Urol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Number-of-references] 36
  • [Other-IDs] NLM/ NIHMS787032; NLM/ PMC4886229
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8. O'Donnell RT, DeNardo SJ, Yuan A, Shen S, Richman CM, Lara PN, Griffith IJ, Goldstein DS, Kukis DL, Martinez GS, Mirick GR, DeNardo GL, Meyers FJ: Radioimmunotherapy with (111)In/(90)Y-2IT-BAD-m170 for metastatic prostate cancer. Clin Cancer Res; 2001 Jun;7(6):1561-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radioimmunotherapy with (111)In/(90)Y-2IT-BAD-m170 for metastatic prostate cancer.
  • PURPOSE: Over 31,000 Americans die of androgen-independent metastatic prostate cancer each year.
  • New strategies that do not involve hormonal manipulation but instead recognize the biochemical and molecular characteristics of prostate cancer are needed.
  • Radioimmunotherapy (RIT) uses a tumor-specific monoclonal antibody to deliver systemic, targeted radiation to cancer.
  • The objectives of this Phase I study of (111)In-2IT-BAD-m170 (for imaging) and (90)Y-2IT-BAD-m170 (for therapy) were to determine the toxicity and maximum tolerated dose (MTD), the specificity for targeting metastatic prostate cancer, and the efficacy for palliation of pain.
  • Patients with adequate renal and liver function, rising prostate-specific antigen, and androgen-independent metastatic prostate cancer were eligible.
  • Pain was assessed objectively by questionnaires before and for 8 weeks after RIT; weekly prostate-specific antigen levels were obtained for 2 months after RIT.
  • RESULTS: The MTD of (90)Y-2IT-BAD-m170 was 0.740 GBq/m(2) for patients that had up to 10% of the axial skeleton involved with prostate cancer.
  • Metastatic prostate cancer was targeted by (111)In-2IT-BAD-m170 in all 17 patients.
  • The mean radiation dose delivered to 39 bone and 18 nodal metastases by (90)Y-2IT-BAD-m170 was 10.5 Gy/GBq (range 2.8-25.1).
  • CONCLUSIONS: This study determined the MTD of (111)In/(90)Y-2IT-BAD-m170 in patients with metastatic prostate cancer.
  • The drugs were well tolerated, targeted metastases, and temporarily palliated pain.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Combined Modality Therapy. Indium Radioisotopes. Prostatic Neoplasms / therapy. Radioimmunotherapy. Yttrium Radioisotopes / therapeutic use
  • [MeSH-minor] Adenocarcinoma / therapy. Aged. Animals. Cohort Studies. Humans. Male. Mice. Middle Aged. Neoplasm Metastasis. Pain / drug therapy. Prostate-Specific Antigen / biosynthesis. Radiometry. Time Factors. Treatment Outcome

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  • (PMID = 11410491.001).
  • [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 / P01-CA47829
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; 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 / 2IT-BAD-Lym-1 monoclonal antibody; 0 / Antibodies, Monoclonal; 0 / Indium Radioisotopes; 0 / Yttrium Radioisotopes; EC 3.4.21.77 / Prostate-Specific Antigen
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9. Emmenegger U, Francia G, Shaked Y, Kerbel RS: Metronomic chemotherapy: principles and lessons learned from applications in the treatment of metastatic prostate cancer. Recent Results Cancer Res; 2010;180:165-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metronomic chemotherapy: principles and lessons learned from applications in the treatment of metastatic prostate cancer.
  • By frequent and protracted administration of conventional cytotoxic drugs without prolonged interruptions, the primary treatment target shifts from the tumor cell population to the tumor vasculature.
  • This "metronomic" way of chemotherapy administration results in antivascular effects, the mechanistic basis of which remains to be fully elucidated.
  • We outline the basic aspects of the metronomic concept, describe the results of clinical applications of such chemotherapy by focusing on studies in metastatic prostate cancer, and discuss certain shortcomings.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic. Endothelial Cells / physiology. Humans. Male. Neoplasm Metastasis. Stem Cells / physiology

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  • (PMID = 20033383.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
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10. Dreicer R: Current status of cytotoxic chemotherapy in patients with metastatic prostate cancer. Urol Oncol; 2008 Jul-Aug;26(4):426-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current status of cytotoxic chemotherapy in patients with metastatic prostate cancer.
  • Despite efforts at early detection with prostate specific antigen-based screening, more than 25,000 patients in the United States will die this year of metastatic prostate cancer.
  • As a consequence both of screening and increased use of androgen deprivation therapy, patients commonly present with low volume, asymptomatic, metastatic disease.
  • Over the past 2 decades chemotherapy for advanced prostate cancer has evolved from a frightful, toxic experience to one that frequently provides clinically meaningful palliation and a modest, but real survival benefit.
  • With the establishment of docetaxel-based chemotherapy as initial therapy, efforts are underway to evaluate the role of second-line systemic therapy options.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Humans. Male. Mitoxantrone / therapeutic use. Neoplasm Metastasis. Taxoids / therapeutic use


11. Timme TL, Satoh T, Tahir SA, Wang H, Teh BS, Butler EB, Miles BJ, Amato RJ, Kadmon D, Thompson TC: Therapeutic targets for metastatic prostate cancer. Curr Drug Targets; 2003 Apr;4(3):251-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic targets for metastatic prostate cancer.
  • Prostate cancer is the most commonly diagnosed non-cutaneous cancer in adult males.
  • Although prostate cancer that is confined to the gland can be cured in many patients using surgery or radiation, these treatments are only effective for localized tumors and the long-term failure rates for these treatments suggests that prostate cancer can metastasize relatively early in the course of the disease.
  • Once prostate cancer has metastasized there are no curative therapies.
  • The greatest challenge in the treatment of advanced prostate cancer is to access and eliminate metastatic cells.
  • Therefore, effective prostate cancer therapy will require novel strategies to target cancer cells both at the site of the primary tumor and at distant metastatic sites.
  • In this article we review several therapeutic targets and approaches that may provide new treatments for metastatic prostate cancer.
  • We discuss the use of small molecules to target specific molecular events associated with metastatic prostate cancer, the use of specific antibodies that target unique metastasis associated molecules and the use of various gene therapy strategies to achieve anti-metastatic activities.
  • [MeSH-major] Prostatic Neoplasms / pathology. Prostatic Neoplasms / therapy
  • [MeSH-minor] Animals. Antibodies / chemistry. Antibodies / therapeutic use. Antineoplastic Agents / chemistry. Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / immunology. Cancer Vaccines / therapeutic use. Genetic Therapy / methods. Humans. Immunotherapy. Male. Neoplasm Metastasis

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  • (PMID = 12643475.001).
  • [ISSN] 1389-4501
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Grant] United States / PHS HHS / / P50-58204; United States / PHS HHS / / R01-50588; United States / PHS HHS / / R01-68814
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Cancer Vaccines
  • [Number-of-references] 113
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12. Swanson G, Thompson I, Basler J, Crawford ED: Metastatic prostate cancer-does treatment of the primary tumor matter? J Urol; 2006 Oct;176(4 Pt 1):1292-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic prostate cancer-does treatment of the primary tumor matter?
  • PURPOSE: In recent years there has been increased interest in adjuvant therapy for prostate cancer.
  • This trend has engendered a tendency toward overlooking the issue of therapy to the primary tumor in advanced disease.
  • We reviewed the effect of treating the principal disease bulk on overall treatment outcome in patients with advanced and metastatic cancer.
  • Specifically we evaluated the role of surgical tumor cytoreduction.
  • MATERIALS AND METHODS: We performed a comprehensive literature review to evaluate the role of surgical debulking on the outcome of advanced cancer, including any published evidence supporting a benefit of this therapy for prostate cancer.
  • RESULTS: Even in cancers for which adjuvant chemotherapy and radiation are used liberally there is a clear benefit to optimal surgical debulking for local control and survival.
  • The beneficial role of maximal surgical cytoreduction has been clearly demonstrated in advanced ovarian cancer and gastrointestinal carcinomatosis.
  • Maximal debulking of brain, liver and lung metastasis has translated into longer survival.
  • Removal of the primary tumor has been proved to increase survival in randomized trials of metastatic renal cell cancer.
  • It appears that patients with node positive and possibly metastatic prostate cancer have a better response to androgen ablation with surgical removal of the gland.
  • CONCLUSIONS: Surgical cytoreduction of cancer results in a more favorable and durable response to systemic therapy.
  • It is reasonable to explore aggressive surgical therapy for advanced prostate cancer.
  • [MeSH-major] Neoplasm Metastasis / prevention & control. Prostatic Neoplasms / pathology. Prostatic Neoplasms / therapy
  • [MeSH-minor] Female. Humans. Male. Neoplasm Staging. Survival Rate


13. Beer TM, Smith DC, Hussain A, Alonso M, Wang J, Giurescu M, Wang Y, Prostate Cancer Clinical Trials Consortium: Phase II study of first-line sagopilone combined with prednisone in patients with metastatic castration-resistant prostate cancer (CRPC). J Clin Oncol; 2009 May 20;27(15_suppl):5059

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of first-line sagopilone combined with prednisone in patients with metastatic castration-resistant prostate cancer (CRPC).
  • : 5059 Background: Epothilones comprise a new class of microtubule stabilizing agents, and sagopilone is a novel, fully synthetic epothilone that has shown significant activity against a broad range of tumor models.
  • METHODS: Chemotherapy-naïve metastatic CRPC patients received sagopilone 16 mg/m<sup>2</sup> IV over 3 hours every 21 days and prednisone 5 mg PO BID.
  • Sites of metastases were: bones, lymph nodes, and viscera in 72%, 68%, and 25% patients, respectively.
  • CONCLUSIONS: Sagopilone is active in metastatic chemotherapy-naïve CRPC patients, with probability of PSA decline, measurable disease responses, and PFS approximating the current standard of docetaxel + prednisone.
  • Further evaluation of this agent in prostate cancer is warranted.

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  • (PMID = 27962969.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Yuan J, Orlandi F, Jefferson M, Li H, Gallardo H, Ku G, Wolchok J, Scher H, Allison J, Slovin SF: Cytokine changes in castrate metastatic prostate cancer (CPMC) patients (pts) treated with ipilimumab (Ipi). J Clin Oncol; 2009 May 20;27(15_suppl):e16149

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytokine changes in castrate metastatic prostate cancer (CPMC) patients (pts) treated with ipilimumab (Ipi).
  • Recent data [Proc Amer Soc Clin Onc, Abstr#5004, 2008] from castrate metastatic PC pts suggested that Ipi was active but was associated with grade 3 autoimmune adverse events (AEs), such as colitis, hepatitis, hypophysitis or rash, which required high dose steroids.
  • Of the 10 pts, 8 had ≥1 AE during treatment.
  • Pts were stratified by ascertainment of clinical benefit (CB) vs. no clinical benefit (NCB) based on time-to-PSA-baseline relapse (TTBR) and also by toxicity (tox) using standard NCI tox criteria.
  • TTBR was defined as time from study entry until the time when a PSA measurement reached or exceeded the baseline value.
  • Pts with a TTBR greater than the median value were judged to have CB; those with a TTBR less than the median value had NCB.
  • Sera at serial time points were analyzed for interferon-gamma (IFN-γ), tumor necrosis factor α and interleukins (IL)-1b, 2, 4, 8, 10, 12, 13 with the Meso Scale Discovery Multiplex Assay (MSD, Gaithersburg, MD).
  • Investigation of the immunophenotype of pts who remain in follow- up and continue to be enrolled is ongoing as well as the impact of prior chemotherapy on development of toxicities.

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  • (PMID = 27963424.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Hussain M, Faulkner J, Vaishampayan U, Lara P, Petrylak D, Colevas D, Sakr W, Crawford ED: Epothilone B (Epo-B) analogue BMS-247550 (NSC #710428) administered every 21 days in patients (pts) with hormone refractory prostate cancer (HRPC). A Southwest Oncology Group Study (S0111). J Clin Oncol; 2004 Jul 15;22(14_suppl):4510

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epothilone B (Epo-B) analogue BMS-247550 (NSC #710428) administered every 21 days in patients (pts) with hormone refractory prostate cancer (HRPC). A Southwest Oncology Group Study (S0111).
  • : 4510 Background: The epothilones are a new class of non-taxane tubulin polymerizing agents with activity both in taxane-sensitive and resistant tumor models.
  • This Phase II trial with a 2-stage design evaluated the efficacy and toxicity of Epo-B in pts with metastatic HRPC.
  • METHODS: Eligible pts had chemotherapy-naive metastatic HRPC, a Zubrod performance status 0-2, and adequate organ function.
  • Of the 48 registered pts 41 were eligible with a median age of 74 years.
  • To date complete data is available for the 28 pts registered to the first stage (22 analyzable, 5 ineligible, 1 did not receive protocol specified treatment).
  • The median survival was not reached at this time.
  • CONCLUSIONS: Early results from this multicenter trial indicate that BMS-247550 has activity in patients with metastatic HRPC.

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  • (PMID = 28016038.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Cetnar JP, Rosen MA, Vaughn DJ, Haas NB, Troxel AB, Song H, Adluru G, Flaherty KT, O'Dwyer PJ, Amaravadi RK: Phase II study of sorafenib and docetaxel in men with metastatic castration resistant prostate cancer (mCRPC). J Clin Oncol; 2009 May 20;27(15_suppl):e16055

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of sorafenib and docetaxel in men with metastatic castration resistant prostate cancer (mCRPC).
  • METHODS: Eligible men had mCRPC and no prior chemotherapy.
  • Treatment consisted of dxl 75 mg/m<sup>2</sup>(day 1) and sorafenib (days 2-19) of a 21 day cycle.
  • Secondary endpoints were vascular response rate (>20% decline in area under the gadolinium curve [AUC60]), toxicity rates, and time to progression (TTP).
  • PSA-only progression (2 consecutive PSA rises) was confirmed by a third PSA rise or radiographic progression after a 21-day drug holiday.
  • Sample size of 69 patients in 1 stage was designed to maximize detection of significant correlations between DCE-MRI and clinical outcomes.
  • DCE-MRI can capture sorafenib's impairment of tumor vasculature in osseous metastases and rebound angiogenesis during drug holidays.

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  • (PMID = 27962998.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Tay MH, George DJ, Gilligan TD, Kelly SM, Appleby L, Taplin ME, Febbo PG, Kantoff PW, Oh WK: Docetaxel plus carboplatin (DC) may have significant activity in hormone refractory prostate cancer (HRPC) patients who have progressed after prior docetaxel-based chemotherapy. J Clin Oncol; 2004 Jul 15;22(14_suppl):4679

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Docetaxel plus carboplatin (DC) may have significant activity in hormone refractory prostate cancer (HRPC) patients who have progressed after prior docetaxel-based chemotherapy.
  • : 4679 Background: Chemotherapy is now increasingly used in HRPC management.
  • The two most frequently used regimens are mitoxantrone-prednisone (MP) and docetaxel-estramustine (DE) beyond which options are limited.
  • Although carboplatin, a drug active in neuroendocrinally differentiated tumor, has modest activity in HRPC as a single agent, we retrospectively report 3 of the 4 patients consecutively treated and responded with salvage docetaxel-carboplatin (DC) following failure to docetaxel-based chemotherapy.
  • METHODS: 4 patients with metastatic HRPC who had failed docetaxel based chemotherapy and at least one line of chemotherapy were treated with docetaxel at 60-70 mg/m<sup>2</sup> and carboplatin at AUC 4 given 3 weekly.
  • RESULTS: 3 of the 4 patients had > 50% PSA decrease, together with improvement of performance status, weight gain and decrease pain medication.
  • Prior treatments include D alone in patient 1, MP, epothilone analogue and DE in patient 2 and DE with bevacizumab in patient 3.
  • The significant response seen in these 3 patients suggest a possible synergistic effect of the two drugs.

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  • (PMID = 28015597.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Hotte SJ, Yu EY, Hirte HW, Higano CS, Gleave M, Chi KN: OGX-427, a 2'methoxyethyl antisense oligonucleotide (ASO), against HSP27: Results of a first-in-human trial. J Clin Oncol; 2009 May 20;27(15_suppl):3506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] OGX-427, a 2'methoxyethyl antisense oligonucleotide (ASO), against HSP27: Results of a first-in-human trial.
  • : 3506 Background: Heat shock protein 27 (Hsp27) is a chaperone protein expressed in many cancers and implicated as a therapeutic "hyper-node" affecting multiple pathways in cancer progression.
  • OGX-427 is a second generation ASO that inhibits Hsp27 expression which in preclinical models inhibited cell growth, induced apoptosis, and enhanced chemotherapy efficacy.
  • METHODS: Eligible patients (pts) had to have metastatic breast, ovarian, prostate, NSCLC, or bladder cancer.
  • Circulating tumor cells (CTC), Hsp27+ CTC and serum Hsp27 levels were evaluated serially.
  • Median age was 62 (range: 33-86) yrs; 16 pts had prostate, 10 breast, 5 ovary and 3 lung ca.
  • Median cycles administered were 2 (0-8) with 2 pts remaining on treatment.
  • At 600 mg DL, one pt had a Gr 3 epistaxis and one pt had a DLT with a Gr 3 cerebral bleed into a metastasis.
  • Three pts with prostate ca had PSA declines of 43%, 58%, 62% and 3 pts with ovarian cancer had CA-125 declines of 27%, 28%, and 41%.
  • Changes in tumor markers suggest single-agent activity.

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  • (PMID = 27961276.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Feyerabend S, Stefanovic S, Gouttefangeas C, Widenmeyer M, Wernet D, Hennenlotter J, Bedke J, Dietz K, Pascolo S, Rammensee H, Stenzl A: HLA-associated multipeptide vaccination in biochemically relapsed prostate cancer patients. J Clin Oncol; 2009 May 20;27(15_suppl):5134

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HLA-associated multipeptide vaccination in biochemically relapsed prostate cancer patients.
  • : 5134 Background: We conduct a phase I/II monocenter clinical trial using multi peptide vaccination in patients with hormone naive, biochemically relapsed prostate cancer.
  • METHODS: Patients (pts) with rising PSA after primary curative surgical treatment without metastatic imageable lesions receive 14 peptides emulsified in Montanide ISA51 subcutaneously, combined with one of four T-cell stimulatory adjuvants versus no adjuvant for 18 months (mo) or until progression.
  • PSA doubling time (DT) and clinical performance are monitored.
  • RESULTS: 25 out of 35 pts have terminated the study treatment so far.
  • During the vaccination period, geometric mean PSA DT increased from 7.8 mo (range 1.5 - 44.8 mo, 25 pts) to 11.8 months (range 2.2 - 571.3 mo, 24pts) whereas 1 pt showed a decreasing PSA value.
  • Overall 8/25 pts (32%) had a mean rise of PSA DT of 81.6 mo and four of them did not receive any further treatment and were evaluable for follow-up (FU) after peptide vaccination (FU median 16 mo, range 5-33).
  • These four pts raised their mean geometric PSA DT from 8.2 mo prior study treatment to 51.9 mo at treatment end and 52.5 mo at end of FU.
  • Two pts had PSA decline or DT increase during FU but not during the treatment period.
  • All pts reacted to at least one of the tumor antigen-derived HLA-class I epitopes after the fourth vaccine injection and up to six peptides were recognized simultaneously by CD8+ T cells in some individuals.
  • Rise of PSA DT delaying standard treatment up to 33 mo and thus, delaying disease specific mortality is feasible.

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  • (PMID = 27964428.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Dipaola RS, Manola J, Li S, Vaughn D, Roth B, Wilding G: A randomized phase II trial of mitoxantrone, estramustine and vinorelbine or 13-cis retinoic acid, interferon and paclitaxel in patients with metastatic hormone refractory prostate cancer: results of ECOG 3899. J Clin Oncol; 2004 Jul 15;22(14_suppl):4594

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A randomized phase II trial of mitoxantrone, estramustine and vinorelbine or 13-cis retinoic acid, interferon and paclitaxel in patients with metastatic hormone refractory prostate cancer: results of ECOG 3899.
  • : 4594 Background: Additional options of chemotherapy are limited for hormone refractory prostate cancer (HRPC), making the study of novel agents and combinations critical.
  • Given data demonstrating that retinoids and interferon reduce Bcl-2 expression, the effect of therapy on Bcl-2 was tested in peripheral blood mononuclear cells (PBMC).
  • RESULTS: Seventy pts with HRPC, without prior chemotherapy, were entered.
  • Partial tumor response was documented in 2/10 pts in arm A and 2/12 pts in B with measurable disease.
  • Bcl-2 expression in PBMCs deceased significantly during therapy only in arm B (p=0.03).
  • Therapy with MEN offers an active non-taxane combination that may warrant further study in pts after progression on taxane therapy.

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  • (PMID = 28015980.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Lee RJ, Stott SL, Nagrath S, Ulkus LE, Dahl DM, Smith MR, Toner M, Maheswaran S, Haber DA: Analyses of circulating tumor cell (CTC) dynamics and treatment response in prostate cancer using the CTC-chip microfluidic device. J Clin Oncol; 2009 May 20;27(15_suppl):5149

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analyses of circulating tumor cell (CTC) dynamics and treatment response in prostate cancer using the CTC-chip microfluidic device.
  • : 5149 Background: The CTC-Chip reliably detects CTCs in patients with localized and metastatic prostate cancer.
  • In localized disease, CTCs may be indicative of tumor invasiveness.
  • In the metastatic setting, CTCs may be useful in monitoring response to therapy.
  • Molecular analyses of CTCs through this minimally invasive technique may provide insights into disease behavior, whereas sampling of metastatic deposits in bone (the predominant site of prostate metastasis) is not feasible.
  • METHODS: Peripheral blood was collected from patients undergoing treatment.
  • Subgroups of patients (n) included: localized disease undergoing prostatectomy (25), and metastatic disease undergoing either androgen deprivation therapy (ADT) (12) or docetaxel chemotherapy (5).
  • In patients with metastatic disease undergoing either ADT or chemotherapy, CTC quantities generally corresponded with changes in serum PSA and radiographic assessments.
  • CONCLUSIONS: These studies are the first to use the highly sensitive CTC-Chip technology to assess dynamic changes in CTCs in patients undergoing prostatectomy, ADT, or chemotherapy.
  • Ongoing larger studies will assess whether patterns of CTC changes predict recurrence or treatment response.
  • Molecular characterization of CTCs may provide new insights into prostate cancer biology, clinical behavior, and therapeutic targets.

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  • (PMID = 27964441.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Ma D, Zhang H, Kennedy B, Parsons T, Olson WC: Antitumor activity of PSMA ADC after progression on docetaxel in a mouse xenograft model of human prostate cancer. J Clin Oncol; 2009 May 20;27(15_suppl):3030

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor activity of PSMA ADC after progression on docetaxel in a mouse xenograft model of human prostate cancer.
  • : 3030 Background: Currently, there are no approved therapies for castration-resistant metastatic prostate cancer that has progressed following docetaxel therapy.
  • Prostate-specific membrane antigen (PSMA) is an attractive target for antibody-targeted therapy of prostate cancer due to its abundant and restricted expression on the surface of prostate cancer cells.
  • We have developed a novel antibody-drug conjugate (ADC) by linking a fully human PSMA monoclonal antibody to monomethylauristatin E (MMAE), a potent tubulin inhibitor.
  • Here, we describe the use of PSMA ADC in a mouse model to treat xenografted human prostate tumors that have progressed following docetaxel therapy.
  • METHODS: Nude mice were implanted subcutaneously with 5 x 10<sup>6</sup> C4-2 human prostate cancer cells.
  • Docetaxel significantly reduced tumor growth (p = 0.025) during the initial phase of the study; however, most of the tumors later progressed.
  • When the tumor volume of an animal in the docetaxel group exceeded 400 mm<sup>3</sup>, the animal was rerandomized to receive continued docetaxel therapy (n = 18) or weekly IV doses of 6 mg/kg PSMA ADC (n = 18).
  • Treatment effects were assessed by measuring tumor volume and overall survival.
  • When tumor volume was assessed to be ≥2,000 mm<sup>3</sup>, animals would be sacrificed.
  • RESULTS: At 134 days following tumor implantation, the survival rate was 100% for animals in the PSMA ADC treatment group; 94% of these mice had tumor sizes <100 mm<sup>3</sup>.
  • In the continued docetaxel treatment group, 14 of 18 animals that were sacrificed when their tumors exceeded 2,000 mm<sup>3</sup>; the survival rate was 22%.
  • Therefore, PSMA ADC treatment significantly shrank tumors and increased overall survival of animals compared to continued docetaxel treatment (p < 0.0001).
  • CONCLUSIONS: PSMA ADC had antitumor activity in mice to xenografted human prostate tumors that had progressed following docetaxel treatment.
  • Treatment with PSMA ADC significantly extended survival in this setting.

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  • (PMID = 27962082.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Sison B, Bond T, Amato RJ, Crawford D, Crighton F: Phase II study of CC-4047 in patients with metastatic hormone-refractory prostate cancer (HRPCa). J Clin Oncol; 2004 Jul 15;22(14_suppl):4701

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of CC-4047 in patients with metastatic hormone-refractory prostate cancer (HRPCa).
  • : 4701 Background: Thalidomide is a potentially effective therapy for patients with metastatic HRPC.
  • CC-4047 is a thalidomide analog with a variety of immunomodulatory and anti-angiogenesis properties similar to thalidomide.
  • This study investigates whether single agent CC-4047 can induce PSA responses and increase time to progression in HRPC.
  • Eligibility included histologically confirmed adenocarcinoma of the prostate, 2 consecutive rises in prostate-specific antigen (PSA) consisting of an absolute change of at least 1 ng/ml separated by at least 28 days, with or without radiographic evidence of disease, castrate levels of serum testosterone (<50 ug/l), failure to antiandrogen withdrawal, ≤ 1 prior chemotherapy regimen, ECOG performance status of ≤ 1, life expectancy ≥ 3 months, and normal organ/marrow function.
  • 4 patients with nodal or visceral tumor without bone involvement.
  • RESULTS: Of the 22 patients, 9 patients have completed 12 weeks of therapy.
  • 1 patient expired secondary to a CNS bleed while on therapeutic doses of coumadin.

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  • (PMID = 28016744.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. De Jager RL, Roman L, Lopatkin N, Karlov P, Breitz H, Earhart R: Results of a phase II study of picoplatin with docetaxel and prednisone in first-line treatment of castration-resistant prostate cancer (CRPC). J Clin Oncol; 2009 May 20;27(15_suppl):5140

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of a phase II study of picoplatin with docetaxel and prednisone in first-line treatment of castration-resistant prostate cancer (CRPC).
  • Recently, a 34-patient Phase I study was performed to investigate the safety and efficacy of Pico in combination with docetaxel (D) + prednisone (pred) as first-line therapy for metastatic CRPC.
  • Picoplatin therapy was well-tolerated at a dose of 120 mg/m<sup>2</sup> and 19 of 32 evaluable pts (59%) achieved a confirmed PSA response.
  • METHODS: 32 patients with chemotherapy-naïve CRPC and disease progression received Pico (120 mg/m<sup>2</sup>) and D (75 mg/m<sup>2</sup>) Q3W with pred 5 mg po bid for up to 10 cycles.
  • Tumor response was measured using RECIST.
  • Of the 24 patients with evaluable post-treatment PSA, 83% (95% CI 64-93%) had PSA decreases <50% of baseline, and in 8 of these (33% of the evaluable population), PSA reached normal levels (< 4 ng/mL).
  • CONCLUSIONS: Picoplatin was safely administered to patients with CRPC as 1<sup>st</sup>-line therapy at 120 mg/m<sup>2</sup> Q3W with full doses of docetaxel and prednisone, resulting in a PSA response rate of 83% of evaluable patients.
  • These results support further development of picoplatin as a novel combination with docetaxel for the treatment of CRPC.

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  • (PMID = 27964433.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Zurita AJ, Liu G, Hutson T, Kozloff M, Shore N, Wilding G, Logothetis CJ, Chen I, Chow Maneval E, George D: Sunitinib in combination with docetaxel and prednisone in patients (pts) with metastatic hormone-refractory prostate cancer (mHRPC). J Clin Oncol; 2009 May 20;27(15_suppl):5166

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sunitinib in combination with docetaxel and prednisone in patients (pts) with metastatic hormone-refractory prostate cancer (mHRPC).
  • : 5166 Background: Overexpression of VEGF and PDGF has been implicated in prostate cancer progression and bone metastases.
  • Sunitinib is an oral, multitargeted inhibitor of VEGFRs, PDGFRs, and other tyrosine kinases which may improve the efficacy of chemotherapy in pts with mHRPC.
  • We performed a multicenter phase I/II study of sunitinib in combination with docetaxel and prednisone as first-line therapy in pts with mHRPC.
  • METHODS: Pts received treatment in a 21-day cycle: sunitinib 37.5 mg/d on days 1-14, docetaxel 75 mg/m<sup>2</sup> on day 1, and prednisone 5 mg BID on days 1-21.
  • Dose reductions were permitted for treatment-related toxicity.
  • Secondary endpoints included tumor response rate (RECIST), safety and patient-reported outcomes.
  • RESULTS: Fifty-five pts were enrolled and 13 remained on study at the time of the data cutoff (1 Oct 08).
  • Six pts completed the study (16 cycles) and continued treatment on another protocol.
  • Pts received a median of 23 weeks of therapy (range, 2-84).
  • The most common treatment-related grade 3-4 AEs were neutropenia (75%), febrile neutropenia (15%), fatigue (15%), stomatitis (7%), and anorexia (7%).
  • PSA responses occurred in 31 pts (56%), with a preliminary median time to PSA progression of 42.1 weeks.
  • Out of 33 pts with measurable disease, thirteen (39%) had a confirmed partial response (PR) and another 7 (21%) had an initial PR.
  • CONCLUSIONS: Sunitinib in combination with docetaxel and prednisone is tolerated and has antitumor activity in pts with mHRPC, as indicated by both PSA and RECIST-defined tumor responses.

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  • (PMID = 27964502.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Armstrong AJ, Halabi S, Tannock IF, George DJ, DeWit R, Eisenberger M: Development of risk groups in metastatic castration-resistant prostate cancer (mCRPC) to facilitate the identification of active chemotherapy regimens. J Clin Oncol; 2009 May 20;27(15_suppl):5137

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of risk groups in metastatic castration-resistant prostate cancer (mCRPC) to facilitate the identification of active chemotherapy regimens.
  • : 5137 Background: Our aim was to develop and validate clinically applicable predictive factors for a >30% PSA decline 3 months following chemotherapy initiation, and to assess the performance of a risk-group based classification in predicting PSA declines and overall survival (OS) in men receiving chemotherapy for mCRPC.
  • Predictive factors for a >30% 3-month decline in PSA levels were identified using multivariate logistic regression in D treated men (n = 656) and validated in M treated men (n = 333).
  • Risk factors were combined to form risk groups to predict PSA declines, OS, tumor, and pain responses.
  • Prostate Cancer Working Group (PCWG2) disease states were evaluated for these outcomes in docetaxel treated men.
  • RESULTS: In multivariate analysis, four independent risk factors predicted for absence of >30% decline in 3-month PSA: significant baseline pain (OR 0.63 p = 0.02), visceral metastases (OR 0.66, p = 0.03), anemia (hemoglobin <13 g/dl, OR 0.72 p = 0.07), and bone scan progression at baseline (OR 0.60 p = 0.009).
  • Predictive accuracy was moderate with a concordance index (c-index) of 0.61.
  • Risk groups (good, intermediate, poor) were developed with median OS of 25.7 (95% CI 23.3-28.6), 18.7 (17.3-19.7), and 12.8 (11.5-14.6) months, respectively (p < 0.0001), and >30% PSA decline in 78, 66, and 58 percent of men (p < 0.001).
  • PCWG2 subtypes (node only, bone metastatic, and visceral disease), were also highly prognostic and predictive but did not predict OS as well as the TAX327 risk groups (c-index 0.56).
  • This classification may facilitate evaluation of new regimens of systemic therapy that warrant definitive testing in comparison to docetaxel and prednisone in phase III trials.

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  • (PMID = 27964425.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Richman CM, Denardo SJ, O'Donnell RT, Yuan A, Natarajan A, Wun T, Tuscano JM, Chew HL, Lara PN, Denardo GL: Combined modality radioimmunotherapy (RIT) in metastatic prostate (PC) and breast cancer (BC) using paclitaxel (PT) and a MUC-1 monoclonal antibody, m170, linked to yttrium-90 (Y-90): A phase I trial. J Clin Oncol; 2004 Jul 15;22(14_suppl):2554

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined modality radioimmunotherapy (RIT) in metastatic prostate (PC) and breast cancer (BC) using paclitaxel (PT) and a MUC-1 monoclonal antibody, m170, linked to yttrium-90 (Y-90): A phase I trial.
  • : 2554 Background: While RIT alone is effective in lymphoma, its application to more radioresistant solid tumors will likely require a combined approach similar to the use of radiosensitizing chemotherapy with external beam radiotherapy.
  • METHODS: Patients with metastatic hormone-refractory PC or advanced BC were imaged with Indium-111-DOTA-peptide-m170 (In-111-m170).
  • Subsequent cohorts received RIT followed by PT (75 mg/m<sup>2</sup>) 48 hours after RIT, a time when most radioactivity is concentrated in tumor and has been eliminated from normal tissues.
  • RESULTS: Bone and soft tissue metastases were targeted by In-111-m170 in 15 of the 16 patients imaged, with no unexpected uptake in normal tissue.
  • With RIT plus PT, 2 of 3 PC patients had neutrophils (ANC)<500/uL.
  • With RIT plus PT, all 3 BC patients had ANC < 500 and 2 of 3 had pl<25K.
  • One patient developed + HAMA (6%) in contrast to 71% of patients in a prior trial using m170 without CSA.
  • CSA was effective in preventing HAMA, suggesting the possibility of repeated "fractionated" therapy that could enhance antitumor response.

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  • (PMID = 28015259.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Yu E, Massard C, Gross M, Wilding G, Posadas E, Culine S, Carducci MA, Trudel G, Paliwal P, Sternberg C: A phase II study of once-daily dasatinib for patients with castration-resistant prostate cancer (CRPC) (CA180085). J Clin Oncol; 2009 May 20;27(15_suppl):5147

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of once-daily dasatinib for patients with castration-resistant prostate cancer (CRPC) (CA180085).
  • The anti-proliferative/anti-metastatic activity as well as osteoclast inhibitory function of dasatinib in pre-clinical models supports its potential as a targeted therapy for prostate cancer.
  • Previously we presented results on BID dosing of dasatinib in the treatment of CRPC (ASCO.
  • METHODS: Male pts with progressive metastatic CRPC, rising PSA, castrate levels of testosterone (< 50 ng/dL) and no prior chemotherapy were enrolled.
  • RESULTS: 47 pts were treated (median treatment duration was 2.3 months).
  • A prolonged PSA doubling time was observed in 32 of 39 pts (82%), including one pt with a PSA response.
  • Of the pts with evaluable bone markers, including those who continued on bisphosphonate therapy, 20/41 (49%) had a ≥ 35% decrease in uNTX and 21/42 (50%) had a decrease from baseline in BAP.
  • In addition, preliminary clinical activity (tumor and PSA response; decreasing bone turnover [uNTX, BAP]), is now confirmed to be similar in pts treated with 100mg QD and BID dosing.
  • These data support the relevance of further studies of dasatinib in metastatic CRPC.

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  • (PMID = 27964443.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Tiffany NM, Ryan CW, Garzotto M, Wersinger EM, Beer TM: High-Dose calcitriol, docetaxel, and estramustine in androgen-independent prostate cancer (AIPC): A phase I/II study. J Clin Oncol; 2004 Jul 15;22(14_suppl):4678

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-Dose calcitriol, docetaxel, and estramustine in androgen-independent prostate cancer (AIPC): A phase I/II study.
  • We sought to test the safety of a 3-drug regimen that combined docetaxel with estramustine and calcitriol.
  • METHODS: Patients with metastatic AIPC received calcitriol 60 mcg PO over 4 hours (15 mcg hourly for 4 doses) on day 1, dexamethasone 8 mg PO BID on days 1-3, estramustine 280 mg PO TID on days 1-5, and docetaxel 60 mg/m<sup>2</sup> (70 mg/m<sup>2</sup> starting in cycle 2 if no ≥ grade 3 toxicity during cycle 1) IV over 60 min on day 2.
  • Treatment was repeated every 21 days for up to 12 cycles.
  • A dose de-escalation scheme for calcitriol was planned if dose limiting toxicities were encountered during the first cycle of treatment in > 1/3 of patients.
  • 8 patients were chemotherapy-naïve and 12 had received prior docetaxel-based therapy (5 received more than 1 prior chemotherapy regimen).
  • The regimen was generally well tolerated and criteria for dose de-escalation were not met.
  • Treatment-related ≥ Grade 3 toxicity included: Hypophosphatemia- 4, Neutropenic fever - 2, perforated diverticulum - 1, edema - 1, vomiting - 1, ALT elevation - 1, anemia - 1, PTT elevation -1.
  • 3 patients had thromboembolic complications and one patient had grade 3 hematuria thought to be due to tumor.
  • 17 patients are evaluable for PSA response at this time.
  • 4 of 7 chemotherapy-naïve patients (57%) met criteria for PSA response (confirmed ≥ 50% decline).
  • 1 of 7 patients (14%) treated with 1 prior docetaxel-containing regimen met these criteria.
  • There were no responses among the 3 patients treated with more than 1 prior chemotherapy regimen.

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  • (PMID = 28015598.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Kantoff PW, Schuetz T, Blumenstein BA, Glode MM, Bilhartz D, Gulley J, Schlom J, Laus R, Godfrey W: Overall survival (OS) analysis of a phase II randomized controlled trial (RCT) of a poxviral-based PSA targeted immunotherapy in metastatic castration-resistant prostate cancer (mCRPC). J Clin Oncol; 2009 May 20;27(15_suppl):5013

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overall survival (OS) analysis of a phase II randomized controlled trial (RCT) of a poxviral-based PSA targeted immunotherapy in metastatic castration-resistant prostate cancer (mCRPC).
  • : 5013 Background: Therapeutic poxviral vaccines for prostate cancer are safe with preliminary evidence of clinical benefit in phase I/II studies.
  • PROSTVAC-VF (PV) comprises 2 recombinant viral vectors (Vaccinia and Fowlpox), each encoding transgenes for prostate specific antigen (PSA) and 3 immune costimulatory molecules (B7.1, ICAM-1, and LFA3: TRICOM).
  • PV is administered subcutaneously in a heterologous prime-boost regimen with concurrent low-dose GM-CSF.
  • METHODS: 122 patients (pts) were treated in a multi-center, double-blind, RCT of a vaccination series.
  • Eligible pts had metastatic disease, a rising PSA despite castrate testosterone levels, and a Gleason score of ≤7.
  • Pts with a history of prior chemotherapy use, visceral metastasis, or narcotic use were excluded.
  • Pt characteristics were similar (means): age (72PV/76C), PSA (134PV/188C), Alk-Phos (142PV/159C), LDH (207PV/218C), Hgb (13PV/13C), and number bone metastatic sites (5.3PV/6.5C).
  • CONCLUSIONS: In a RCT, PV immunotherapy was associated with an 8.5 month improvement in median OS in men with mCRPC.
  • These data provide evidence of prolonged anti-tumor activity, but need to be confirmed in a larger phase III study.

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  • (PMID = 27962903.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Mohebtash M, Madan RA, Arlen PM, Rauckhorst M, Tsang KY, Cereda V, Vergati M, Poole DJ, Dahut WL, Schlom J, Gulley JL: Phase I trial of targeted therapy with PSA-TRICOM vaccine (V) and ipilimumab (ipi) in patients (pts) with metastatic castration-resistant prostate cancer (mCRPC). J Clin Oncol; 2009 May 20;27(15_suppl):5144

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of targeted therapy with PSA-TRICOM vaccine (V) and ipilimumab (ipi) in patients (pts) with metastatic castration-resistant prostate cancer (mCRPC).
  • : 5144 Background: There are few treatment options for mCRPC pts.
  • Ipi blocks CTLA-4, a T-cell downregulatory receptor, has clinical activity in mCRPC as monotherapy and has also been shown to enhance anti-tumor responses in combination with V in preclinical studies.
  • Median PSA doubling time (DT) ↑ from 2.2 mo at baseline to 3.7 on study (p = 0.17).
  • Median PSA DT ↑ > 3-fold from 2.6 mo at baseline to 8.2 on study (p = 0.01) in DL4.
  • The 24 chemo-naïve pts had PSA DT ↑ from 2.5 to 6 mo (p = 0.003).
  • 2 of 14 had no irAE, 12 showed ≥ G2 irAE temporally associated with PSA ↓.
  • 5 of 9 pts had > 2-5 fold ↑ in T-cell responses by ELISPOT assay and 4 of 13 had significant ↓ in their IL-6 levels.

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  • (PMID = 27964446.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Basch EM, Sit L, Fruscione M, Burke L, Kane R, George D, Carducci MA, Matthew P, Beer TM, Scher HI: Pain and analgesic use in men with metastatic prostate cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e20515

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pain and analgesic use in men with metastatic prostate cancer.
  • : e20515 Background: Pain is an important endpoint in metastatic prostate cancer and was the basis for the 1996 FDA approval of mitoxantrone.
  • The prevalence and distribution of pain severity at specific points in the prostate cancer disease continuum are not well defined.
  • METHODS: A questionnaire that includes the Brief Pain Inventory and additional pain/analgesia items was developed as a collaboration between the DOD/PCF-supported Prostate Cancer Clinical Trials Consortium (PCCTC) and FDA Study Endpoints and Labeling Design (SEALD) team.
  • RESULTS: Between August-December 2008, 325 men with prostate cancers representing different disease states being seen in outpatient clinics of participating centers were each queried once.
  • More than half (n=175) self-reported metastatic disease, including 129 with bone metastases.
  • Among those with bone metastases, 76 (59%) reported experiencing any level of pain in the last week; 49 (38%) reported a worst pain score ≥4/10 of which 38 (78%) used analgesics over the past week and 31 (63%) used daily analgesia.
  • Among the 49 patients with pain scores ≥4/10, current or past docetaxel use was reported by 32 (65%), androgen deprivation therapy by 47 (96%), and 28 (57%) had been or were currently enrolled in a clinical trial.
  • CONCLUSIONS: Pain is sufficiently prevalent in men with metastatic prostate cancer to enable prospective assessment of palliation endpoints in clinical trials.

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  • (PMID = 27960916.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Braud AC, Joly F, Rios M, Felizot L, Fargeot P, Servent V, Laguerre B, Turpin F, Pein F: Preservation of Activities Daily Living (ADL) in a phase-II impact study of oral capecitabine and vinorelbine in the treatment of metastatic carcinomas in patients 70 and older: The GERICO-01 Study by the French FNCLCC Group. J Clin Oncol; 2004 Jul 15;22(14_suppl):8160

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preservation of Activities Daily Living (ADL) in a phase-II impact study of oral capecitabine and vinorelbine in the treatment of metastatic carcinomas in patients 70 and older: The GERICO-01 Study by the French FNCLCC Group.
  • METHODS: In Gerico-01, with pts 70 years or older, the primary endpoint of the study was the autonomy preservation as measured by the ADL in 6 item; 2nd objectives were toxicity (NCI-CTC v2), PK study of V, the serum PSA or CA 15-3 levels variation and the tumor targets evaluation (RECIST); the primary tumors were either metastatic disease from a primary Breast, or a lung or a prostate Ca.
  • The treatment was Q-3 weeks an oral combination chemotherapy (CT) with C day 1-14 at a starting dose of 750 mg/m<sup>2</sup> twice a day and oral V, days 1 and 8 at a starting dose of 45 mg/m<sup>2</sup>/d.
  • C+V was discontinued in progressive disease, or the loss of 2 or more ADL criteria, or any grade III-IV toxicities.
  • RESULTS: Between december 2002 and 2003, 65 pts were included in 8 different French centers and 12 are still under treatment.
  • The pts' median age was 75 yrs (70-86); the primary was a breast in 28, a prostate in 31 and a lung Ca in 6 pts.
  • Among breast carcinoma there were 5 partial remission, 1 in prostate and 1 in lung ca, stable disease was seen in 2 breast, 9 prostate, 1 lung; C+V was stopped in 9 progressive disease, 3 cases of toxicity, 1 pt. refusal.

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  • (PMID = 28015421.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Morris MJ, Kelly WK, Slovin S, Sauter N, Eicher C, Regan K, Curley T, Delacruz A, Reuter V, Scher HI: Phase I trial of exogenous testosterone (T) for the treatment of castrate metastatic prostate cancer (PC). J Clin Oncol; 2004 Jul 15;22(14_suppl):4560

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of exogenous testosterone (T) for the treatment of castrate metastatic prostate cancer (PC).
  • : 4560 Background: Standard treatment for metastatic PC is androgen withdrawal.
  • METHODS: Eligible patients (pts) had metastatic PC with progression on scans or PSA rises >25% over baseline, had T levels <30 mg/dl, were castrate for ≥1 year, and had failed anti-androgen withdrawal.
  • Pts were treated with T-containing transdermal patches or gel.
  • Three cohorts of 3-6 pts each were defined by treatment duration: 1 week of T, 4 weeks of T, and treatment with T until progression.
  • Antitumor effects were gauged by post-treatment PSA assays and imaging studies.
  • No pt was taken off study for tumor flare, defined as an increase in tumor-related symptoms within the first two weeks of therapy.
  • Therapy was well tolerated.
  • There were no grade 4 events, and only 1 grade 3 event (transaminitis) was felt to be possibly related to drug.
  • Median treatment duration for cohort 3 was 59 days (range 27-124).
  • 1 pt achieved a ≥50% post-treatment PSA decline; 2 pts had stable PSAs; no pts had a radiographic response.
  • CONCLUSIONS: Administration of T to patients with advanced PC for 1 week, 4 weeks, or until disease progression is safe, and not limited by tumor flare.
  • Combinations of T with other agents that modulate AR may be a more productive strategy than continuous monotherapy.
  • Support: Prostate Cancer Foundation, PepsiCo, Sacerdote Fund, NIH CA102544 No significant financial relationships to disclose.

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  • (PMID = 28015943.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Araujo J, Armstrong AJ, Braud EL, Posadas E, Lonberg M, Gallick GE, Trudel GC, Paliwal P, Agrawal S, Logothetis CJ: Dasatinib and docetaxel combination treatment for patients with castration-resistant progressive prostate cancer: A phase I/II study (CA180086). J Clin Oncol; 2009 May 20;27(15_suppl):5061

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dasatinib and docetaxel combination treatment for patients with castration-resistant progressive prostate cancer: A phase I/II study (CA180086).
  • : 5061 Background: Dasatinib, a potent inhibitor of SRC family kinases, inhibits in vitro prostate cancer cell proliferation and migration.
  • We report promising preliminary results of dasatinib in combination with docetaxel (D) for treatment of metastatic castration-resistant prostate cancer (CRPC).
  • METHODS: Male pts with progressive CRPC and castrate levels of testosterone (≤50 ng/dL) requiring chemotherapy were enrolled.
  • 2) was to determine drug-drug interactions.
  • Secondary endpoints were: changes in PSA, bone scans and tumor size, bone metabolism [urinary N-telopeptide (uNTX) and bone alkaline phosphatase (BAP)] and PK.
  • RESULTS: 46 pts were treated with 28 pts still on therapy.
  • Median treatment duration (n = 18, pts off study) was 4.2 months (0.13-9.63).
  • PSA response was seen in 13/32 (41%) pts, clinical benefit (PR + SD) for RECIST-evaluable pts was 21/21, [7 PR, 5 uPR and 4 SD (at ≥21 wks) and 5 SD at ≥6 wk)].
  • CONCLUSIONS: Dasatinib and D at doses up to 120 mg QD and 75 mg/m<sup>2</sup> are safe with manageable toxicities and no drug-drug interactions.
  • These data confirm the antitumor and antiosteoclast activity of dasatinib in combination with D and serve as the basis for the ongoing phase III study of this combination.

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  • (PMID = 27962978.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Fleisher M, Danila DC, Leversha M, Rathkopf D, Slovin S, Anand A, Koscuiszka M, Haqq C, Scher HI: Circulating tumor cells (CTC) in patients with metastatic castration-resistant prostate cancer (CRPC) receiving abiraterone acetate (AA) after failure of docetaxel-based chemotherapy. J Clin Oncol; 2009 May 20;27(15_suppl):5049

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Circulating tumor cells (CTC) in patients with metastatic castration-resistant prostate cancer (CRPC) receiving abiraterone acetate (AA) after failure of docetaxel-based chemotherapy.
  • : 5049 Background: Selecting targeted therapies and assessing outcome in patients (pts) with CRPC are significant unmet medical needs.
  • METHODS: AA (1000 mg QD oral) was studied in pts with metastatic CRPC who had progressed on docetaxel based chemotherapy.
  • We monitored changes in CTC number with therapy, and performed FISH for AR in CTC as previously described.
  • RESULTS: At MSKCC, 54 pts were screened and 48 treated; 38 pts received prednisone from the start of treatment.
  • Prior systemic therapy included > 3 hormonal therapies in 63%; while 71% received 1, 29% had 2 lines of chemotherapy.
  • Metastatic sites were bone alone in 10 pts (21%), bone and lymph nodes in 21 (44%), 15 (31%) with visceral disease, 2 with soft tissue alone.
  • Baseline CTC count was > 5 in 35 pts, whereas 13 pts had <5; CTC changes with treatment are presented in table below.
  • Pts in Group A were treated on protocol for a median of 8.9 m, compared to 2.8 m in group B (P <0.001).
  • Among pts with baseline CTC > 5, the CTC decline to <5 was associated with a decline in PSA by >50% (p< 0.001).
  • From 28 pts with FISH in CTC, 13 (47%) pts had AR amplification, 8 (29%) pts had copy number gain, and 5 (10%) pts had no evident AR copy number abnormalities; FISH failed in 2 pts.
  • CONCLUSIONS: Changes in CTC with treatment may represent valuable intermediary endpoints for clinical benefit.
  • We are prospectively testing pre and post-therapy CTC, and separately AR FISH profiles and clinical outcomes in COU-AA-301, a phase III trial for CRPC patients who have received docetaxel based chemotherapy.

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  • (PMID = 27962948.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. Campana F, Raymond E, Misset JL, Cvitkovic E, Cvitkovic F: Activity of oxaliplatin and 5-fluorouracil/folinic acid (FOLFOX2) in elderly patients with simultaneous advanced colon (ACC) and Hormone refractory prostate cancer (HRPC). J Clin Oncol; 2004 Jul 15;22(14_suppl):8241

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of oxaliplatin and 5-fluorouracil/folinic acid (FOLFOX2) in elderly patients with simultaneous advanced colon (ACC) and Hormone refractory prostate cancer (HRPC).
  • Tumor response was evaluated clinically by ultrasound, CT-Scan and CEA.
  • PSA was also used to assess the response of prostate cancer.
  • RESULTS: Two patients (pts) (PS 1; age:72 and 74) with measurable liver metastasis (colon cancer), non measurable but symptomatic bone metastasis (prostate cancer), and elevated baseline PSA values (12.5 and 255 ng/ml) were evaluable for toxicity and response.
  • FOLFOX2 induced objective responses (60% and 70% tumor regression that lasted 8+ and 6 months) in colon cancer liver metastasis.
  • Chemotherapy was associated with pain relief and significant reductions of PSA values (90% decrease in one pt and normalization in the other).
  • CONCLUSION: Our clinical experience suggests that front-line FOLFOX2 chemotherapy is safe and active to control tumor progression of synchronous advanced colon and hormone-refractory prostate cancers in elderly males.

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  • (PMID = 28016662.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. Hudes G, Tagawa S, Whang Y, Qi M, Qin X, Puchalski T, Prabhakar U, O'Brien K, Eisenberger M: A phase I study of CNTO328, an anti-interleukin (IL)-6 monoclonal antibody combined with docetaxel in subjects with metastatic castration-resistant prostate cancer (CRPC). J Clin Oncol; 2009 May 20;27(15_suppl):5063

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of CNTO328, an anti-interleukin (IL)-6 monoclonal antibody combined with docetaxel in subjects with metastatic castration-resistant prostate cancer (CRPC).
  • : 5063 Background: IL-6 is a potential mediator of prostate cancer morbidity and mortality and may protect prostate cancer cells from chemotherapy-induced apoptosis.
  • CNTO328, a chimeric anti-IL-6 antibody, has been shown to inhibit prostate tumor growth in xenograft mouse models.
  • METHODS: Chemotherapy-naïve patients with metastatic CRPC were administered CNTO328 in combination with T (75 mg/m2 q3w) in 3 dose-escalation cohorts (6 mg/kg q2w, and 9 and 12 mg/kg q3w) following an initial run-in cycle of T alone to examine the effect of CNTO328 on T pharmacokinetics (PK).
  • Prostate specific antigen (PSA), radiological response, and C-reactive protein (CRP), the best-known surrogate of serum IL-6 bioactivity, were also assessed.
  • 36 patients with KPS ≥70, median age 66 (range 43-82) received 6 (median) cycles of T (range 1-37).
  • 32 patients received at least one dose of CNTO328 in combination with T and are evaluable.
  • CONCLUSIONS: CNTO328 with T is well tolerated and demonstrates biological and clinical activity in CRPC that warrants further study.

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  • (PMID = 27962976.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Strada MR, Frascaroli M, Jedrychowska I, Palumbo R, Poggi G, Bernardo A, Villani G, Melazzini M, Bernardo G: Prospective phase II study of integrated rehabilitative treatment in oncologic patients with neuromotor damage from vertebral metastases. J Clin Oncol; 2004 Jul 15;22(14_suppl):8207

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prospective phase II study of integrated rehabilitative treatment in oncologic patients with neuromotor damage from vertebral metastases.
  • : 8207 Background: Breast, lung and prostate cancer are associated with a high incidence of bone and osteomedullar metastases, often responsible of a neuromotor damage.
  • A prospective study was designed to verify the feasibility and activity of an integrated rehabilitative protocol in pts with neuromotor damage from vertebral metastases.
  • METHODS: Treatment was performed throughout the following steps, with short-term objectives:.
  • Primary tumor was breast carcinoma in 21 pts (47%), lung cancer in 12 pts (27%), prostate carcinoma in 8 pts (18%), ependyma, testis, non-Hodgkin lymphoma and multiple myeloma in each one of the remaining 4 pts.
  • Most pts (82%) had received combined chemo-radiotherapy; while radiotherapy and chemotherapy alone were given in 6 and 3 pts, respectively.
  • Treatment compliance was good, with no drop-out; improvement of QoL was observed in 93% of pts (43/45) by FACT-G.
  • CONCLUSIONS: Our results show that such an integrated rehabilitative program in metastatic pts with neuromotor damage from vertebral metastases produced a good clinical activity in both preventing the damages following neurological deficit and optimizing the residual motor potentialities, also improving patient QoL throughout the achievement of the best possible autonomy.

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  • (PMID = 28016814.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Slovin SF, Beer TM, Higano CS, Tejwani S, Hamid O, Picus J, Harzstark A, Scher HI, Lan Z, Lowy I, Prostate Cancer Clinical Trials Consortium: Initial phase II experience of ipilimumab (IPI) alone and in combination with radiotherapy (XRT) in patients with metastatic castration-resistant prostate cancer (mCRPC). J Clin Oncol; 2009 May 20;27(15_suppl):5138

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Initial phase II experience of ipilimumab (IPI) alone and in combination with radiotherapy (XRT) in patients with metastatic castration-resistant prostate cancer (mCRPC).
  • : 5138 Background: IPI is a fully human, monoclonal anti-CTLA-4 antibody capable of enhancing anti-tumor immunity.
  • In preclinical models, XRT releases tumor antigens and enhances anti-tumor activity of CTLA-4 blockade.
  • (1) IPI alone n=16, (2) IPI + XRT n=15 chemotherapy naïve (NoCHEMO), and (3) IPI + XRT n=14 chemotherapy experienced (CHEMO) pts.
  • Median time to PSA decline was 5.7 wks (r 3 to 21 wks); median duration 23 wks (r 3 to 84+ wks).
  • In one pt dosed with IPI alone, PSA ≤ 0.05 ng/ml, as well as a CR of bone, nodal and prostate lesions continue for 54+ and 84+ wks, respectively.
  • CONCLUSIONS: irAEs in the 10 mg/kg cohorts are similar in type and rate to IPI in melanoma. irAEs and PSA declines occurred in chemotherapy naïve and post chemotherapy patients, and with or without XRT.
  • Time to response can be delayed, with a durable median response of 23 wks.

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  • (PMID = 27964424.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. Bendell JC, Weiss GJ, Infante JR, Chiorean EG, Borad M, Tibes R, Jones SF, Langmuir VK, Kroll S, Burris HA: Final results of a phase I study of TH-302, a hypoxia-activated cytotoxic prodrug (HAP). J Clin Oncol; 2009 May 20;27(15_suppl):2573

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Final results of a phase I study of TH-302, a hypoxia-activated cytotoxic prodrug (HAP).
  • : 2573 Background: TH-302 is a 2-nitroimidazole prodrug of the DNA alkylator, bromo-isophosphoramide mustard (Br-IPM).
  • TH-302 is essentially inactive under normoxia but in severe hypoxia and in the presence of certain reductases, it is reduced and Br-IPM is released.
  • METHODS: Eligible patients (pts) had ECOG ≤1, advanced or metastatic solid tumors, evaluable by RECIST, and acceptable hematologic, liver and renal function.
  • TH-302 was administered intravenously over 30-60 minutes on Day 1, 8 and 15 of a 28-day cycle.
  • Primary tumor: prostate (8), colorectal (8), lung (5) other (8).
  • The most common TH-302-related AEs were nausea, skin lesions, vomiting and fatigue.
  • Cmax and AUC for TH-302 and Br-IPM increased linearly with no accumulation at Day 15.
  • CONCLUSIONS: Weekly TH-302 has remarkably little hematologic toxicity.
  • Skin and mucosal AEs have developed at the higher dose levels.
  • TH-302 is the first HAP to demonstrate tumor responses in Phase I.
  • Studies in combination with chemotherapy are ongoing.

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  • (PMID = 27961897.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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42. Hauser KA, Karafa M, Seyidova-Khoshknabi D, Davis MP, Walsh D: Prevalence and risk factors of vitamin D insufficiency in cancer. J Clin Oncol; 2009 May 20;27(15_suppl):9581

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence and risk factors of vitamin D insufficiency in cancer.
  • : 9581 Background: Low vitamin D has been linked to increased cancer incidence and reduced prognosis.
  • Little is known about prevalence and risks of insufficiency in cancer.
  • METHODS: Electronic medical records of all adult solid tumor patients treated at The Cleveland Clinic in 2006-2007 were reviewed.
  • Data extracted: demographics (age, gender, race), cancer site (primary and metastatic, ICD-9 codes) and first 25 hydroxy vitamin D level [25OHD] during the study period.
  • Laboratory data (calcium, hepatic and renal function), medications prescribed (anticonvulsants, antineoplastic, corticosteroids, vitamin D) and treatment procedures (chemotherapy and radiotherapy) in 2 months preceding vitamin D were recorded.
  • Most common cancers: breast (19%), prostate (18%), skin (13%).
  • They were more likely female (66% vs 47%), and to have breast, hepatobiliary, skin or thyroid cancer, than those not tested (both p<0.001).
  • Insufficiency was associated with male gender, race (African American), month of test (Feb-Apr, Oct), cancer type (hepatobiliary, genitourinary, pancreas, upper gastrointestinal), metastatic disease, low albumin, high bilirubin and AST, and lack of antineoplastic or vitamin D medication (all p<0.01).
  • Multivariable predictors were cancer type, test month, African American race, low albumin, and lack of antineoplastic or vitamin D medication (all p<0.01).
  • CONCLUSIONS: Vitamin D insufficiency is highly prevalent among cancer patients tested.
  • This study is limited by selection bias but indicates need for prospective vitamin D evaluation in cancer.

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  • (PMID = 27963701.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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43. Gallagher RE, Ferrari A, Kaubisch A, Makower D, Stein C, Rajdev L, Gucalp R, Wadler S, Mandeli J, Sarta C: Arsenic trioxide (ATO) in metastatic hormone-refractory prostate cancer (HRPC): Results of phase II trial T99-0077. J Clin Oncol; 2004 Jul 15;22(14_suppl):4638

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenic trioxide (ATO) in metastatic hormone-refractory prostate cancer (HRPC): Results of phase II trial T99-0077.
  • : 4638 Background: Chemotherapy regimens for HRPC frequently produce clinical responses, as measured by a decline in serum prostate-specific antigen (PSA) or, less frequently, by objective criteria but have, at best, a modest effect on survival.
  • In the effort to discover alternative effective therapy, ATO was tested for efficacy in HRPC, based on in vitro evidence of anti-prostate cancer cell activity and on remarkable clinical effectiveness in acute promyelocytic leukemia (APL), partly due to induction of APL cell terminal differentiation.
  • METHODS: Patient (pt) eligibility required failure of ≥2 prior hormonal therapies ± chemotherapy, PSA ≥10 ng/mL with metastatic disease and ECOG performance status ≤2.
  • The primary endpoint was confirmed ≥50% reduction in PSA and/or >30% tumor shrinkage by RECIST criteria after 16 weeks of treatment.
  • Since ATO might produce an early PSA increase due to tumor cell differentiation, only pts who completed 2 cycles (schedule 1) or 6 weeks maintenance (schedule 2) were considered evaluable.
  • RESULTS: Of 19 pts registered, 15 were evaluable; 7/15 had failed previous chemotherapy.
  • Grade 3/4 toxicity occurred in 13 pts, requiring dose reductions in 4 and protocol removal in 2 cases; causes were (pt #): neutropenia (4), anemia (2), diarrhea (2), fluid/electrolyte disturbances (2, 1 with pericardial tamponade), fatigue (2), musculoskeletal symptoms (2), and skin rash (1).
  • CONCLUSIONS: ATO monotherapy has limited efficacy for the treatment of HRPC, associated with moderate toxicity.
  • A high incidence of decreased PSA velocity suggests an early cytostatic rather than differentiation effect on tumor cells.

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  • (PMID = 28015774.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Aguero MF, Venero M, Brown DM, Smulson ME, Espinoza LA: Phenoxodiol inhibits growth of metastatic prostate cancer cells. Prostate; 2010 Aug;70(11):1211-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phenoxodiol inhibits growth of metastatic prostate cancer cells.
  • BACKGROUND: Phenoxodiol, a synthetic analog of Genistein, is being assessed in several clinical studies against a range of cancer types and was shown to have a good efficacy and safety profile.
  • In this study we tested the effects of Phenoxodiol against prostate cancer cell lines.
  • METHODS: Cell-cycle analysis, plasmatic membrane damage, clonogenic assay, comet assay, and Western blot methodologies were employed to assess the effects of Phenoxodiol on prostate cancer cell lines.
  • An in vivo model confirmed the potential therapeutic efficacy of Phenoxodiol when administered orally to tumor bearing mice.
  • RESULTS: Phenoxodiol treatment promoted a marked inhibition of proliferation and loss of colony formation in LNCaP cells in a dose- and time-dependent manner.
  • Similar effects were also observed in the metastatic prostate cell lines PC3 and DU145.
  • Oral administration of Phenoxodiol induced a considerable growth inhibition of malignant tumors generated by inoculation of LNCaP cells into Balb/c nu/nu athymic mice.
  • CONCLUSIONS: These data demonstrated that Phenoxodiol promotes apoptosis, as determined by PARP-1 degradation, via mitochondrial depolarization and G1/S cell-cycle arrest thereby confirming that it is active against androgen-dependent and independent prostate cancer cells.
  • Although a precise target for Phenoxodiol has not been identified, these data contribute to our understanding of the mechanism by which this drug promotes cell death in prostate cancer cells, and warrants the continued clinical development of Phenoxodiol as a therapeutic for the treatment of metastatic prostate cancer.
  • [MeSH-major] Isoflavones / pharmacology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Comet Assay. DNA Damage. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / metabolism. Neoplasms, Hormone-Dependent / pathology. Poly(ADP-ribose) Polymerase Inhibitors. Poly(ADP-ribose) Polymerases / metabolism. Xenograft Model Antitumor Assays

  • Genetic Alliance. consumer health - Prostate cancer.
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  • [Copyright] 2010. (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20564423.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoflavones; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 995FT1W541 / phenoxodiol; EC 2.4.2.30 / PARP1 protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
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45. Nyirády P, Sárdi E, Beko G, Szucs M, Horváth A, Székely E, Szentmihályi K, Romics I, Blázovics A: [Effects of bioactive molecules of Beta vulgaris L. ssp. esculenta var. rubra on metastatic prostate cancer]. Orv Hetil; 2010 Sep 12;151(37):1495-503
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effects of bioactive molecules of Beta vulgaris L. ssp. esculenta var. rubra on metastatic prostate cancer].
  • Several reports are known about the effects of nutrition supplements in the improvement of quality of life of patients with tumor, however, the physiological background remains largely unknown.
  • METHODS: Natural table beet product come from commercial service was given twice 10 g daily for 1 month for 24 patients (mean age 68+/-8 years) with hormone-resistant and metastatic prostate cancer treated with taxan chemotherapy, who report themselves first, mean 3,6+/-2,8 years ago with their complains.
  • 18 men's data were amenable after treatment for evaluation.
  • In addition to routine laboratory examination values of HbA1c, 9 cytokines and levels of 3 growth factors, the global parameters of redox-homeostasis, few elements of their metal-ions, Zn- and level of free protoporfirin, trans-metilating processes before and 1 month after treatment were determined.
  • CONCLUSIONS: According to results, it seems that moderate and permanent consumption of table beet product affects the life expectancy of patients favorably; however, due to the increasing values of EGF, medical control is necessary for patients with prostate cancer treated by chemotherapy.
  • [MeSH-major] Adenocarcinoma / drug therapy. Beta vulgaris. Phytotherapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Chromatography, High Pressure Liquid. Humans. Luminescent Measurements. Male. Middle Aged. Plant Extracts / therapeutic use. Taxoids / therapeutic use. Trace Elements / blood. Treatment Outcome


46. Small EJ, Smith MR, Seaman JJ, Petrone S, Kowalski MO: Combined analysis of two multicenter, randomized, placebo-controlled studies of pamidronate disodium for the palliation of bone pain in men with metastatic prostate cancer. J Clin Oncol; 2003 Dec 1;21(23):4277-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined analysis of two multicenter, randomized, placebo-controlled studies of pamidronate disodium for the palliation of bone pain in men with metastatic prostate cancer.
  • PURPOSE: Bone metastases occur in approximately 80% of patients with advanced prostate cancer.
  • The purpose of this study was to evaluate the effect of an intravenous bisphosphonate, pamidronate disodium, on pain control in metastatic prostate cancer patients.
  • PATIENTS AND METHODS: Two multicenter, double-blind, randomized, placebo-controlled trials were conducted in patients with bone pain due to metastatic prostate cancer, with disease progression after first-line hormonal therapy.
  • Efficacy was measured via self-reported pain score (Brief Pain Inventory), analgesic use, the proportion of patients with a skeletal-related event (SRE; defined as pathologic fracture, radiation or surgery to bone, spinal cord compression, or hypercalcemia), and a pilot quantitative measurement of mobility.
  • Laboratory evaluations included serum prostate-specific antigen, interleukin-6, bone alkaline phosphatase, and urinary bone resorption markers.
  • CONCLUSION: Pamidronate disodium failed to demonstrate a significant overall treatment benefit compared with placebo in palliation of bone pain or reduction of SREs.
  • Evaluation of more potent bisphosphonates in patients with prostate cancer is warranted.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Neoplasms / drug therapy. Diphosphonates / therapeutic use. Pain / drug therapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Double-Blind Method. Humans. Male. Middle Aged. Palliative Care. Placebos. Retrospective Studies. Treatment Outcome


47. Michaelson MD, Kaufman DS, Kantoff P, Oh WK, Smith MR: Randomized phase II study of atrasentan alone or in combination with zoledronic acid in men with metastatic prostate cancer. Cancer; 2006 Aug 1;107(3):530-5
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  • [Title] Randomized phase II study of atrasentan alone or in combination with zoledronic acid in men with metastatic prostate cancer.
  • BACKGROUND: Metastatic prostate cancer is characterized by the presence of osteoblastic bone metastases.
  • Bone metastases account for most of the morbidity from this disease.
  • METHODS: The effects of atrasentan alone versus combination therapy with atrasentan and zoledronic acid were investigated on bone turnover markers in men with bone metastases from prostate cancer.
  • Forty-four men were randomized to receive either atrasentan alone or combination therapy, and 33 completed at least 12 weeks of treatment and were included in the primary analysis.
  • RESULTS: Treatment with the combination resulted in significantly lower serum levels of N-telopeptide, a marker of bone resorption, compared with treatment with atrasentan alone.
  • No Grade 4 or 5 treatment-related toxicities were observed.
  • There was minimal clinical efficacy, with no objective responses and only 1 prostate-specific antigen (PSA) response.
  • CONCLUSIONS: There is no evidence for additive or synergistic effects of combination therapy with atrasentan and zoledronic acid on bone turnover markers in men with metastatic prostate cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols. Diphosphonates / administration & dosage. Imidazoles / administration & dosage. Prostatic Neoplasms / drug therapy. Pyrrolidines / administration & dosage
  • [MeSH-minor] Aged. Aged, 80 and over. Alkaline Phosphatase / analysis. Biomarkers, Tumor / analysis. Bone Density Conservation Agents / administration & dosage. Bone Density Conservation Agents / adverse effects. Bone Neoplasms / metabolism. Bone Neoplasms / secondary. Bone and Bones / enzymology. Bone and Bones / metabolism. Disease Progression. Dyspnea / complications. Edema / complications. Humans. Male. Middle Aged. Neoplasm Metastasis. Treatment Outcome

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  • [Copyright] Copyright 2006 American Cancer Society.
  • (PMID = 16804927.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1K12CA87723
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 0 / Pyrrolidines; 6XC1PAD3KF / zoledronic acid; EC 3.1.3.1 / Alkaline Phosphatase; V6D7VK2215 / atrasentan
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48. Yashi M, Nukui A, Kurokawa S, Ochi M, Ishikawa S, Goto K, Kobayashi Y, Muraishi O, Tokue A: Elevated serum progastrin-releasing peptide (31-98) level is a predictor of short response duration after hormonal therapy in metastatic prostate cancer. Prostate; 2003 Sep 1;56(4):305-12
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  • [Title] Elevated serum progastrin-releasing peptide (31-98) level is a predictor of short response duration after hormonal therapy in metastatic prostate cancer.
  • BACKGROUND: The neuroendocrine (NE) pathway has been attracting attention as a mechanism for the androgen-independent progression because the neuropeptide provokes tumor growth and inhibits apoptosis under androgen-deprived milieu in prostate cancer cells.
  • METHODS: Serum ProGRP status was determined with an enzyme-linked immunosorbent assay (ELISA) in 460 men with benign and malignant prostatic diseases, chronic renal failure, and healthy controls.
  • Seventy patients with metastatic prostate cancer including four patients (5.7%) with NE carcinoma who underwent hormonal therapy were enrolled in the prognostic analyses by Cox proportional hazards model.
  • RESULTS: The serum status steadily shifted toward predominant expression of ProGRP with the progression of prostate cancer into metastatic and androgen-independent stages.
  • Univariate analysis revealed that the deteriorated performance status (PS) and extent of bony disease (EOD), and high serum alkaline phosphatase (ALP), serum ProGRP, and nadir prostate-specific antigen (PSA) levels were associated with a lower progression-free survival (PFS) rate (P < 0.005).
  • Serum ProGRP was the most significant predictor among pre-treatment factors in this model (P = 0.0094).
  • CONCLUSIONS: The neuropeptide precursor ProGRP is a distinct serum marker that is useful to know the NE milieu and provides prognostic information in patients with advanced prostate cancer.
  • Standard therapy for metastatic prostate cancer may make progress when further studies will clarify the causative link between serum ProGRP level and androgen-independent disease progression.
  • [MeSH-major] Biomarkers, Tumor / analysis. Gastrointestinal Hormones / analysis. Neoplasm Metastasis. Neoplasm Staging / methods. Peptide Fragments / analysis. Peptides / analysis. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Recombinant Proteins / analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Androgens / pharmacology. Antineoplastic Agents, Hormonal / pharmacology. Drug Resistance, Neoplasm. Enzyme-Linked Immunosorbent Assay. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis. Prostate-Specific Antigen / analysis. Treatment Outcome

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12858359.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Gastrointestinal Hormones; 0 / Peptide Fragments; 0 / Peptides; 0 / Recombinant Proteins; 0 / pro-gastrin-releasing peptide (31-98); EC 3.4.21.77 / Prostate-Specific Antigen
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49. Slipman CW, Patel RK, Siegelman ES, Cirigliano M, Bhat AL, Isaac Z, Lenrow D: Metastatic prostate cancer to the spine and a PSA of 5666: a case report. Pain Physician; 2001 Oct;4(4):317-21
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  • [Title] Metastatic prostate cancer to the spine and a PSA of 5666: a case report.
  • Prostate cancer is the most commonly diagnosed cancer and the second most common cause of cancer death among American men.
  • To our knowledge, the highest reported prostate specific antigen (PSA) level on initial presentation is 3280 ng/mL.
  • A magnetic resonance imaging study of the lumbar spine revealed numerous osseous metastatic lesions, and the PSA level was found to be 5666 ng/mL.
  • He was treated with oral narcotics and a Duragesic patch to achieve analgesia and bicalutamide (Casodex) and leuprolide acetate (Lupron) therapy for androgen blockade.
  • Later in his course, he required chemotherapy due to hormone-refractory prostate cancer.
  • The objective of this report is to discuss the first patient with metastatic prostate cancer to the spine with PSA level greater than 3,500 ng/mL.

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  • (PMID = 16902677.001).
  • [ISSN] 1533-3159
  • [Journal-full-title] Pain physician
  • [ISO-abbreviation] Pain Physician
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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50. Fontana A, Falcone A, Derosa L, Di Desidero T, Danesi R, Bocci G: Metronomic chemotherapy for metastatic prostate cancer: a 'young' concept for old patients? Drugs Aging; 2010 Sep 01;27(9):689-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metronomic chemotherapy for metastatic prostate cancer: a 'young' concept for old patients?
  • Prostate cancer is a common disease in the elderly, and the number of older prostate cancer patients will probably increase with both the aging of the population and the increased rate of screening.
  • In elderly patients with several co-morbidities, cancer management can be complex, and the risk of administering toxic therapy in this setting should be carefully evaluated.
  • Metronomic chemotherapy, i.e. low-dose, long-term, frequently administered chemotherapy, has been shown to have a significant stabilizing effect on cancer and a positive impact on the quality of life of patients, including those with prostate cancer.
  • Given the low toxicity profile of metronomic chemotherapy, elderly patients or patients with co-morbidities may be candidates for a first-line or second-line oral metronomic approach when standard chemotherapies are contraindicated or not acceptable to the patient.
  • Moreover, the possibility of patients being able to spend more time at home is an important component of a palliative treatment such as metronomic chemotherapy.
  • Unfortunately, and despite these considerations, very few data are available on the activity and safety of metronomic chemotherapy in elderly patients.
  • However, retrospective analyses conducted in a small cohort of patients have been published and, notwithstanding their limitations, indicate that novel metronomic schedules are well tolerated, safe and show potentially interesting activity in elderly, 'unfit' (poor performance status) patients with metastatic prostate cancer.
  • Therefore, evaluation of metronomic chemotherapy strategies in prospective, randomized, phase II/III clinical studies of elderly patients with metastatic prostate cancer appears to be warranted.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Drug Administration Schedule. Humans. Male. Neoplasm Metastasis

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  • [Cites] Clin Prostate Cancer. 2003 Dec;2(3):167-72 [15040860.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4899-905 [18794539.001]
  • [Cites] Cancer. 2003 Oct 15;98(8):1643-8 [14534880.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]
  • [Cites] Curr Opin Support Palliat Care. 2007 Oct;1(3):187-91 [18685361.001]
  • [Cites] Cancer Treat Rev. 2009 Oct;35(6):522-7 [19487081.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):242-5 [18182665.001]
  • [Cites] J Urol. 2007 Jun;177(6):2136-40; discussion 2140 [17509300.001]
  • [Cites] J Clin Oncol. 2008 Jan 1;26(1):76-82 [18165643.001]
  • [Cites] Cancer Chemother Pharmacol. 2009 Jun;64(1):189-93 [19151974.001]
  • [Cites] Anticancer Drugs. 2006 Sep;17(8):961-7 [16940806.001]
  • [Cites] CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49 [19474385.001]
  • [Cites] Nat Clin Pract Urol. 2009 Feb;6(2):76-85 [19198621.001]
  • [Cites] Med Oncol. 2010 Jun;27(2):363-7 [19365737.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]
  • [Cites] Br J Cancer. 2008 Apr 22;98 (8):1312-9 [18362940.001]
  • [Cites] Clin Cancer Res. 2009 Aug 1;15(15):4954-62 [19622584.001]
  • [Cites] Invest New Drugs. 2010 Oct;28(5):684-9 [19669699.001]
  • [Cites] Cancer Immunol Immunother. 2007 May;56(5):641-8 [16960692.001]
  • [Cites] Eur Urol. 2009 Jun;55(6):1368-75 [18706755.001]
  • [Cites] J Am Geriatr Soc. 2010 May;58(5):986-8 [20722827.001]
  • [Cites] Semin Oncol. 2008 Dec;35(6):597-617 [19027464.001]
  • [Cites] Nihon Ronen Igakkai Zasshi. 2009 May;46(3):264-8 [19521048.001]
  • [Cites] Cancer Res. 2002 May 15;62(10):2731-5 [12019144.001]
  • [Cites] Ann Oncol. 2005 Aug;16(8):1243-52 [15905308.001]
  • [Cites] Tumori. 2009 Jan-Feb;95(1):130; author reply 131 [19366074.001]
  • [Cites] Nat Rev Clin Oncol. 2010 Jan;7(1):13-21 [19997075.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12917-22 [14561896.001]
  • [Cites] Ann Hematol. 2009 Dec;88(12):1257-9 [19330332.001]
  • [Cites] Tumori. 2007 Nov-Dec;93(6):647 [18338509.001]
  • (PMID = 20809660.001).
  • [ISSN] 1179-1969
  • [Journal-full-title] Drugs & aging
  • [ISO-abbreviation] Drugs Aging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
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51. Lein M, Wirth M, Miller K, Eickenberg HU, Weissbach L, Schmidt K, Haus U, Stephan C, Meissner S, Loening SA, Jung K: Serial markers of bone turnover in men with metastatic prostate cancer treated with zoledronic Acid for detection of bone metastases progression. Eur Urol; 2007 Nov;52(5):1381-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serial markers of bone turnover in men with metastatic prostate cancer treated with zoledronic Acid for detection of bone metastases progression.
  • OBJECTIVES: This study assessed the usefulness of serial measurements of bone turnover markers in men with metastatic prostate cancer treated with zoledronic acid to detect disease progression.
  • METHODS: Serum measurements of total alkaline phosphatase (tALP), bone-specific alkaline phosphatase (bALP), cross-linked N-terminal (NTx) and cross-linked C-terminal (CTx) telopeptides of type I collagen, amino-terminal procollagen propeptides of type I collagen (PINP), C-terminal telopeptides of type I collagen (ICTP), and prostate-specific antigen (PSA) were performed in 77 prostate cancer patients suffering from bone metastases and treated with zoledronic acid up to 15 mo.
  • Fifty patients were with and 27 patients without objective evidence of metastatic bone progression during the administration of zoledronic acid.
  • In patients with metastatic bone progression PINP, tALP, bALP, and ICTP were significantly higher at weeks 24, 36, 48, and 60 after starting treatment with zoledronic acid compared with patients without progression.
  • In addition to the information of prostate-specific antigen as a monitoring parameter, the bone formation marker showed a better distinction between patients with and without disease progression.
  • CONCLUSIONS: Selected bone turnover markers provide valuable information regarding progression of bone metastasis in men with metastatic prostate cancer under bisphosphonate therapy.
  • [MeSH-major] Biomarkers, Tumor / blood. Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / blood. Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Prostatic Neoplasms / blood
  • [MeSH-minor] Aged. Alkaline Phosphatase / blood. Collagen Type I / blood. Disease Progression. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Follow-Up Studies. Humans. Male. Middle Aged. Peptide Fragments / blood. Peptides / blood. Procollagen / blood. Prognosis. Prospective Studies. Prostate-Specific Antigen / blood

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  • (PMID = 17321667.001).
  • [ISSN] 0302-2838
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Bone Density Conservation Agents; 0 / Collagen Type I; 0 / Diphosphonates; 0 / Imidazoles; 0 / Peptide Fragments; 0 / Peptides; 0 / Procollagen; 0 / collagen type I trimeric cross-linked peptide; 6XC1PAD3KF / zoledronic acid; EC 3.1.3.1 / Alkaline Phosphatase; EC 3.4.21.77 / Prostate-Specific Antigen
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52. 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

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  • (PMID = 16531199.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; EC 3.4.21.77 / Prostate-Specific Antigen
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53. Okegawa T, Kinjo M, Nutahara K, Higashihara E: Pretreatment serum level of HER2/nue as a prognostic factor in metastatic prostate cancer patients about to undergo endocrine therapy. Int J Urol; 2006 Sep;13(9):1197-201
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  • [Title] Pretreatment serum level of HER2/nue as a prognostic factor in metastatic prostate cancer patients about to undergo endocrine therapy.
  • BACKGROUND: Overexpression of the HER2 receptor protein and amplification of the HER2 gene has been implicated in tumor development and progression, and has been associated with a poor prognosis in several types of cancer.
  • The aim of this study was to evaluate whether pretreatment serum HER2 levels can be used to predict biochemical recurrence-free survival in prostate cancer patients about to undergo endocrine therapy.
  • METHODS: The study population consisted of 379 untreated patients with histologically diagnosed prostate cancer: 197 with T2N0M0, 93 with T3N0M0, 19 with TxN1Mx, and 70 with TxNxM1.
  • Serum HER2 levels were assessed in the prostate cancer patients prior to treatment as well as in a control group of 100 patients with histologically confirmed non-cancer.
  • RESULTS: The mean level of HER2 in serum was significantly higher in prostate cancer patients than non-prostate cancer patients (P = 0.006).
  • Also, the serum HER2 level was significantly higher in bone metastatic cancer patients (14.3 +/- 6.3 ng/mL) than in non-metastatic patients (T2: 11.9 +/- 2.3 ng/mL, P = 0.003; T3: 12.2 +/- 2.8 ng/mL, P = 0.011).
  • The metastatic patients were divided into those with low and high HER2 levels using a cutoff value of 12.6 ng/mL based on receiver-operating characteristic curves.
  • The biochemical recurrence-free rate was significantly poorer in patients with a high HER2 level (P = 0.0078, log-rank test).
  • Multivariate Cox logistic regression analysis demonstrated that the pretreatment serum HER2 value (P = 0.022), serum prostate-specific antigen value (P = 0.018), and extent of disease score (P = 0.027) were independent predictors of recurrence.
  • CONCLUSIONS: The pretreatment serum HER2 level may be a useful independent prognostic factor that is associated with a high risk of biochemical recurrence in metastatic prostate cancer patients about to undergo endocrine therapy.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Biomarkers, Tumor / blood. Bone Neoplasms / blood. Neoplasm Recurrence, Local / blood. Prostatic Neoplasms / blood. Receptor, ErbB-2 / blood
  • [MeSH-minor] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Aged. Anilides / therapeutic use. Disease-Free Survival. Follow-Up Studies. Humans. Male. Neoplasm Staging. Nitriles. Prognosis. Prostate-Specific Antigen / blood. Retrospective Studies. Survival Rate. Tosyl Compounds. Treatment Outcome


54. Cho KS, Oh HY, Lee EJ, Hong SJ: Identification of enhancer of zeste homolog 2 expression in peripheral circulating tumor cells in metastatic prostate cancer patients: a preliminary study. Yonsei Med J; 2007 Dec 31;48(6):1009-14
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  • [Title] Identification of enhancer of zeste homolog 2 expression in peripheral circulating tumor cells in metastatic prostate cancer patients: a preliminary study.
  • PURPOSE: Enhancer of zeste homolog 2 (EZH2), a kind of transcriptional repressor, is reportedly over-expressed in metastatic prostate cancer.
  • In this study, we analyzed EZH2 mRNA in circulating tumor cells (CTCs) in peripheral blood as a biomarker in patients with metastatic prostate cancer.
  • PATIENTS AND METHODS: Ber-EP4 coated immunomagnetic beads were used to harvest CTCs, and mRNA was isolated by oligo- dT conjugated immunomagnetic beads.
  • The sensitivity of this test for detection of EZH2 mRNA was determined by serial dilutions of a human prostate cancer cell line.
  • Blood samples were collected from 20 patients each with metastatic or localized prostate cancer and 10 healthy volunteers.
  • RESULTS: Sensitivity experiments showed that the test was highly sensitive as it could detect 10 tumor cells per 5 mL.
  • EZH2 mRNA expression density in the metastatic prostate cancer group was significantly higher than in the control (p=0.023) and localized prostate cancer groups (p=0.019).
  • There was no difference between the control and localized prostate cancer groups (p > 0.05).
  • CONCLUSION: EZH2 mRNA expression in circulating epithelial cells represents a promising marker for detecting early metastasis in prostate cancer.
  • However, more specific and sensitive techniques for detection of CTCs are needed to avoid mononuclear cell contamination.
  • [MeSH-minor] Aged. Humans. Male. Middle Aged. Neoplasm Metastasis. Polycomb Repressive Complex 2. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • [Cites] Clin Cancer Res. 2002 Jun;8(6):1794-9 [12060619.001]
  • [Cites] Prostate. 2007 Apr 1;67(5):547-56 [17252556.001]
  • [Cites] Urology. 2003 Feb;61(2):277-81 [12597930.001]
  • [Cites] J Natl Cancer Inst. 2003 May 7;95(9):661-8 [12734317.001]
  • [Cites] J Urol. 2000 Jun;163(6):2022-9 [10799250.001]
  • [Cites] J Urol. 2000 Jul;164(1):101-5 [10840432.001]
  • [Cites] J Urol. 2001 Aug;166(2):416-9 [11458039.001]
  • [Cites] Urology. 2001 Sep;58(3):386-92 [11549486.001]
  • [Cites] J Urol. 2002 Feb;167(2 Pt 1):528-34 [11792912.001]
  • [Cites] Br J Cancer. 2004 Jan 26;90(2):443-8 [14735191.001]
  • [Cites] Cancer Res. 1992 Nov 1;52(21):6110-2 [1382851.001]
  • [Cites] Urology. 1994 Jun;43(6):765-75 [7515202.001]
  • [Cites] Cancer Res. 1994 Dec 15;54(24):6306-10 [7527294.001]
  • [Cites] J Clin Oncol. 1994 Dec;12(12):2634-9 [7527455.001]
  • [Cites] J Clin Oncol. 1995 May;13(5):1195-200 [7537803.001]
  • [Cites] Cancer. 1996 Jul 1;78(1):10-6 [8646704.001]
  • [Cites] J Urol. 1996 Nov;156(5):1560-6 [8863538.001]
  • [Cites] Urology. 1997 Aug;50(2):184-8 [9255285.001]
  • [Cites] J Clin Oncol. 1997 Dec;15(12):3451-7 [9396397.001]
  • [Cites] Urology. 2005 Mar;65(3):616-21 [15780403.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 23;102(34):12177-82 [16091473.001]
  • [Cites] Genes Chromosomes Cancer. 2006 Jul;45(7):639-45 [16575874.001]
  • [Cites] Nature. 2002 Oct 10;419(6907):624-9 [12374981.001]
  • (PMID = 18159594.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2
  • [Other-IDs] NLM/ PMC2628187
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55. Dearnaley DP, Sydes MR, Mason MD, Stott M, Powell CS, Robinson AC, Thompson PM, Moffat LE, Naylor SL, Parmar MK, Mrc Pr05 Collaborators: A double-blind, placebo-controlled, randomized trial of oral sodium clodronate for metastatic prostate cancer (MRC PR05 Trial). J Natl Cancer Inst; 2003 Sep 3;95(17):1300-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A double-blind, placebo-controlled, randomized trial of oral sodium clodronate for metastatic prostate cancer (MRC PR05 Trial).
  • BACKGROUND: The most frequent site of metastases from prostate cancer is bone.
  • Bisphosphonates reduce excessive bone turnover while preserving bone structure and mineralization in patients with other tumor types.
  • We conducted a double-blind, placebo-controlled, randomized trial to determine whether the first-generation bisphosphonate sodium clodronate could improve bone progression-free survival (BPFS) times among men with bone metastases from prostate cancer.
  • METHODS: Between June 1994 and July 1998, 311 men who were starting or responding to first-line hormone therapy for bone metastases were randomly assigned to receive oral sodium clodronate (2080 mg/day) or placebo for a maximum of 3 years.
  • Secondary endpoints included overall survival, treatment toxicity, and change in World Health Organization (WHO) performance status.
  • Time-to-event data were analyzed using the log-rank chi-square test and Kaplan-Meier curves.
  • However, the clodronate group reported more gastrointestinal problems and increased lactate dehydrogenase levels and required more frequent modification of the trial drug dose (HR for any adverse event = 1.71, 95% CI = 1.21 to 2.41; P =.002).
  • Results of subgroup analyses suggested that clodronate might be more effective the sooner after diagnosis of metastatic bone disease it is started.
  • CONCLUSION: These results suggest that further studies of the effect of newer generation bisphosphonates on BPFS in men with metastatic prostate cancer are warranted.
  • [MeSH-major] Analgesics, Non-Narcotic / administration & dosage. Bone Neoplasms / complications. Bone Neoplasms / drug therapy. Clodronic Acid / administration & dosage. Pain / prevention & control. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Aged. Androgen Antagonists / administration & dosage. Antineoplastic Agents, Hormonal / administration & dosage. Digestive System / drug effects. Diphosphonates / administration & dosage. Disease-Free Survival. Double-Blind Method. Drug Administration Schedule. Drug Therapy, Combination. Great Britain. Humans. Imidazoles / administration & dosage. Male. Middle Aged. Odds Ratio. Research Design. Survival Analysis. Treatment Outcome


56. Mottet N, Lucas C, Sene E, Avances C, Maubach L, Wolff JM: Intermittent androgen castration: a biological reality during intermittent treatment in metastatic prostate cancer? Urol Int; 2005;75(3):204-8
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  • [Title] Intermittent androgen castration: a biological reality during intermittent treatment in metastatic prostate cancer?
  • INTRODUCTION: To assess the effects of intermittent maximal androgen blockade (IMAB) on testosterone (T) levels during on- and off-treatment periods.
  • MATERIALS AND METHODS: A total of 51 patients with metastatic prostate cancer underwent a 6-months period of continuous maximal androgen blockade (MAB) consisting of leuprorelin (3.75 mg at monthly intervals) plus flutamide (250 mg t.i.d.) followed by IMAB.
  • During each cycle, the cut-off prostate-specific antigen (PSA) levels to stop and resume treatment were 4 and 10 ng/ml, respectively.
  • IMAB continued until progression under treatment occurred.
  • Before treatment, 4 patients had a T lower than normal laboratory value but these recovered all to a normal T value at the end of the first cycle.
  • During the 6 cycles, only 8 patients did not recover a normal T at least once during the off-treatment periods (OTP).
  • The mean T values at the end of each OTP did not change during these 6 cycles (Anova test, p=0.621) with a mean stable recovery delay of 32-43 days (Anova test, p=0.722).
  • CONCLUSION: IMAB protocol with an initial 6-month treatment period can result in an intermittent castration with the recovery of normal T levels in most patients during six consecutive cycles of treatment.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Flutamide / therapeutic use. Leuprolide / therapeutic use. Prostate-Specific Antigen / blood. Prostatic Neoplasms / drug therapy. Testosterone / blood
  • [MeSH-minor] Aged. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Hormonal / therapeutic use. Biomarkers, Tumor / blood. Drug Administration Schedule. Follow-Up Studies. Humans. Male. Neoplasm Metastasis. Prospective Studies. Treatment Outcome

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16215305.001).
  • [ISSN] 0042-1138
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 3XMK78S47O / Testosterone; 76W6J0943E / Flutamide; EC 3.4.21.77 / Prostate-Specific Antigen; EFY6W0M8TG / Leuprolide
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57. Sasaki T, Komiya A, Suzuki H, Shimbo M, Ueda T, Akakura K, Ichikawa T: Changes in chromogranin a serum levels during endocrine therapy in metastatic prostate cancer patients. Eur Urol; 2005 Aug;48(2):224-9; discussion 229-30
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  • [Title] Changes in chromogranin a serum levels during endocrine therapy in metastatic prostate cancer patients.
  • INTRODUCTION: The concept of neuroendocrine (NE) differentiation in prostate cancer has become more widely recognized as its diagnostic, prognostic, and therapeutic usefulness.
  • PATIENTS AND METHODS: We enrolled 38 patients with stage D prostate cancer who underwent endocrine therapy by medical or surgical castration and oral antiandrogen.
  • According to PSA response, serum levels of CGA as a marker of NE differentiation were measured at the multiple points of time;.
  • (1) pre-treatment, (2) complete response (CR), (3) a nadir level of PSA, (4) PSA failure or hormone independent progression.
  • We compared these serum values in relation to efficacy of endocrine therapy.
  • Serum CGA increased as intervals of endocrine therapy became longer with positive correlation (p < 0.05).
  • CONCLUSION: During endocrine therapy in metastatic prostate cancer patients, serum CGA values were not related to serum PSA levels, and increased as treatment periods became longer.
  • It is suggested that CGA velocity has potential to predict androgen independent progression after endocrine therapy.
  • [MeSH-major] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Chromogranins / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Analysis of Variance. Biomarkers, Tumor / blood. Disease Progression. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Prostate-Specific Antigen / blood. Statistics, Nonparametric


58. Johansen JS, Brasso K, Iversen P, Teisner B, Garnero P, Price PA, Christensen IJ: Changes of biochemical markers of bone turnover and YKL-40 following hormonal treatment for metastatic prostate cancer are related to survival. Clin Cancer Res; 2007 Jun 1;13(11):3244-9
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  • [Title] Changes of biochemical markers of bone turnover and YKL-40 following hormonal treatment for metastatic prostate cancer are related to survival.
  • PURPOSE: Elevated serum levels of biochemical markers of bone turnover and YKL-40 in patients with metastatic prostate cancer (PC) at the time of diagnosis are associated to poor prognosis.
  • In this study, we evaluated the value of these biomarkers in monitoring the patients during hormonal treatment.
  • EXPERIMENTAL DESIGN: Serum procollagen type I N-terminal propeptide (PINP), bone-specific alkaline phosphatase (BAP), CTX-I, and YKL-40 were determined by ELISA in a longitudinal study of 106 patients with metastatic PC during treatment with total androgen ablation or parenteral estrogen.
  • Median observation time was 4.9 years (range, 3.6-6.2).
  • RESULTS: After 6 months treatment, serum PINP, BAP, and YKL-40 decreased (P < 0.0001), but not serum CTX-I compared with baseline values.
  • Multivariate Cox analysis including the biomarkers 6 months after the start of treatment showed that Soloway score (HR, 3.9; P = 0.013), WHO tumor grade (HR, 3.9; P = 0.004), and serum PINP (HR, 2.2; P < 0.0001) were independent prognostic variables of survival.
  • Scoring the biomarkers during treatment as time-dependent covariates in univariate Cox regression analysis showed that increases in serum PINP (HR, 2.0; P < 0.0001), BAP (HR, 2.1; P < 0.0001), and YKL-40 (HR, 2.1; P < 0.0001) were predictors of early death.
  • CONCLUSIONS: Serial monitoring of serum PINP, BAP, CTX-I, and YKL-40 in metastatic PC patients during hormonal treatment provided information of prognosis.
  • [MeSH-major] Bone and Bones / drug effects. Glycoproteins / biosynthesis. Hormones / metabolism. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adipokines. Aged. Aged, 80 and over. Biomarkers, Tumor. Humans. Lectins. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Transplantation. Peptide Fragments / chemistry. Procollagen / chemistry. Retrospective Studies. Treatment Outcome

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  • (PMID = 17545529.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adipokines; 0 / Biomarkers, Tumor; 0 / CHI3L1 protein, human; 0 / Glycoproteins; 0 / Hormones; 0 / Lectins; 0 / Peptide Fragments; 0 / Procollagen; 0 / procollagen Type I N-terminal peptide
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59. Curtis KK, Adam TJ, Chen SC, Pruthi RK, Gornet MK: Anaemia following initiation of androgen deprivation therapy for metastatic prostate cancer: a retrospective chart review. Aging Male; 2008 Dec;11(4):157-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaemia following initiation of androgen deprivation therapy for metastatic prostate cancer: a retrospective chart review.
  • OBJECTIVE: Haemoglobin levels often decline into the anaemic range with androgen deprivation therapy (ADT).
  • We conducted a chart review of patients receiving ADT for metastatic prostate cancer to assess anaemia-related symptoms.
  • METHODS: 135 stage IV prostate cancer cases were reviewed for treatment type; haemoglobin values before and after treatment; and symptoms of anaemia.
  • Mean haemoglobin levels before and after for all treatment forms, for leuprolide alone, and for combination leuprolide/bicalutamide were calculated and evaluated for significant differences.
  • The numbers of patients developing symptoms were recorded and the effects of specific therapies evaluated.
  • Leuprolide and bicalutamide combination treatment caused a mean decline of -0.78 g/dL (p=0.0426).
  • Contingency analysis with Fisher's exact test shows patients receiving leuprolide therapy alone versus other forms of ADT were significantly less likely to have symptoms (chi(2)=0.0190).
  • CONCLUSIONS: The present study confirms that ADT results in a significant drop in haemoglobin levels into the anaemic range.
  • [MeSH-major] Androgen Antagonists / adverse effects. Anemia / chemically induced. Antineoplastic Agents, Hormonal / adverse effects. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Anilides / adverse effects. Anilides / therapeutic use. Combined Modality Therapy. Goserelin / adverse effects. Goserelin / therapeutic use. Hemoglobins / analysis. Humans. Leuprolide / adverse effects. Leuprolide / therapeutic use. Linear Models. Male. Neoplasm Metastasis. Nitriles / adverse effects. Nitriles / therapeutic use. Retrospective Studies. Tosyl Compounds / adverse effects. Tosyl Compounds / therapeutic use

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  • (PMID = 18937151.001).
  • [ISSN] 1473-0790
  • [Journal-full-title] The aging male : the official journal of the International Society for the Study of the Aging Male
  • [ISO-abbreviation] Aging Male
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents, Hormonal; 0 / Hemoglobins; 0 / Nitriles; 0 / Tosyl Compounds; 0F65R8P09N / Goserelin; A0Z3NAU9DP / bicalutamide; EFY6W0M8TG / Leuprolide
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60. Mimeault M, Johansson SL, Vankatraman G, Moore E, Henichart JP, Depreux P, Lin MF, Batra SK: Combined targeting of epidermal growth factor receptor and hedgehog signaling by gefitinib and cyclopamine cooperatively improves the cytotoxic effects of docetaxel on metastatic prostate cancer cells. Mol Cancer Ther; 2007 Mar;6(3):967-78
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  • [Title] Combined targeting of epidermal growth factor receptor and hedgehog signaling by gefitinib and cyclopamine cooperatively improves the cytotoxic effects of docetaxel on metastatic prostate cancer cells.
  • The epidermal growth factor receptor (EGFR) and hedgehog cascades provide a critical role in prostate cancer progression and contribute to the resistance to clinical therapies and disease relapse.
  • Therefore, we evaluated, for the first time, the antiproliferative and cytotoxic effects induced by a combination of selective inhibitors of EGFR tyrosine kinase and smoothened hedgehog signaling element, gefitinib and cyclopamine, with a current chemotherapeutic drug used in the clinics, docetaxel, on some metastatic prostate cancer cell lines.
  • Immunohistochemical analyses revealed that sonic hedgehog (SHH) expression was enhanced in 39% of primary prostatic adenocarcinomas (Gleason scores 4-10) compared with the corresponding normal tissues of the same prostate gland from 32 prostate cancer patients.
  • The confocal microscopy and Western blot analyses have also indicated the high expression levels of SHH and EGFR in metastatic LNCaP, DU145, and PC3 cells.
  • Moreover, the results revealed that the drugs, alone or in combination, at lower concentrations inhibited the growth of EGF plus SHH-stimulated and serum-stimulated androgen-responsive LNCaP-C33 and androgen-independent LNCaP-C81, DU145, and PC3 cells.
  • Importantly, the combined docetaxel, gefitinib, and cyclopamine also caused a higher rate of apoptotic death of prostate cancer cells compared with individual agents.
  • The cytotoxic effects induced by these drugs in PC3 cells seem to be mediated in part through the cellular ceramide production and activation of caspase cascades via a mitochondrial pathway and the release of cytochrome c into the cytosol.
  • Additionally, the combined agents were more effective at suppressing the invasiveness of PC3 cells through Matrigel in vitro than the single drugs.
  • These findings indicate that the combined use of inhibitors of EGF-EGFR and hedgehog signaling with docetaxel could represent a more promising strategy for treatment in patients with metastatic and androgen-independent prostate cancer.

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  • (PMID = 17363490.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA138791; United States / NCI NIH HHS / CA / CA 88184
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hedgehog Proteins; 0 / Quinazolines; 0 / SHH protein, human; 0 / Taxoids; 0 / Veratrum Alkaloids; 15H5577CQD / docetaxel; 9007-43-6 / Cytochromes c; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib; ZH658AJ192 / cyclopamine
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61. Sato N, Akakura K, Isaka S, Nakatsu H, Tanaka M, Ito H, Masai M, Chiba Prostate Study Group: Intermittent androgen suppression for locally advanced and metastatic prostate cancer: preliminary report of a prospective multicenter study. Urology; 2004 Aug;64(2):341-5
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  • [Title] Intermittent androgen suppression for locally advanced and metastatic prostate cancer: preliminary report of a prospective multicenter study.
  • OBJECTIVES: To clarify the effect of intermittent androgen suppression on the time to androgen-independent progression and changes in quality of life (QOL).
  • METHODS: Patients with locally advanced or metastatic prostate cancer were treated with a combination of leuprolide acetate and flutamide for 36 weeks.
  • When the serum prostate-specific antigen (PSA) levels at 24 and 32 weeks were less than 4.0 ng/mL, treatment was withheld until the PSA level reached 15 ng/mL or the pretreatment level.
  • This cycle of on-treatment and off-treatment was repeated until PSA failure (three consecutive increases in PSA level greater than 4.0 ng/mL during the on-treatment period) or symptomatic progression was observed.
  • RESULTS: Forty-nine patients (26 with T3N0M0, 8 with T2-T3N1M0, 2 with T4N0M0, and 13 with T2-T3N0M1) were enrolled.
  • The mean off-treatment duration in cycles 1, 2, and 3 was 46.1, 36.9, and 23.3 weeks, respectively.
  • In the off-treatment period, statistically significant improvements in the QOL score were observed in the categories of potency (11.4 versus 2.4) and social/family well-being (20.3 versus 16.1) compared with those in the on-treatment period.
  • CONCLUSIONS: Our interim analysis indicated that QOL is remarkably improved during the off-treatment period.
  • Intermittent androgen suppression would be a viable option for treatment of advanced prostate cancer, although a randomized controlled study is required to determine whether intermittent androgen suppression prolongs the time to androgen-independent cancer.
  • [MeSH-major] Adenocarcinoma / secondary. Androgens. Antineoplastic Agents, Hormonal / therapeutic use. Flutamide / therapeutic use. Leuprolide / therapeutic use. Neoplasms, Hormone-Dependent / secondary. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Biomarkers, Tumor / blood. Disease Progression. Drug Administration Schedule. Follow-Up Studies. Gonadotropin-Releasing Hormone / agonists. Humans. Male. Neoplasm Proteins / blood. Pilot Projects. Prospective Studies. Prostate-Specific Antigen / blood. Quality of Life. Surveys and Questionnaires. Testosterone / blood. Treatment Failure

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  • (PMID = 15302491.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 33515-09-2 / Gonadotropin-Releasing Hormone; 3XMK78S47O / Testosterone; 76W6J0943E / Flutamide; EC 3.4.21.77 / Prostate-Specific Antigen; EFY6W0M8TG / Leuprolide
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62. Montgomery RB, Goldman B, Tangen CM, Hussain M, Petrylak DP, Page S, Klein EA, Crawford ED, Southwest Oncology Group: Association of body mass index with response and survival in men with metastatic prostate cancer: Southwest Oncology Group trials 8894 and 9916. J Urol; 2007 Nov;178(5):1946-51; discussion 1951
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  • [Title] Association of body mass index with response and survival in men with metastatic prostate cancer: Southwest Oncology Group trials 8894 and 9916.
  • PURPOSE: We evaluated the effect of body mass index on prostate specific antigen response, and progression-free and overall survival in men with androgen dependent or androgen independent metastatic prostate cancer.
  • The first study included 1,006 men treated with androgen deprivation for metastatic prostate cancer.
  • The second study included 671 patients treated with chemotherapy for metastatic, androgen independent prostate cancer.
  • RESULTS: Among men with androgen dependent disease, higher body mass index was associated with longer overall (p <0.001) and progression-free (p = 0.009) survival, as well as with an increased likelihood of achieving a prostate specific antigen nadir less than 4 ng/ml (p = 0.008).
  • Among men with androgen independent prostate cancer, no clear association could be detected between body mass index and progression-free survival, overall survival or prostate specific antigen response.
  • CONCLUSIONS: This study revealed higher body mass index to be associated with better overall and progression-free survival in patients with androgen dependent metastatic prostate cancer.
  • [MeSH-major] Adenocarcinoma / therapy. Antineoplastic Agents, Hormonal / therapeutic use. Body Mass Index. Flutamide / therapeutic use. Orchiectomy / methods. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Biomarkers, Tumor / blood. Disease-Free Survival. Follow-Up Studies. Humans. Male. Prognosis. Proportional Hazards Models. Prostate-Specific Antigen / blood. Retrospective Studies. Risk Factors. Southwestern United States / epidemiology. Survival Rate / trends

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  • [CommentIn] J Urol. 2007 Nov;178(5):1842-3 [17868740.001]
  • (PMID = 17868721.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA32102; United States / NCI NIH HHS / CA / CA38926
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 76W6J0943E / Flutamide; EC 3.4.21.77 / Prostate-Specific Antigen
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63. Dyrstad SW, Shah P, Rao K: Chemotherapy for prostate cancer. Curr Pharm Des; 2006;12(7):819-37
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  • [Title] Chemotherapy for prostate cancer.
  • Androgen deprivation in patients with metastatic prostate cancer produces palliation of symptoms, reduction in PSA levels, and temporary regression of tumor in most patients.
  • The response from these drugs is usually very short.
  • Once these measures have been exhausted, the clinician is left with limited treatment options that include radionuclides and cytotoxic chemotherapy.
  • It is the objective of this article to review the experience with chemotherapy in prostate cancer and then to discuss the role of radionuclide agents, emerging agents, and herbal therapies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Clinical Trials as Topic. Humans. Male. Plant Preparations / therapeutic use. Radiopharmaceuticals / therapeutic use

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  • (PMID = 16515498.001).
  • [ISSN] 1381-6128
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Plant Preparations; 0 / Radiopharmaceuticals
  • [Number-of-references] 49
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64. Johannsen M, Wilke K, Schnorr D, Loening SA: [Taxanes in the chemotherapy of hormone-refractory prostate carcinoma]. Urologe A; 2004 Feb;43(2):160-7
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  • [Title] [Taxanes in the chemotherapy of hormone-refractory prostate carcinoma].
  • [Transliterated title] Taxane in der Chemotherapie des hormonrefraktären Prostatakarzinoms.
  • Prostate cancer represents one of the most prevalent malignancies in men.
  • Standard therapy of metastatic prostate cancer consists of androgen deprivation, which is a palliative therapy yielding a clinical response of limited duration.
  • In hormone-refractory prostate cancer (HRPC), response to chemotherapy with regimens available until about ten years ago has been disappointing.
  • Nowadays, due to increasing life expectancy and earlier diagnosis and therapy of prostate cancer, more patients with hormone-refractory disease are still in relatively good overall condition.
  • With the taxanes, much more effective cytostatic substances for chemotherapy of HRPC are available today.
  • Using modern taxane-based chemotherapy, effective palliation of pain can be achieved in 50-70% of patients with HRPC, while retaining an acceptable quality of life.
  • There is also evidence for improved overall survival after taxane-based chemotherapy, although this remains to be proven by ongoing studies.
  • This article presents an overview of current studies investigating the outcome after taxane-based chemotherapy, as well as new therapeutic approaches in combination with docetaxel.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents / therapeutic use. Pain / drug therapy. Palliative Care / methods. Prostatic Neoplasms / drug therapy. Taxoids / therapeutic use
  • [MeSH-minor] Drug Resistance, Neoplasm. Humans. Male. Treatment Outcome

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  • [Cites] Oncology. 2003;64(4):300-5 [12759524.001]
  • [Cites] Ann Oncol. 2001 Sep;12(9):1273-9 [11697840.001]
  • [Cites] J Clin Oncol. 2001 May 1;19(9):2509-16 [11331330.001]
  • [Cites] Urology. 1999 Dec;54(6A Suppl):22-9 [10606281.001]
  • [Cites] Urologe A. 2003 Nov;42(11):1453-60 [14624343.001]
  • [Cites] J Clin Oncol. 1992 Nov;10(11):1754-61 [1383436.001]
  • [Cites] Cancer. 2003 Dec 15;98(12):2592-8 [14669278.001]
  • [Cites] Cancer. 2000 Jul 15;89(2):431-6 [10918176.001]
  • [Cites] BJU Int. 2003 Dec;92(9):890-5 [14632841.001]
  • [Cites] Urology. 1995 Aug;46(2):142-8 [7624983.001]
  • [Cites] Cancer J. 2003 Jul-Aug;9(4):286-92 [12967139.001]
  • [Cites] Am J Clin Pathol. 2001 Aug;116(2):234-9 [11488070.001]
  • [Cites] J Clin Oncol. 1994 Oct;12(10):2005-12 [7523606.001]
  • [Cites] Urology. 2002 Sep;60(3 Suppl 1):1-6 [12231036.001]
  • [Cites] J Urol. 2003 Nov;170(5):1709-16 [14532760.001]
  • [Cites] Cancer. 2003 Nov 15;98(10):2192-8 [14601089.001]
  • [Cites] Urol Clin North Am. 2001 Aug;28(3):555-65 [11590814.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 17):14-8 [10604263.001]
  • [Cites] Cancer. 2002 Mar 1;94(5):1457-65 [11920502.001]
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7314-20 [14612529.001]
  • [Cites] Urology. 2001 Jul;58(1):59-64 [11445480.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2506-13 [10561316.001]
  • [Cites] Mol Cancer Ther. 2003 Sep;2(9):873-84 [14555706.001]
  • [Cites] Semin Oncol. 2001 Aug;28(4 Suppl 15):8-15 [11685723.001]
  • [Cites] J Clin Oncol. 1999 Jun;17(6):1664-71 [10561202.001]
  • [Cites] Oncology (Williston Park). 2002 Jun;16(6 Suppl 6):63-72 [12108899.001]
  • [Cites] Br J Cancer. 2002 Jul 1;87(1):21-7 [12085250.001]
  • [Cites] J Clin Oncol. 1996 Jun;14(6):1756-64 [8656243.001]
  • [Cites] Expert Opin Drug Saf. 2003 Mar;2(2):141-6 [12904114.001]
  • [Cites] Cancer. 2003 Jul 15;98(2):269-76 [12872344.001]
  • [Cites] J Clin Invest. 1995 Apr;95(4):1869-76 [7706494.001]
  • [Cites] Urology. 1999 Dec;54(6A Suppl):30-5 [10606282.001]
  • [Cites] Cancer. 1993 Oct 15;72(8):2457-60 [8104680.001]
  • [Cites] Br J Dermatol. 2002 Apr;146(4):709-10 [11966714.001]
  • [Cites] J Clin Oncol. 2001 Jan 1;19(1):44-53 [11134194.001]
  • [Cites] Int J Immunopharmacol. 1998 Nov;20(11):669-77 [9848398.001]
  • [Cites] Int Immunopharmacol. 2003 Dec;3(13-14):1699-714 [14636822.001]
  • [Cites] Ophthalmology. 2002 Jun;109(6):1188-91 [12045065.001]
  • [Cites] Cancer Res. 1997 Jan 15;57(2):229-33 [9000560.001]
  • [Cites] Cancer Sci. 2003 May;94(5):459-66 [12824894.001]
  • [Cites] Cancer. 2002 Feb 1;94(3):847-53 [11857321.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):958-67 [10071290.001]
  • [Cites] Cancer. 2003 Oct 15;98(8):1627-34 [14534878.001]
  • [Cites] J Clin Oncol. 1997 Sep;15(9):3156-63 [9294479.001]
  • [Cites] J Clin Oncol. 2003 Jan 1;21(1):123-8 [12506180.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 17):19-23 [10604264.001]
  • [Cites] Semin Oncol. 2001 Aug;28(4 Suppl 15):71-6 [11685733.001]
  • [Cites] Semin Oncol. 2001 Aug;28(4 Suppl 15):16-21 [11685724.001]
  • [Cites] Ann Plast Surg. 2000 Oct;45(4):438-41 [11037169.001]
  • [Cites] Cancer. 2003 Nov 1;98(9):1855-62 [14584067.001]
  • [Cites] Cancer Invest. 2002;20(5-6):634-43 [12197218.001]
  • [Cites] Cancer. 2003 Nov 1;98(9):1842-8 [14584065.001]
  • (PMID = 14991117.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel
  • [Number-of-references] 62
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65. Wörmann B, Wolff JM: [Systemic treatment of metastatic prostate cancer]. Urologe A; 2010 Feb;49(2):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] [Systemic treatment of metastatic prostate cancer].
  • [Transliterated title] Die systemische Therapie des metastasierten Prostatakarzinoms.
  • Systemic treatment of advanced prostate cancer is multifaceted.
  • First-line therapy is antihormonal treatment with androgen deprivation or antiandrogens.
  • Chemotherapy is effective in hormone refractory (castration resistant) prostate cancer.
  • Use of bisphosphonates is standard in metastatic bone disease.
  • Treatment of patients with metastatic prostate cancer is palliative.
  • New approaches and new drugs will increase the therapeutic possibilities considerably.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Bone Neoplasms / secondary. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Androgen Antagonists / adverse effects. Androgen Antagonists / therapeutic use. Combined Modality Therapy. Diphosphonates / therapeutic use. Disease Progression. Humans. Male. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / mortality. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Orchiectomy. Palliative Care. Quality of Life. Survival Analysis

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  • [Cites] Aktuelle Urol. 2009 May;40(3):159-63 [19399720.001]
  • [Cites] J Clin Oncol. 2009 Feb 1;27(4):644-6 [19103725.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]
  • [Cites] Cochrane Database Syst Rev. 2002;(4):CD003851 [12519611.001]
  • [Cites] BJU Int. 2008 Feb;101(4):440-3 [17941935.001]
  • [Cites] CMAJ. 2009 May 26;180(11):E62-71 [19407261.001]
  • [Cites] Urol Oncol. 2008 Jul-Aug;26(4):420-5 [18593621.001]
  • [Cites] Cancer. 2009 Aug 15;115(16):3670-9 [19536890.001]
  • [Cites] Scand J Urol Nephrol. 2006;40(6):441-52 [17130095.001]
  • [Cites] Oncologist. 2009 Apr;14(4):391-8 [19342474.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]
  • [Cites] Urol Oncol. 2008 Jul-Aug;26(4):426-9 [18593622.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Aug;86(8):3467-77 [11502765.001]
  • [Cites] J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68 [12359855.001]
  • [Cites] J Clin Oncol. 2007 Apr 20;25(12):1596-605 [17404365.001]
  • [Cites] J Clin Oncol. 2006 Apr 20;24(12):1868-76 [16622261.001]
  • [Cites] J Clin Oncol. 2004 Jul 15;22(14):2927-41 [15184404.001]
  • [Cites] BJU Int. 2007 Jun;99(6):1383-9 [17346269.001]
  • [Cites] N Engl J Med. 2009 Aug 20;361(8):745-55 [19671656.001]
  • [Cites] Cochrane Database Syst Rev. 2006 Oct 18;(4):CD006250 [17054286.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3984-90 [16921051.001]
  • [Cites] JAMA. 2009 Aug 26;302(8):866-73 [19706860.001]
  • [Cites] J Clin Oncol. 2009 Apr 20;27(12):2022-9 [19289629.001]
  • [Cites] Nucl Med Commun. 2007 Aug;28(8):623-30 [17625384.001]
  • [Cites] J Clin Oncol. 2001 Sep 15;19(18 Suppl):61S-63S [11560975.001]
  • [Cites] Urol Oncol. 2008 Jul-Aug;26(4):430-7 [18593623.001]
  • [Cites] CA Cancer J Clin. 2002 May-Jun;52(3):154-79 [12018929.001]
  • [Cites] Clin Prostate Cancer. 2002 Dec;1(3):163-71 [15046691.001]
  • [Cites] Lancet. 2000 Apr 29;355(9214):1491-8 [10801170.001]
  • [Cites] Urol Oncol. 2008 Jul-Aug;26(4):415-9 [18593620.001]
  • (PMID = 20180063.001).
  • [ISSN] 1433-0563
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Diphosphonates
  • [Number-of-references] 36
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66. Kobayashi M, Wood PA, Hrushesky WJ: Circadian chemotherapy for gynecological and genitourinary cancers. Chronobiol Int; 2002 Jan;19(1):237-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Circadian chemotherapy for gynecological and genitourinary cancers.
  • The circadian timing of surgery, anticancer drugs, radiation therapy, and biologic agents can result in improved toxicity profiles, tumor control, and host survival.
  • Optimally timed cancer chemotherapy with doxorubicin or pirarubicin (06:00h) and cisplatin (18:00h) enhanced the control of advanced ovarian cancer while minimizing side effects, and increased the response rate in metastatic endometrial cancer.
  • Therapy of metastatic bladder cancer with doxorubicin-cisplatin was made more tolerable by this same circadian approach resulting in a 57% objective response rate.
  • This optimally timed therapy is also effective in the adjuvant setting, decreasing the expected frequency of metastasis from locally advanced bladder cancer.
  • Circadian fluorodeoxyuridine (FUDR) continuous infusion (70% of the daily dose given between 15:00h and 21:00h) has been shown effective for metastatic renal cell carcinoma resulting in 29% objective response and stable disease of more than 1 yr duration in the majority of patients.
  • In a multicenter trial in patients with metastatic renal cell cancer, patients were randomized to a flat or a circadian-modified FUDR infusion.
  • Hormone refractory metastatic prostate cancer has been treated with circadian-timed FUDR chemotherapy; however, without objective response.
  • Biological agents such as interferon-alpha and IL-2 have shown low but effective disease control in metastatic renal cell cancer, however, with much toxicity.
  • In summary, the timing of anthracycline, platinum, and fluoropyrimidine-based drug therapies during the 24h is relevant to the toxic therapeutic ratio of these agents in the treatment of gynecologic and genitourinary cancers.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Chronotherapy. Doxorubicin / analogs & derivatives. Genital Neoplasms, Female / drug therapy. Urogenital Neoplasms / drug therapy
  • [MeSH-minor] Animals. Carcinoma, Renal Cell / drug therapy. Carcinoma, Renal Cell / secondary. Cell Cycle. Circadian Rhythm. Cisplatin / administration & dosage. Endometrial Neoplasms / drug therapy. Female. Floxuridine / administration & dosage. Humans. Kidney Neoplasms / drug therapy. Male. Ovarian Neoplasms / drug therapy. Prostatic Neoplasms / drug therapy. Rats. Urinary Bladder Neoplasms / drug therapy. Urinary Bladder Neoplasms / secondary

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  • (PMID = 11962679.001).
  • [ISSN] 0742-0528
  • [Journal-full-title] Chronobiology international
  • [ISO-abbreviation] Chronobiol. Int.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA31635; United States / NCI NIH HHS / CA / R01CA50749
  • [Publication-type] Journal Article; 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.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 039LU44I5M / Floxuridine; 80168379AG / Doxorubicin; D58G680W0G / pirarubicin; Q20Q21Q62J / Cisplatin
  • [Number-of-references] 33
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67. Drouin SJ, Rouprêt M, Wallerand H, Houédé N: [Chemotherapy in early stage of hormone-resistant metastatic prostate cancer: what are the indications?]. Prog Urol; 2010 Jun;20 Suppl 3:S192-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Chemotherapy in early stage of hormone-resistant metastatic prostate cancer: what are the indications?].
  • [Transliterated title] Chimiothérapie en phase précoce d'hormonorésistance des cancers de prostate métastatiques: quelles indications?
  • Treatment of hormone-refractory prostate cancer remains a source of debate.
  • Since 2004, docétaxel-based chemotherapy has become the standard treatment as it has demonstrated efficacy on overall survival in two randomized studies.
  • In some studies, chemotherapy seems to be also effective on pain relief.
  • The adverse effects occur more frequently than with others chemotherapy (mitoxantrone) but are moderated and aren't responsible of specific mortality.
  • These facts encourage to begin the chemotherapy as earlier as possible even before metastases appear.
  • Some studies have even raised the issue of an initiation of chemotherapy before the onset of hormone independence.
  • The treated patients have a limited life expectancy and a 2 months gain of survival may be of limited value.
  • Thus, an early initiation of chemotherapy must be discussed case by case, on an individual basis.
  • The prognosis factors and alternative therapeutic options based on new molecules used in metastatic cancer might also be considered for the therapeutic decision.
  • [MeSH-major] Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Drug Resistance, Neoplasm. Humans. Male. Neoplasm Metastasis. Neoplasm Staging. Taxoids / therapeutic use

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  • [Copyright] Copyright (c) 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20620964.001).
  • [ISSN] 1166-7087
  • [Journal-full-title] Progrès en urologie : journal de l'Association française d'urologie et de la Société française d'urologie
  • [ISO-abbreviation] Prog. Urol.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Taxoids; 15H5577CQD / docetaxel
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68. Lebret T, Méjean A: [Role of hormonotherapy in the treatment of metastatic prostate cancer]. Prog Urol; 2008 Nov;18 Suppl 7:S332-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Role of hormonotherapy in the treatment of metastatic prostate cancer].
  • [Transliterated title] Place de l'hormonothérapie dans le traitement du cancer de prostate métastatique.
  • Androgen privation is considered as the referent first line treatment for metastatic prostate cancer.
  • Based on LHRH agonist, different therapeutic schedule included maximum androgenic blockage, intermittent treatment and associations with other drugs like oestrogen leading to possible hormonal manipulations.
  • Since metastasis is confirmed, immediate treatment with continue LHRH agonist is the French Association of Urology (AFU) AFU recommendations treatment for metastatic prostate cancer but intermittent treatment can be considered as an option.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Gonadotropin-Releasing Hormone / analogs & derivatives. Humans. Male. Neoplasm Metastasis / drug therapy

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  • (PMID = 19070812.001).
  • [ISSN] 1166-7087
  • [Journal-full-title] Progrès en urologie : journal de l'Association française d'urologie et de la Société française d'urologie
  • [ISO-abbreviation] Prog. Urol.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone
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69. Moser L, Schubert T, Hinkelbein W: Hormone-refractory and metastatic prostate cancer - palliative radiotherapy. Front Radiat Ther Oncol; 2008;41:117-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hormone-refractory and metastatic prostate cancer - palliative radiotherapy.
  • Prostate cancer progression is commonly manifested by obstructive uropathy, regional lymphatic metastases and hematogenous metastases to the axial skeleton.
  • Radiotherapy is a mainstay in the palliation of symptomatic metastatic prostate cancer and is most often used for the palliation of painful metastatic bone lesions, resulting in a relief of pain in about 80-90% of patients and a reduction of analgesics.
  • In metastatic disease compromising the integrity of the spinal cord or a nerve root, radiotherapy can be used as an urgent intervention to minimize neurological dysfunction and local progression or as an adjunct to surgical decompression.
  • Symptoms of metastatic lymphadenopathy like leg edema and back discomfort caused by pelvic or paraaortic metastases are related to the immediate anatomic structures affected.
  • Radiotherapy for localized hormone-refractory prostate cancer has an excellent local control rate; nevertheless, the prognosis is poor, the majority of patients failing with distant metastasis within few years.
  • The role of radiotherapy in hormone-refractory and metastatic prostate cancer, considering the patient's individual situation, are presented and discussed.
  • [MeSH-major] Drug Resistance, Neoplasm. Neoplasm Metastasis / radiotherapy. Palliative Care / methods. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Humans. Male


70. Lu-Yao G, Moore DF, Oleynick J, Dipaola RS, Yao SL: Use of hormonal therapy in men with metastatic prostate cancer. J Urol; 2006 Aug;176(2):526-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of hormonal therapy in men with metastatic prostate cancer.
  • PURPOSE: Bilateral orchiectomy or luteinizing hormone releasing hormone agonists represent the standard of care for metastatic prostate cancer.
  • In this population based study we assessed the use rates of these therapies in men who died of prostate cancer.
  • MATERIAL AND METHODS: A total of 9,110 men 65 years or older who died of prostate cancer in 1991 to 2000 were identified through the population based Surveillance, Epidemiology and End Results, and Medicare linked database to determine hormonal therapy use rates.
  • RESULTS: Approximately 38% of black and 25% of white men did not receive hormonal therapy before dying of prostate cancer.
  • After adjusting for cancer status at diagnosis and other potential confounding factors black race and residence in low income areas were associated with lower hormonal therapy use (relative risk 0.73, 95% CI 0.67 to 0.80 and 0.91, 95% CI 0.85 to 0.98, respectively).
  • Hormonal therapy use was most comprehensive in the Northeast.
  • CONCLUSIONS: A substantial number of men who die as a consequence of prostate cancer never receive hormonal therapy.
  • The use of hormonal therapy varies significantly.
  • Further studies are warranted to determine factors that may be associated with the incomplete use of hormonal therapy for metastatic prostate cancer.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Humans. Male. Neoplasm Metastasis. SEER Program

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  • (PMID = 16813882.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal
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71. Carson AP, Howard DL, Carpenter WR, Taylor YJ, Peacock S, Schenck AP, Godley PA: Trends and racial differences in the use of androgen deprivation therapy for metastatic prostate cancer. J Pain Symptom Manage; 2010 May;39(5):872-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trends and racial differences in the use of androgen deprivation therapy for metastatic prostate cancer.
  • CONTEXT: Androgen deprivation therapy (ADT) is widely used to manage the symptoms of advanced prostate cancer and has been shown to slow the progression of the disease.
  • OBJECTIVES: The purpose of this study was to assess use trends for ADT overall and by type (orchiectomy and luteinizing hormone-releasing hormone [LHRH] agonists) and the factors associated with time to receipt for metastatic prostate cancer.
  • METHODS: Data from the Surveillance, Epidemiology, and End Results (SEER) cancer registry and Medicare claims database were obtained for 5,273 men, aged 65 years and older and diagnosed with Stage IV prostate cancer during 1991-1999 from seven SEER regions.
  • An accelerated failure time regression model with log-normal distribution was used to examine factors associated with mean time to receipt of ADT.
  • RESULTS: African-American men were less likely than white men to receive any ADT after diagnosis (P<0.001).
  • Differences were noted in the time to receipt of ADT, with African-American men having a longer mean time to receipt of orchiectomy (time ratio [TR]=1.50; 95% confidence interval [CI]=1.03, 2.17) or LHRH agonist (TR=1.42; 95% CI=1.06, 1.89) than white men.
  • CONCLUSION: African-American men with metastatic prostate cancer were significantly less likely to receive ADT and, when treated, had a slightly longer time to receipt than white men, which has implications for patients and physicians involved in the palliative management of metastatic prostate cancer.

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  • [Copyright] Copyright 2010. Published by Elsevier Inc.
  • [Cites] J Clin Oncol. 2001 Sep 1;19(17):3750-7 [11533098.001]
  • [Cites] J Natl Cancer Inst. 2001 Mar 7;93(5):388-95 [11238701.001]
  • [Cites] J Natl Cancer Inst. 2002 Mar 6;94(5):334-57 [11880473.001]
  • [Cites] J Urol. 2002 Jul;168(1):9-12 [12050481.001]
  • [Cites] Med Care. 2002 Aug;40(8 Suppl):IV-3-18 [12187163.001]
  • [Cites] Stat Med. 2002 Nov 30;21(22):3493-510 [12407686.001]
  • [Cites] J Natl Cancer Inst. 2003 Jul 2;95(13):981-9 [12837834.001]
  • [Cites] Urol Oncol. 2003 Jul-Aug;21(4):245-54 [12954493.001]
  • [Cites] J Natl Cancer Inst. 2003 Nov 19;95(22):1702-10 [14625261.001]
  • [Cites] J Gen Intern Med. 2004 Feb;19(2):146-55 [15009794.001]
  • [Cites] Med Care. 2004 Mar;42(3):239-50 [15076823.001]
  • [Cites] Bull N Y Acad Med. 1972 Jun;48(5):751-66 [4555718.001]
  • [Cites] Cancer. 1973 Nov;32(5):1126-30 [4585929.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(5):1658-62 [6461861.001]
  • [Cites] Urology. 1989 May;33(5 Suppl):45-52 [2523611.001]
  • [Cites] Urology. 1989 May;33(5 Suppl):57-62 [2523612.001]
  • [Cites] Br J Urol. 1991 May;67(5):502-8 [1828183.001]
  • [Cites] Br J Urol. 1997 Feb;79(2):235-46 [9052476.001]
  • [Cites] Cancer. 1998 Jul 15;83(2):320-30 [9669815.001]
  • [Cites] Med Care. 1998 Sep;36(9):1337-48 [9749657.001]
  • [Cites] Cancer. 2005 Feb 1;103(3):538-45 [15612083.001]
  • [Cites] Cancer. 2005 Apr 15;103(8):1615-24 [15742331.001]
  • [Cites] JAMA. 2005 Jul 13;294(2):238-44 [16014598.001]
  • [Cites] J Natl Cancer Inst. 2006 Jun 21;98(12):839-45 [16788157.001]
  • [Cites] J Urol. 2006 Aug;176(2):526-31 [16813882.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2006 Oct 1;66(2):395-402 [16904843.001]
  • [Cites] J Clin Oncol. 2006 Sep 20;24(27):4448-56 [16983113.001]
  • [Cites] J Clin Oncol. 2007 Apr 20;25(12):1596-605 [17404365.001]
  • [Cites] J Urol. 2001 Jan;165(1):104-7 [11125375.001]
  • [Cites] J Clin Epidemiol. 2000 Dec;53(12):1258-67 [11146273.001]
  • [Cites] Cochrane Database Syst Rev. 2002;(1):CD003506 [11869665.001]
  • (PMID = 20471547.001).
  • [ISSN] 1873-6513
  • [Journal-full-title] Journal of pain and symptom management
  • [ISO-abbreviation] J Pain Symptom Manage
  • [Language] ENG
  • [Grant] United States / PHS HHS / / U55/CCR921930-02; United States / NCI NIH HHS / CA / 1U01CA114629; United States / NCI NIH HHS / PC / N01-PC-35139; United States / NCI NIH HHS / PC / N02 PC015105; United States / NIMHD NIH HHS / MD / P60MD000244; United States / NCI NIH HHS / CA / U01 CA114629; United States / NIMHD NIH HHS / MD / P60 MD000239; United States / NIMHD NIH HHS / MD / P60 MD000244; United States / NCI NIH HHS / CA / 2R25CA057726; United States / NCI NIH HHS / CA / N01PC35136; United States / NCI NIH HHS / CA / N01PC35139; United States / NCI NIH HHS / PC / N01-PC-35136; United States / NCI NIH HHS / CA / R25 CA057726
  • [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 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone
  • [Other-IDs] NLM/ NIHMS362675; NLM/ PMC3878612
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72. Tan WW: Novel agents and targets in managing patients with metastatic prostate cancer. Cancer Control; 2006 Jul;13(3):194-8
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  • [Title] Novel agents and targets in managing patients with metastatic prostate cancer.
  • BACKGROUND: Docetaxel has recently been found to improve survival in patients with metastatic androgen-independent prostate cancer (AIPC).
  • Chemotherapy as a first-line option leaves room for improvement, while second-line options are multiple and somewhat controversial.
  • METHODS: Clinically relevant articles focusing on chemotherapy drugs for metastatic prostate cancer and their mechanism of action and efficacy were reviewed from January 2004 through April 2006.
  • However, for doublets with docetaxel or second-line chemotherapy, multiple studies have shown interesting and promising results with calcitriol, thalidomide, bevacizumab, satraplatin, vaccines, ixabepilone, and atrasentan.
  • CONCLUSIONS: Docetaxel should be considered for first-line treatment of metastatic AIPC.
  • Due to its progression-free survival of only 6 months, more effective drugs and drug combinations need to be developed to treat patients with AIPC.
  • Combination treatments with docetaxel and other new agents are promising, but adequately powered phase III trials need to be conducted with survival as the principal endpoint for these promising drug combinations.
  • [MeSH-major] Adenocarcinoma / therapy. Bone Neoplasms / therapy. Prostatic Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Humans. Male


73. Silva BM, Neto JA, Lima RL: [Analysis of complications in metastatic prostate cancer patients submitted to bilateral orchiectomy]. Rev Col Bras Cir; 2010 Aug;37(4):269-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Analysis of complications in metastatic prostate cancer patients submitted to bilateral orchiectomy].
  • [Transliterated title] Análise de complicações em pacientes portadores de câncer de próstata metastático submetidos à orquiectomia bilateral.
  • METHODS: That's an analytical transversal study with a sample of 25 patients, between 58 to 82 years, carriers of metastatic prostate cancer, submitted to the bilateral orchiectomy in the Professor Alberto Antunes University Hospital 's (HUPAA-UFAL), in the period of January of 2003 to December of 2008.
  • 86% of the interviewed ones had related to be satisfied with the results of the procedure and had affirmed that they can have a normal daily life, with significant improvement of the clinical stage.
  • About the adjuvant treatments, only 36% had carried through, being most common, chemotherapy (36%) and x-ray (29%).
  • CONCLUSION: The bilateral orchiectomy constitutes in a good alternative for metastatic prostate cancer patients, in a way that it is observed satisfaction of the majority of the patients in relation to the improvement of the symptoms and the presented complications had not great impact in the daily life of the same ones.
  • [MeSH-minor] Aged. Aged, 80 and over. Cross-Sectional Studies. Humans. Male. Middle Aged. Neoplasm Metastasis. Postoperative Complications / epidemiology. Postoperative Complications / etiology

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  • (PMID = 21085843.001).
  • [ISSN] 1809-4546
  • [Journal-full-title] Revista do Colégio Brasileiro de Cirurgiões
  • [ISO-abbreviation] Rev Col Bras Cir
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
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74. Sissung TM, Thordardottir S, Gardner ER, Figg WD: Current status of thalidomide and CC-5013 in the treatment of metastatic prostate cancer. Anticancer Agents Med Chem; 2009 Dec;9(10):1058-69
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  • [Title] Current status of thalidomide and CC-5013 in the treatment of metastatic prostate cancer.
  • Thalidomide is emerging as a potentially important therapeutic option in the treatment of metastatic prostate cancer.
  • Although the mechanism of action of this agent remains elusive in malignancies of the prostate, recent data has indicated that thalidomide may play a role in inflammation, immunomodulation, and anti-angiogenesis.
  • Lenalidomide (CC-5013), a thalidomide analogue with improved activity and safety profile in certain disease contexts, is in the early stages of development in prostate cancer.
  • This review will provide the current status of the history, mechanism, metabolism, and clinical use of thalidomide in metastatic prostate cancer.
  • It will also describe the mechanism and clinical use of lenalidomide as it pertains to malignancies of the prostate.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Prostatic Neoplasms / drug therapy. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use
  • [MeSH-minor] Animals. Humans. Male. Treatment Outcome

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  • (PMID = 19719457.001).
  • [ISSN] 1875-5992
  • [Journal-full-title] Anti-cancer agents in medicinal chemistry
  • [ISO-abbreviation] Anticancer Agents Med Chem
  • [Language] eng
  • [Grant] United States / PHS HHS / / HHSN261200800001E; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
  • [Number-of-references] 95
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75. Smith MR: Bisphosphonates to prevent skeletal complications in men with metastatic prostate cancer. J Urol; 2003 Dec;170(6 Pt 2):S55-7; discussion S57-8
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  • [Title] Bisphosphonates to prevent skeletal complications in men with metastatic prostate cancer.
  • PURPOSE: The literature on clinical trials of bisphosphonates in men with metastatic prostate cancer is reviewed to familiarize the reader with biology of bone metastases and rationale for use of bisphosphonates.
  • MATERIALS AND METHODS: A MEDLINE review of the literature on prostate cancer and bisphosphonates was performed.
  • RESULTS: In uncontrolled clinical trials bisphosphonates improved pain and analgesic scores in men with symptomatic bone metastases.
  • In a randomized controlled trial of men with bone metastases and progressive disease after first line hormonal therapy zoledronic acid decreased the skeletal related events, a composite end point defined as fracture, surgery or radiation therapy to bone, or change in antineoplastic therapy for bone pain.
  • Randomized controlled trials with other bisphosphonates reported no significant benefit in men with bone metastases.
  • Problems with the study populations, drug bioavailability and potency, statistical power and end point definition may have contributed to the negative results of these other studies.
  • CONCLUSIONS: Zoledronic acid decreases the risk of skeletal related events in men with bone metastases and disease progression after first line hormonal therapy.
  • Additional clinical research is needed to evaluate the optimal timing, schedule and duration of bisphosphonate treatment in men with metastatic prostate cancer.
  • Additional research is also necessary to determine whether bisphosphonates can prevent bone metastases in men with high risk nonmetastatic prostate cancer.
  • [MeSH-major] Bone Neoplasms / prevention & control. Bone Neoplasms / secondary. Diphosphonates / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Analgesics, Non-Narcotic / therapeutic use. Antimetabolites / therapeutic use. Clodronic Acid / therapeutic use. Humans. Imidazoles / therapeutic use. Male. Retrospective Studies

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  • (PMID = 14610411.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics, Non-Narcotic; 0 / Antimetabolites; 0 / Diphosphonates; 0 / Imidazoles; 0813BZ6866 / Clodronic Acid; 6XC1PAD3KF / zoledronic acid
  • [Number-of-references] 26
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76. Sakai H, Kanetake H: [First line therapy in the treatment of metastatic prostate cancer]. Gan To Kagaku Ryoho; 2003 Jan;30(1):43-9
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  • [Title] [First line therapy in the treatment of metastatic prostate cancer].
  • Hormonal therapy has been the main treatment for advanced prostate cancer for the past six decades.
  • Maximum androgen blockade (MAB), combination therapy with castration and antiandrogens, has been compared with castration monotherapy since the late 1980s.
  • Recently published meta-analyses have revealed that MAB with non-steroidal antiandrogens is slightly superior to monotherapy (surgical or medical castration) in the treatment of advanced prostate cancer, and that MAB has more adverse effects.
  • Some studies indicated that the survival of metastatic prostate cancer patients treated with immediate therapy was similar to that of men in whom treatment was delayed.
  • Hormonal therapy has side effects and is costly, and delayed treatment may be beneficial to elderly men with silent metastasis.
  • Intermittent hormonal therapy is a controversial approach to management of advanced prostate cancer, although laboratory data suggest that intermittent androgen deprivation may prolong the duration of androgen dependence.
  • Intermittent hormonal therapy for patients with metastatic prostate cancer needs to be assessed in a randomized trial to determine the effect on overall survival and quality of life.
  • Our results in a randomized clinical trial of chemo-endocrine therapy versus endocrine therapy alone suggested that the addition of chemotherapy (cisplatin plus pirarubicin) to initial endocrine therapy might be beneficial to patients with advanced prostate cancer, especially an aggressive form of prostate cancer.
  • However, chemo-endocrine therapy should be considered an experimental approach at present.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Orchiectomy. Prostatic Neoplasms / therapy
  • [MeSH-minor] Anilides / therapeutic use. Combined Modality Therapy. Flutamide / therapeutic use. Gonadotropin-Releasing Hormone / agonists. Humans. Male. Nitriles. Quality of Life. Tosyl Compounds

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  • (PMID = 12557704.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents, Hormonal; 0 / Nitriles; 0 / Tosyl Compounds; 33515-09-2 / Gonadotropin-Releasing Hormone; 76W6J0943E / Flutamide; A0Z3NAU9DP / bicalutamide
  • [Number-of-references] 32
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77. Kelly WK, Slovin SF: Chemotherapy for androgen- independent prostate cancer: myth or reality. Curr Oncol Rep; 2000 Sep;2(5):394-401
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  • [Title] Chemotherapy for androgen- independent prostate cancer: myth or reality.
  • In the past, the treatment options for patients with metastatic prostate cancer that progressed despite castrate levels of testosterone was limited, and no therapies provided an improvement in survival.
  • With the widespread use of prostate-specific antigen (PSA) to monitor their clinical course, patients have presented with less extensive disease and a better performance status.
  • Clinical trial methodology has improved as well, through incorporation of post-therapy changes in PSA to evaluate novel agents.
  • These data suggest that prostate cancer is not as resistant to chemotherapy as it was once thought to be.
  • [MeSH-major] Androgens / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Prostate-Specific Antigen / analysis. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Antibiotics, Antineoplastic / pharmacology. Antibiotics, Antineoplastic / therapeutic use. Antineoplastic Agents, Hormonal / pharmacology. Antineoplastic Agents, Hormonal / therapeutic use. Clinical Trials as Topic. Drug Resistance, Neoplasm. Endpoint Determination. Estramustine / pharmacology. Estramustine / therapeutic use. Humans. Male. Testosterone / blood

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  • [Cites] Ann Oncol. 1999 Jan;10(1):33-8 [10076719.001]
  • [Cites] J Clin Oncol. 1999 May;17 (5):1397-406 [10334524.001]
  • [Cites] J Clin Oncol. 1999 Jan;17(1):74-81 [10458220.001]
  • [Cites] J Clin Oncol. 1994 Apr;12(4):689-94 [7512127.001]
  • [Cites] Ann Oncol. 1998 Nov;9(11):1199-204 [9862050.001]
  • [Cites] J Clin Oncol. 1992 Nov;10(11):1754-61 [1383436.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3160-6 [10506613.001]
  • [Cites] J Urol. 1992 Mar;147(3 Pt 2):931-4 [1371564.001]
  • [Cites] Cancer Res. 1988 Nov 15;48(22):6262-71 [2846150.001]
  • [Cites] J Clin Oncol. 1996 Mar;14 (3):709-15 [8622015.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2506-13 [10561316.001]
  • [Cites] J Natl Cancer Inst. 1996 Nov 20;88(22):1623-34 [8931606.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3461-7 [10550143.001]
  • [Cites] Clin Cancer Res. 1998 Jul;4(7):1765-72 [9676853.001]
  • [Cites] Cancer. 1993 Dec 15;72(12 Suppl):3793-8 [8252492.001]
  • [Cites] Scand J Urol Nephrol. 1981;15(3):201-5 [7323739.001]
  • [Cites] J Clin Oncol. 1999 Jun;17(6):1664-71 [10561202.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):921-6 [10071285.001]
  • [Cites] Cancer Res. 1990 Jun 15;50(12):3748-53 [2340521.001]
  • [Cites] J Clin Oncol. 1999 Mar;17 (3):948-57 [10071289.001]
  • [Cites] Clin Cancer Res. 1997 Dec;3(12 Pt 1):2371-6 [9815636.001]
  • [Cites] J Clin Oncol. 1996 Jun;14(6):1756-64 [8656243.001]
  • [Cites] Cancer. 1998 Nov 1;83(9):1989-94 [9806658.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(2):405-11 [10637256.001]
  • [Cites] Clin Cancer Res. 1999 Apr;5(4):831-7 [10213219.001]
  • [Cites] Cancer. 1993 Feb 1;71(3 Suppl):1098-109 [7679039.001]
  • [Cites] J Natl Cancer Inst. 1999 Nov 3;91(21):1869-76 [10547394.001]
  • [Cites] Cancer. 1993 Oct 15;72(8):2457-60 [8104680.001]
  • [Cites] J Clin Oncol. 1993 Apr;11(4):607-15 [7683043.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):958-67 [10071290.001]
  • [Cites] J Clin Oncol. 1997 Sep;15(9):3156-63 [9294479.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3816-21 [10577854.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3828-34 [10577856.001]
  • [Cites] Cancer Res. 1992 Aug 15;52(16):4433-40 [1353706.001]
  • (PMID = 11122870.001).
  • [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 / Androgens; 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 35LT29625A / Estramustine; 3XMK78S47O / Testosterone; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 40
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78. Macpherson GR, Franks M, Tomoaia-Cotisel A, Ando Y, Price DK, Figg WD: Current status of thalidomide and its role in the treatment of metastatic prostate cancer. Crit Rev Oncol Hematol; 2003 Jun 27;46 Suppl:S49-57
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  • [Title] Current status of thalidomide and its role in the treatment of metastatic prostate cancer.
  • Concurrent with its evaluation in various clinical trials for cancer, thalidomide's mechanism of action is sought and new analogues with improved efficacy and pharmacological profile are emerging.
  • This review is a critical evaluation of thalidomide metabolism, molecular targets, anti-angiogenic activity and clinical efficacy with an emphasis on metastatic prostate cancer.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Prostatic Neoplasms / drug therapy. Thalidomide / therapeutic use
  • [MeSH-minor] Animals. Clinical Trials as Topic. Humans. Male. Signal Transduction / drug effects

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  • (PMID = 12850527.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 4Z8R6ORS6L / Thalidomide
  • [Number-of-references] 86
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79. Curtis KK, Pruthi RK, Fonseca R, Gornet MK: Transfusion-dependent anemia after initiation of androgen deprivation therapy for metastatic prostate cancer. Urology; 2007 Oct;70(4):811.e5-8
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  • [Title] Transfusion-dependent anemia after initiation of androgen deprivation therapy for metastatic prostate cancer.
  • Androgen deprivation therapy (ADT) is a commonly used treatment for metastatic prostate cancer.
  • A 78-year-old patient with metastatic prostate cancer had transfusion-dependent anemia develop while on ADT.
  • The anemia, which had been well managed with iron therapy before ADT, was worsened by the loss of bone marrow-stimulating testosterone effects.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Androgen Antagonists / adverse effects. Anemia / chemically induced. Antineoplastic Agents, Hormonal / adverse effects. Blood Transfusion. Leuprolide / adverse effects. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Gastrointestinal Hemorrhage / chemically induced. Gastrointestinal Hemorrhage / therapy. Hemoglobins / analysis. Humans. Male. Telangiectasia, Hereditary Hemorrhagic / complications


80. Lloyd A, Penson D, Dewilde S, Kleinman L: Eliciting patient preferences for hormonal therapy options in the treatment of metastatic prostate cancer. Prostate Cancer Prostatic Dis; 2008;11(2):153-9
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  • [Title] Eliciting patient preferences for hormonal therapy options in the treatment of metastatic prostate cancer.
  • Treatment choices for metastatic prostate cancer are complex and can involve men balancing survival versus quality of life.
  • The present study aims to elicit patient preferences with respect to the attributes of treatments for metastatic prostate cancer through a discrete choice experiment (DCE) questionnaire.
  • Men with recently diagnosed localized prostate cancer were asked to envisage that they had metastatic disease when completing a survey.
  • As expected, men with prostate cancer placed considerable importance on gains in survival; however, avoiding side effects of treatment was also clearly important.
  • Survival gains should be considered alongside side effects when discussing treatment options in metastatic disease.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Flutamide / therapeutic use. Nitriles / therapeutic use. Patient Satisfaction. Prostatic Neoplasms / drug therapy. Tosyl Compounds / therapeutic use
  • [MeSH-minor] Aged. Choice Behavior. Cross-Sectional Studies. Diarrhea / chemically induced. Diarrhea / psychology. Drug Administration Schedule. Drug Costs. Drug Therapy / psychology. Erectile Dysfunction / chemically induced. Erectile Dysfunction / psychology. Gynecomastia / chemically induced. Gynecomastia / psychology. Health Surveys. Hematuria / chemically induced. Hematuria / psychology. Humans. Life Expectancy. Male. Middle Aged. Patient Acceptance of Health Care

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  • (PMID = 17637761.001).
  • [ISSN] 1476-5608
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents, Hormonal; 0 / Nitriles; 0 / Tosyl Compounds; 76W6J0943E / Flutamide; A0Z3NAU9DP / bicalutamide
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81. Moss RA, Petrylak DP: Cytotoxic chemotherapy for prostate cancer: Who and when? Curr Treat Options Oncol; 2006 Sep;7(5):370-7
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  • [Title] Cytotoxic chemotherapy for prostate cancer: Who and when?
  • The survival benefit demonstrated by docetaxel-based therapy in two randomized trials, Southwest Oncology Group (SWOG) 99-16 and TAX 327, has changed the perception of chemotherapy in men with hormone-refractory prostate cancer from nihilism to optimism.
  • These survival improvements are of similar magnitude to those found in trials that established chemotherapeutic regimens for metastatic breast, lung, or colorectal cancer.
  • The timing of chemotherapy in the aforementioned solid tumors is much more clearly defined than in men with metastatic prostate cancer.
  • Traditionally, chemotherapy in men with hormone-resistant prostate cancer was reserved for symptomatic patients only; the inclusion of symptomatic and asymptomatic patients in SWOG 99-16 and TAX 327 has raised several questions regarding the optimal use of chemotherapy in these patients.
  • When is the best time to initiate docetaxel-based chemotherapy?
  • Is it appropriate to use chemotherapy in high-risk patients as adjuvant therapy?
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Prostatic Neoplasms / drug therapy. Taxoids / administration & dosage
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / administration & dosage. Chemotherapy, Adjuvant. Humans. Male. Randomized Controlled Trials as Topic. Risk. Survival Rate

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  • [Cites] Ann Oncol. 1999 Jan;10(1):33-8 [10076719.001]
  • [Cites] J Clin Oncol. 2001 May 1;19(9):2509-16 [11331330.001]
  • [Cites] Br J Urol. 1997 Feb;79(2):196-202 [9052470.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]
  • [Cites] BJU Int. 2006 Jul;98(1):11-9 [16566811.001]
  • [Cites] J Clin Oncol. 2002 Apr 15;20(8):2171-80 [11956279.001]
  • [Cites] J Clin Oncol. 1997 Jan;15(1):382-8 [8996165.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]
  • [Cites] JAMA. 1999 May 5;281(17):1591-7 [10235151.001]
  • [Cites] Urology. 2005 Jun;65(6 Suppl):8-12 [15939077.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2506-13 [10561316.001]
  • [Cites] J Clin Oncol. 2005 Nov 10;23(32):8242-6 [16278479.001]
  • [Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]
  • [Cites] Br J Cancer. 2004 Oct 18;91(8):1425-7 [15467765.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3461-7 [10550143.001]
  • [Cites] J Urol. 2004 Jul;172(1):141-5 [15201755.001]
  • [Cites] Oncology (Williston Park). 2005 Apr;19(5):631-6 [15945343.001]
  • [Cites] BJU Int. 2000 Oct;86(6):675-80 [11069375.001]
  • [Cites] J Clin Oncol. 1996 Jun;14(6):1756-64 [8656243.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 17):28-33 [10604266.001]
  • [Cites] Cancer. 1993 Feb 1;71(3 Suppl):1098-109 [7679039.001]
  • [Cites] J Clin Oncol. 1999 May;17(5):1499-507 [10334537.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):958-67 [10071290.001]
  • [Cites] Urology. 2003 Dec 29;62 Suppl 1:141-6 [14747052.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):1025-33 [15020604.001]
  • [Cites] J Clin Oncol. 2005 May 1;23(13):2918-25 [15860850.001]
  • [Cites] Urol Oncol. 2003 May-Jun;21(3):219-27 [12810210.001]
  • [Cites] J Urol. 2005 Aug;174(2):646-50; discussion 650 [16006930.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8147-51 [15623588.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4568-71 [14673043.001]
  • [Cites] Semin Oncol. 1983 Sep;10(3 Suppl 3):1-2 [6686721.001]
  • (PMID = 16904054.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel
  • [Number-of-references] 32
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82. Small EJ, Ryan CJ: The case for secondary hormonal therapies in the chemotherapy age. J Urol; 2006 Dec;176(6 Pt 2):S66-71
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  • [Title] The case for secondary hormonal therapies in the chemotherapy age.
  • PURPOSE: Virtually all patients with high risk localized and metastatic prostate cancer who are treated with androgen deprivation therapy eventually have progressive clinical or biochemical disease despite this therapy.
  • Despite this fact numerous therapies are available that target the interaction of androgen and androgen receptor in the castrate testosterone milieu and many clinical investigations are under way in this area.
  • MATERIALS AND METHODS: This literature review focuses on the current clinical literature in support of secondary hormonal therapy.
  • These observations suggest that secondary hormonal therapies remain a reasonable clinical approach.
  • Receptor directed approaches to secondary hormonal therapy are antiandrogen withdrawal, sequential use of antiandrogens and estrogenic compounds.
  • Ligand directed therapies are adrenal cortex inhibitors, such as ketoconazole and others in clinical development.
  • Furthermore, in the context of androgen independent tumor growth in patients with metastatic disease clinicians are now faced with the choice of using chemotherapy or secondary hormonal manipulations.
  • CONCLUSIONS: The modest activity of these secondary therapies challenges the notion that advancing prostate cancer uniformly becomes hormone refractory.
  • It offers an alternative to the early use of chemotherapy in patients with androgen independent disease.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Drug Therapy, Combination. Humans. Male. Treatment Outcome

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  • (PMID = 17084172.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents
  • [Number-of-references] 39
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83. Bhandari MS, Petrylak DP, Hussain M: Clinical trials in metastatic prostate cancer--has there been real progress in the past decade? Eur J Cancer; 2005 Apr;41(6):941-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical trials in metastatic prostate cancer--has there been real progress in the past decade?
  • Hormone refractory prostate cancer remains a challenge.
  • While only palliative treatment strategies were available for the past several decades, many promising agents have been investigated over the past decade.
  • Of those the taxanes appeared with significant anti-tumor activity and recently, two large randomized controlled trials demonstrated for the first time, a survival and palliative benefit with docetaxel based chemotherapy.
  • In the current era, recurrent disease after local treatment for localized disease is diagnosed long before evidence of systemic disease.
  • With earlier institution of hormonal treatments, patients are becoming "hormone refractory" earlier in the course of their disease with considerable long life expectancy.
  • Hence, there is a greater need than ever for more treatment options for this expanding group of patients.
  • A number of new systemic therapies have recently emerged, based on a deeper understanding of prostate cancer biology.
  • Novel chemotherapeutics such as the epothilones, molecularly targeted therapies against angiogenesis, the proteosome and endothelin receptor antagonists, as well as biological agents such as anti-sense oligonucleotides are being tested as part of the armamentarium.
  • Key to progress in the therapy of this fatal disease is the commitment and timely enrolment of prostate cancer patients in clinical trials.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Clinical Trials as Topic / trends. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents, Phytogenic / therapeutic use. Humans. Male. Suramin / therapeutic use. Taxoids / therapeutic use. Treatment Outcome


84. Moreno JG, O'Hara SM, Gross S, Doyle G, Fritsche H, Gomella LG, Terstappen LW: Changes in circulating carcinoma cells in patients with metastatic prostate cancer correlate with disease status. Urology; 2001 Sep;58(3):386-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Changes in circulating carcinoma cells in patients with metastatic prostate cancer correlate with disease status.
  • OBJECTIVES: To investigate the diurnal variations in circulating tumor cells (CTCs) in metastatic carcinoma of the prostate (CAP) and to determine whether the change in CTCs correlated with disease progression.
  • RESULTS: Male controls (n = 22) exhibited 0.8 +/- 1.2 events per 7 mL blood compared with 5.9 +/- 4.7 in 10 samples from patients with localized CAP and 46.6 +/- 65.6 events in 10 samples from patients with metastatic CAP.
  • Ten patients were serially analyzed during a 6-month period for serum prostate-specific antigen and CTCs.
  • The correlation between the prostate-specific antigen level and CTC number was fair.
  • Two patients received chemotherapy that caused substantial fluctuations in the CTCs with less pronounced changes in the prostate-specific antigen level.
  • CONCLUSIONS: We conclude that the level of CTCs can be quantified in the circulation of patients with metastatic CAP and that the change in CTCs correlates with disease progression with no diurnal variations.


85. Lechevallier E, Culine S, Benchikh El Fegoun A: [Chemotherapy with docetaxel in prostate cancer. A case report]. Prog Urol; 2010 Mar;20 Suppl 1:S80-3
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  • [Title] [Chemotherapy with docetaxel in prostate cancer. A case report].
  • [Transliterated title] Place de la chimiothérapie par docétaxel dans le cancer de la prostate. A propos d'un cas.
  • There is nothing to support Docetaxel as a first line treatment in metastatic prostate cancer.
  • Hormonal treatment is still the gold standard.
  • Chemotherapy should be initiated in symptomatic patients or if patients are at high risk of developing metastasis (PSADT < 3 months).
  • Quality of life is the main endpoint of chemotherapy in metastatic prostate cancer, that should be monitored clinically.
  • There is no gold standard for second line chemotherapy in castrate resistant prostate cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Prostatic Neoplasms / drug therapy. Taxoids / therapeutic use

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  • (PMID = 20493453.001).
  • [ISSN] 1166-7087
  • [Journal-full-title] Progrès en urologie : journal de l'Association française d'urologie et de la Société française d'urologie
  • [ISO-abbreviation] Prog. Urol.
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel
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86. Gravis G, Salem N, Bladou F, Viens P: [Prostate cancer and chemotherapy]. Bull Cancer; 2007 Jul;94(7 Suppl):F21-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Prostate cancer and chemotherapy].
  • [Transliterated title] Chimiothérapie et cancer de la prostate.
  • Androgen deprivation in patients with metastatic prostate cancer produces palliation of symptoms, PSA decrease and tumoral regression in most patients.
  • Chemotherapy with mitoxantrone has been shown to palliate symptoms but did not extend survival.
  • Two large randomized trials showed a survival benefit for pts with HRPC treated with docetaxel with a reduction risk of death by 21-24%, and significant improvement in palliation of symptoms and quality of life.
  • Current data have demonstrated that neoadjuvant or adjuvant chemotherapy is relatively safe and feasible.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant. Clinical Trials, Phase III as Topic. Drug Administration Schedule. Estramustine / therapeutic use. Humans. Male. Mitoxantrone / therapeutic use. Prednisone / therapeutic use. Prostate-Specific Antigen / blood. Randomized Controlled Trials as Topic. Taxoids / therapeutic use

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  • (PMID = 17845990.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel; 35LT29625A / Estramustine; BZ114NVM5P / Mitoxantrone; EC 3.4.21.77 / Prostate-Specific Antigen; VB0R961HZT / Prednisone
  • [Number-of-references] 70
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87. Lissoni P, Malugani F, Casu M, Bukovec R, Egardi R, Bordin V, Fumagalli E, Mengo S, Gardani G: Effect of bicalutamide therapy on prolactin response to L-dopa in metastatic prostate cancer patients. Neuro Endocrinol Lett; 2002 Feb;23(1):61-3
Hazardous Substances Data Bank. BICALUTAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of bicalutamide therapy on prolactin response to L-dopa in metastatic prostate cancer patients.
  • OBJECTIVES: The secretion of prolactin (PRL), which is a growth factor for prostate cancer cell proliferation, has been proven to present profound alterations in advanced prostate cancer patients, consisting of abnormally elevated baseline levels and paradoxical response to L-dopa.
  • Moreover, the efficacy of standard therapies for prostate cancer may be mediated at least in part by changes in PRL secretion.
  • The present study was carried out to analyze the effects of the new antiandrogen agent bicalutamide on basal levels of PRL and on its response to L-dopa in metastatic prostate cancer patients.
  • MATERIAL & METHODS: The study included 10 metastatic prostate cancer patients.
  • They were investigated with L-dopa test before therapy and after one month of treatment.
  • Mean PRL basal levels decreased after bicalutamide therapy, without, however, significant differences.
  • Before therapy, a paradoxical increase in PRL levels after L-dopa occurred in 4 patients, 3 of them showed basal concentrations of PRL within the normal range.
  • Moreover, bicalutamide therapy significantly reduced PRL increase in response to L-dopa.
  • CONCLUSIONS: This study would suggest that the measurement of the only basal levels is not sufficient to define as normal the secretion of PRL in advanced prostate cancer, because of the possible existence of altered response to the dynamic tests for PRL secretion.
  • Moreover, the study shows that the antitumor therapy with the new anti-androgen bicalutamide may reduce PRL secretion and improve its paradoxical secretion in response to L.-Dopa.
  • Further studies will be required to better define the possible prognostic impact of changes in PRL secretion on the efficacy of treatments for metastatic prostate cancer.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Levodopa. Prolactin / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / drug therapy

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  • (PMID = 11880864.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Nitriles; 0 / Tosyl Compounds; 46627O600J / Levodopa; 9002-62-4 / Prolactin; A0Z3NAU9DP / bicalutamide
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88. Rocco B, Ferrari M, Scardino E, Matei DV, Verweij F, Varela R, De Cobelli O: Gn-RH antagonist possible response, after Gn-RH agonist failure in a man with metastatic prostate cancer. Anticancer Res; 2005 Jan-Feb;25(1B):577-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gn-RH antagonist possible response, after Gn-RH agonist failure in a man with metastatic prostate cancer.
  • Gn-RH agonists or surgical castration are considered standard treatment for patients affected by metastatic prostate cancer.
  • Despite greater cost, chemical castration is often considered the treatment of choice as it is psychologically better tolerated.
  • We report our experience of one patient undergoing treatment with Gn-RH agonist who developed an early resistance to the administered drug, with serum testosterone levels within the range of normality.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Gonadotropin-Releasing Hormone / agonists. Gonadotropin-Releasing Hormone / antagonists & inhibitors. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Humans. Leuprolide / therapeutic use. Male. Neoplasm Metastasis. Prostate-Specific Antigen / blood. Testosterone / blood. Time Factors

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  • (PMID = 15816630.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone; 3XMK78S47O / Testosterone; EC 3.4.21.77 / Prostate-Specific Antigen; EFY6W0M8TG / Leuprolide
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89. Bouchot O, Lenormand L, Karam G, Prunet D, Gaschignard N, Malinovsky JM, Buzelin JM: Intermittent androgen suppression in the treatment of metastatic prostate cancer. Eur Urol; 2000 Nov;38(5):543-9
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  • [Title] Intermittent androgen suppression in the treatment of metastatic prostate cancer.
  • BACKGROUND: To assess the feasibility of intermittent androgen suppression in patients with metastatic prostate cancer and to quantify the improvement in the quality of life.
  • METHODS: Forty-three patients with M1 b prostate cancer were treated by intermittent hormonal deprivation using luteinizing hormone-releasing hormone (LHRH) analogue alone (n = 11), or associated with an antiandrogen (n = 32).
  • The prospective nonrandomized study required an initial therapy period of 12 months with a stable biological response during 6 months (PSA, testosterone).
  • Treatment was resumed when the serum PSA value recovered to 20 ng/ml, or when local failure or new bone metastasis occurred.
  • RESULTS: The mean follow-up time was 43.7 months.
  • After the initial 12 months of androgen suppression, one patient with a minimal disease was off-therapy with a follow-up of 18 months.
  • For the 42 other patients, the mean off-therapy period was 6.7 months.
  • In the second therapy period (9-12 months), 7 patients were hormono-independent and died with a mean survival time of 27 months; 35 patients were responders.
  • The mean off-therapy length in the second cycle was short (3.8 months).
  • After this time, androgen suppression therapy was reintroduced permanently, but 10 patients were hormono-independent.
  • No difference was observed in the EORTC QLQ-C30 between therapy and off-therapy periods, only a rapid decrease in adverse events due to the hormonal deprivation was reported in all cases during the off-therapy period.
  • CONCLUSIONS: Intermittent androgen suppression in patients with M1 b prostate cancer could be associated with a significant period off-therapy in the first cycle (55.8%), and with a chance of second hormone response.
  • But in the second cycle, the off-therapy period length was short and required a careful follow-up.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Feasibility Studies. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Metastasis. Prospective Studies. Quality of Life


90. Fujikawa K, Awakura Y, Okabe T, Watanabe R, Nishimura S: [Cost-utility analysis of androgen ablation therapy in metastatic prostate cancer]. Nihon Hinyokika Gakkai Zasshi; 2003 May;94(4):503-11; discussion 511-2
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  • [Title] [Cost-utility analysis of androgen ablation therapy in metastatic prostate cancer].
  • BACKGROUND: As Bayoumi, et al pointed out in their article (J. Natl. Cancer Inst.
  • 2000, vol 92, p 1731), it is evident that treatment of prostate cancer with Luteinizing Hormone Releasing Hormone (LHRH) analogue costs more than treatment by bilateral orchiectomy.
  • However, patients with metastatic prostate cancer are usually treated with LHRH analogue.
  • Does this mean that urologist choose higher cost and less Quality-Adjusted Life Year (QALY) treatment?
  • Therefore, we urologists should re-analyze their conclusion whether the treatment with LHRH analogue is really strictly dominated (high cost and low effect).
  • The base case was assumed to be a 65-year-old man with symptomatic metastatic prostate cancer.
  • The model used time horizon of 10 years.
  • Five androgen ablation therapies were evaluated as first-line therapy: diethylstilbestrol diphosphate (DES), orchiectomy, orchiectomy + nonsteroidal antiandrogen (NSAA), LHRH analogue and LHRH analogue + NSAA.
  • RESULTS: While DES was the least expensive therapy with the lowest QALY, LHRH analogue monotherapy was the second most expensive therapy with the longest QALY.
  • Incremental cost-effectiveness ratios relative to DES of LHRH (yen 4,288,295/QALY) was cheaper than that of orchiectomy when quality of life (QOL) weight of orchiectomy was assumed to be 0.94 relative to that of LHRH analogue.
  • Cost/QALY of LHRH analogue relative to DES is yen 4,288,295/QALY, which we considered to represent a good value.
  • Choice of therapy depends on the patient's preference.
  • [MeSH-major] Androgen Antagonists / economics. Antineoplastic Agents, Hormonal / economics. Orchiectomy / economics. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / economics. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cost-Benefit Analysis. Costs and Cost Analysis. Diethylstilbestrol / economics. Diethylstilbestrol / therapeutic use. Gonadotropin-Releasing Hormone / analogs & derivatives. Gonadotropin-Releasing Hormone / economics. Humans. Male. Quality of Life. Quality-Adjusted Life Years

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  • (PMID = 12795165.001).
  • [ISSN] 0021-5287
  • [Journal-full-title] Nihon Hinyōkika Gakkai zasshi. The japanese journal of urology
  • [ISO-abbreviation] Nippon Hinyokika Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone; 731DCA35BT / Diethylstilbestrol
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91. Perachino M, Cavalli V, Bravi F: Testosterone levels in patients with metastatic prostate cancer treated with luteinizing hormone-releasing hormone therapy: prognostic significance? BJU Int; 2010 Mar;105(5):648-51
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  • [Title] Testosterone levels in patients with metastatic prostate cancer treated with luteinizing hormone-releasing hormone therapy: prognostic significance?
  • OBJECTIVE: To determine if the testosterone level achieved with androgen-deprivation therapy (ADT) is directly related to survival and risk of death in men with metastatic prostate cancer, as agonistic analogues of luteinizing hormone-releasing hormones (LHRH) are indicated for palliative treatment of these patients, but there is no consensus about the utility of serum testosterone measurements during the follow-up, and their possible prognostic value.
  • PATIENTS AND METHODS: We retrospectively reviewed 129 consecutive patients with a histological diagnosis of metastatic bony-only prostate cancer and previously untreated with ADT.
  • Testosterone and prostate-specific antigen (PSA) levels were measured in all patients every 3 months for the duration of the follow-up.
  • The following variables were recorded: age, stage, Gleason score, basal PSA level, basal testosterone level, PSA nadir, time to PSA nadir, testosterone after 6 months, testosterone nadir and time to testosterone nadir.
  • Data were analysed using Cox's proportional hazards models, with the primary endpoint being cancer-specific survival.
  • With a mean follow-up of 47.5 (29.7) months, 71 patients were dead (55%) and 78 were alive (45%) at the time of analysis.
  • Based on the present results, lowering the testosterone level as much as possible should be the goal of ADT in patients with metastatic prostate cancer, as this might affect patient survival.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Goserelin / therapeutic use. Prostatic Neoplasms / drug therapy. Testosterone / blood
  • [MeSH-minor] Aged. Aged, 80 and over. Epidemiologic Methods. Humans. Male. Middle Aged. Prognosis. Treatment Outcome


92. Dreicer R: Chemotherapy for advanced prostate cancer: docetaxel and beyond. Hematol Oncol Clin North Am; 2006 Aug;20(4):935-46, x
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  • [Title] Chemotherapy for advanced prostate cancer: docetaxel and beyond.
  • To place appropriately into context the current status of chemotherapy as a management option for patients with hormone-refractory metastatic prostate cancer, it is important to reflect on the widely held historical belief that advanced prostate cancer is a chemotherapeutic-insensitive neoplasm.
  • This article focuses on three disease subsets: (1)metastatic, hormone-refractory, chemotherapy-naive prostate cancer;(2) metastatic, hormone-refractory, progressive prostate cancer after frontline chemotherapy; and (3) locally advanced prostate cancer.
  • Yagoda and Petrylak evaluated the results of 26 phase II trials of antineoplastics in advanced prostate cancer published between 1987 and 1991 and found the average objective response rate was less than 10% with only a few studies having response rates in the 10% to 20%range.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Chemotherapy, Adjuvant / methods. Disease Progression. Humans. Male

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  • (PMID = 16861124.001).
  • [ISSN] 0889-8588
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 60
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93. Gulley J, Dahut WL: Chemotherapy for prostate cancer: finally an advance! Am J Ther; 2004 Jul-Aug;11(4):288-94
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  • [Title] Chemotherapy for prostate cancer: finally an advance!
  • Patients with metastatic prostate cancer can be treated with androgen deprivation strategies; however, most patients will eventually develop androgen-independent prostate cancer (AIPC).
  • Until recently, chemotherapy has been shown to palliate symptoms of disease but not improve survival.
  • This firmly cements docetaxel-based therapies as the standard of care for patients with metastatic androgen-independent disease.
  • In addition, this foundation provides a platform for the translation of novel agents into new combination cancer therapies.
  • In this paper, we not only review standard treatment options available for AIPC including the recently completed docetaxel trials, but also present some of the promising new drug combinations of currently available drugs.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Prostatic Neoplasms / drug therapy. Taxoids / therapeutic use
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials, Phase III as Topic. Humans. Male

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  • (PMID = 15266221.001).
  • [ISSN] 1075-2765
  • [Journal-full-title] American journal of therapeutics
  • [ISO-abbreviation] Am J Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel
  • [Number-of-references] 37
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94. Tsukamoto S, Miyanaga N, Kawai K, Akaza H: [Evidence-based medicine for urological cancer chemotherapy]. Gan To Kagaku Ryoho; 2000 Feb;27(2):183-91

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Evidence-based medicine for urological cancer chemotherapy].
  • We reviewed the treatment results of urological cancer chemotherapy from the standpoint of evidence based medicine.
  • In the treatment of advanced transitional cell carcinoma of the urothelium, M-VAC (MTX + VBL + ADM + CDDP) is regarded as the standard regimen; however, durable event-free survival is rare.
  • There is no level 1 evidence to date showing that the use of neoadjuvant or adjuvant cisplatin-based regimens will improve survival in cases of locally advanced bladder cancer.
  • Immunotherapy with interferon or interleukin-2 produces a small survival advantage in patients with metastatic renal cell carcinoma.
  • There is no evidence that adjuvant interferon-alpha administration will improve the survival in those with non-metastatic renal cell carcinoma.
  • Systematized cisplatin-based treatment protocols have been established in patients with advanced testicular germ cell tumor by means of many randomized controlled trials.
  • Several clinical trials are under way to prove the efficacy of high dose chemotherapy (with autologous stem-cell support) in patients with poor risk germ cell tumors.
  • We do not yet have sufficient data to conclude whether maximal androgen blockade will prolong the survival in patients with metastatic prostate cancer, nor to conclude whether neoadjuvant androgen depletion treatment improve disease free survival of the patients after radical prostatectomy.
  • [MeSH-major] Carcinoma, Transitional Cell / drug therapy. Evidence-Based Medicine. Urologic Neoplasms / drug therapy

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  • (PMID = 10700888.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] JAPAN
  • [Number-of-references] 47
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95. Turner SL, Gruenewald S, Spry N, Gebski V, Metastron Users Group: Less pain does equal better quality of life following strontium-89 therapy for metastatic prostate cancer. Br J Cancer; 2001 Feb 2;84(3):297-302
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Less pain does equal better quality of life following strontium-89 therapy for metastatic prostate cancer.
  • 93 patients with hormone refractory metastatic prostate cancer were entered on a prospective study to measure reduction in pain and changes in quality of life (QoL) after the administration of 150 MegaBequerel (MBq) Strontium-89 (Sr-89).
  • QoL was assessed using a validated instrument, the Functional Living Index - Cancer (FLIC) questionnaire.
  • Pain response was measured using the Radiation Therapy Oncology Group scoring system.
  • The lack of correlation of PSA response and clinical parameters indicates that in the palliative setting, PSA may not provide a useful surrogate for treatment outcome.
  • [MeSH-major] Bone Neoplasms / complications. Pain / prevention & control. Prostatic Neoplasms / pathology. Quality of Life. Strontium / therapeutic use
  • [MeSH-minor] Diarrhea / chemically induced. Follow-Up Studies. Hematologic Diseases / chemically induced. Humans. Male. Nausea / chemically induced. Neoplasm Metastasis. Prospective Studies. Prostate-Specific Antigen / blood. Prostate-Specific Antigen / drug effects. Spinal Cord Compression / chemically induced. Strontium Radioisotopes / therapeutic use. Surveys and Questionnaires. Treatment Outcome. Vomiting / chemically induced


96. Wang J, Halford S, Rigg A, Roylance R, Lynch M, Waxman J: Adjuvant mitozantrone chemotherapy in advanced prostate cancer. BJU Int; 2000 Oct;86(6):675-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adjuvant mitozantrone chemotherapy in advanced prostate cancer.
  • OBJECTIVE: To assess the role of mitozantrone, active in relapsed prostate cancer, as an adjuvant to hormonal treatment in patients with advanced prostate cancer.
  • PATIENTS AND METHODS: Between October 1990 and May 1995, 96 patients were entered into a stratified, randomized, single-institution study of hormonal therapy with a luteinizing hormone-releasing hormone agonist and flutamide, with or without four cycles of adjuvant mitozantrone.
  • RESULTS: Patients with localized prostate cancer receiving adjuvant chemotherapy had a higher initial objective response rate (95% vs 53%, P = 0.008) and median survival (80 vs 36 months, P = 0.04) than patients who were treated with hormonal therapy alone.
  • There was no advantage to adjuvant chemotherapy in patients with metastatic prostate cancer.
  • There were insignificant advantages to chemotherapy in overall response rates (55% vs 39%, P = 0.3) and PSA responses (82% vs 64%, P = 0.11).
  • There was no difference between the patient groups in time to treatment failure.
  • CONCLUSION: There was a survival advantage in using adjuvant mitozantrone in patients with locally advanced prostate cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Mitoxantrone / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant / methods. Flutamide / administration & dosage. Humans. Male. Middle Aged. Neoplasm Metastasis. Prostate-Specific Antigen / blood. Receptors, LHRH / antagonists & inhibitors. Survival Analysis. Treatment Outcome


97. Wu K, Zeng J, Li L, Fan J, Zhang D, Xue Y, Zhu G, Yang L, Wang X, He D: Silibinin reverses epithelial-to-mesenchymal transition in metastatic prostate cancer cells by targeting transcription factors. Oncol Rep; 2010 Jun;23(6):1545-52
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  • [Title] Silibinin reverses epithelial-to-mesenchymal transition in metastatic prostate cancer cells by targeting transcription factors.
  • Silibinin, a naturally occurring flavanone isolated from milk thistle extract, has been shown to possess strong anticancer efficacy against both androgen-dependent and androgen-independent prostate cancer, wherein it inhibits not only cell growth, but also cell invasion and metastasis.
  • Inhibitory effects of silibinin on prostate cancer invasion, motility and migration were previously observed in the highly bone metastatic ARCaP M cell line; however, mechanisms of such efficacy are not completely elucidated.
  • The epithelial-to-mesenchymal transition (EMT) is a crucial step in the progression of prostate cancer, reversal or inhibition of EMT by drugs thus provides a new approach to prostate cancer therapy.
  • In the present study, we found that silibinin treatment resulted in the up-regulation of cytokeratin-18 and down-regulation of vimentin and MMP2, which was consistent with morphologic reversal of EMT phenotype leading to be epithelial.
  • Overall these findings demonstrate silibinin was able to reverse EMT to suppress the invasive property of metastatic prostate cancer cells at the transcriptional level.
  • [MeSH-major] Antioxidants / pharmacology. Epithelial Cells / metabolism. Mesoderm / metabolism. Prostatic Neoplasms / drug therapy. Silymarin / pharmacology. Transcription Factors / metabolism
  • [MeSH-minor] Blotting, Western. Cell Adhesion. Cell Line. Cell Movement. Cell Proliferation. Down-Regulation. Fluorescent Antibody Technique. Humans. Keratin-18 / genetics. Keratin-18 / metabolism. Male. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 2 / metabolism. NF-kappa B / genetics. NF-kappa B / metabolism. Neoplasm Metastasis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation. Vimentin / genetics. Vimentin / metabolism

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  • (PMID = 20428808.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Keratin-18; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Silymarin; 0 / Transcription Factors; 0 / Vimentin; 4RKY41TBTF / silybin; EC 3.4.24.24 / Matrix Metalloproteinase 2
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98. Qian DZ, Rademacher BL, Pittsenbarger J, Huang CY, Myrthue A, Higano CS, Garzotto M, Nelson PS, Beer TM: CCL2 is induced by chemotherapy and protects prostate cancer cells from docetaxel-induced cytotoxicity. Prostate; 2010 Mar 1;70(4):433-42
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  • [Title] CCL2 is induced by chemotherapy and protects prostate cancer cells from docetaxel-induced cytotoxicity.
  • BACKGROUND: Metastatic prostate cancer is either inherently resistant to chemotherapy or rapidly acquires this phenotype after chemotherapy exposure.
  • METHODS: We compared the gene expression profiles in individual human prostate cancer specimens before and after exposure to chemotherapy collected from previously untreated patients who participated in a clinical trial of preoperative chemotherapy.
  • Subsequently, we used the gain- and loss-of-function approach in vitro to identify a potential mechanism underlying chemotherapy resistance.
  • RESULTS: Among the molecular signatures associated with treatment, several genes that regulate the inflammatory response and chemokine activity were upregulated including a significant increase in transcripts encoding the CC chemokine CCL2.
  • Docetaxel increased CCL2 expression in prostate cancer cell lines in vitro.
  • In contrast, overexpression of CCL2 or recombinant CCL2 protein stimulated prostate cancer cell proliferation and rescued cells from docetaxel-induced cytotoxicity.
  • The addition of a PI3K/AKT inhibitor Ly294002 reversed the CCL2 protection and was additive to docetaxel-induced toxicity.
  • CONCLUSION: These results support a mechanism of chemotherapy resistance mediated by cellular stress responses involving the induction of CCL2 expression and suggest that inhibiting CCL2 activity could enhance therapeutic responses to taxane-based therapy.

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  • [Copyright] Prostate 70: 433-442, 2010. (c) 2009 Wiley-Liss, Inc.
  • [Cites] Urol Oncol. 2006 May-Jun;24(3):254-9 [16678060.001]
  • [Cites] Nat Clin Pract Urol. 2005 Feb;2(2):92-100; quiz 1 p following 112 [16474654.001]
  • [Cites] J Immunol. 2006 Aug 15;177(4):2651-61 [16888027.001]
  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1308-14 [17317842.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):256-69 [17384581.001]
  • [Cites] Prostate. 2007 Aug 1;67(11):1182-93 [17520666.001]
  • [Cites] Neoplasia. 2007 Jul;9(7):556-62 [17710158.001]
  • [Cites] Cancer. 2007 Sep 15;110(6):1248-54 [17674353.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9417-24 [17909051.001]
  • [Cites] Clin Cancer Res. 2007 Oct 1;13(19):5825-33 [17908975.001]
  • [Cites] Clin Cancer Res. 2008 Jun 1;14(11):3562-70 [18519790.001]
  • [Cites] Mol Cell Biol. 2008 Jul;28(13):4407-23 [18443042.001]
  • [Cites] J Biol Chem. 2008 Sep 5;283(36):25057-73 [18611860.001]
  • [Cites] Autophagy. 2008 Oct;4(7):969-71 [18758234.001]
  • [Cites] Nat Rev Cancer. 2008 Nov;8(11):887-99 [18846100.001]
  • [Cites] Clin Exp Metastasis. 2009;26(2):161-9 [19002595.001]
  • [Cites] Mol Cell Biol. 1999 Dec;19(12):8469-78 [10567572.001]
  • [Cites] Nucleic Acids Res. 2002 Jan 1;30(1):218-20 [11752298.001]
  • [Cites] Genes Dev. 2002 Jan 15;16(2):183-97 [11799062.001]
  • [Cites] Nat Rev Immunol. 2002 Sep;2(9):664-74 [12209135.001]
  • [Cites] Cell Cycle. 2003 Mar-Apr;2(2):143-8 [12695666.001]
  • [Cites] Expert Rev Anticancer Ther. 2003 Jun;3(3):261-8 [12820771.001]
  • [Cites] J Cell Biochem. 2004 Jan 1;91(1):100-17 [14689584.001]
  • [Cites] Oncogene. 2004 Jan 15;23(2):426-33 [14724571.001]
  • [Cites] Clin Cancer Res. 2004 Feb 15;10(4):1306-11 [14977829.001]
  • [Cites] Nat Rev Cancer. 2004 Jul;4(7):540-50 [15229479.001]
  • [Cites] Cancer Res. 2004 Sep 15;64(18):6626-34 [15374977.001]
  • [Cites] J Biol Chem. 1998 Feb 27;273(9):4928-36 [9478937.001]
  • [Cites] Cancer Res. 1998 Apr 15;58(8):1609-15 [9563469.001]
  • [Cites] Int J Oncol. 1998 Oct;13(4):659-64 [9735392.001]
  • [Cites] J Biol Chem. 1999 Mar 19;274(12):8208-16 [10075725.001]
  • [Cites] Inflamm Res. 2004 Oct;53(10):576-84 [15597153.001]
  • [Cites] Clin Cancer Res. 2005 Jul 15;11(14):5233-40 [16033841.001]
  • [Cites] CA Cancer J Clin. 2005 Sep-Oct;55(5):300-18; quiz 323-5 [16166075.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):287-97 [16226704.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):634-42 [16428510.001]
  • [Cites] Neoplasia. 2006 Jul;8(7):578-86 [16867220.001]
  • (PMID = 19866475.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA119125; United States / NCI NIH HHS / CA / U54CA126540; United States / NCI NIH HHS / CA / CA97186; United States / NCI NIH HHS / CA / CA097186-06; United States / NCRR NIH HHS / RR / 3M01RR00334-33S2; United States / NCI NIH HHS / CA / P50 CA097186; United States / NCRR NIH HHS / RR / M01 RR000334; United States / NCI NIH HHS / CA / P50 CA097186-06; United States / NCI NIH HHS / CA / 1 R01 CA119125-01; United States / NCI NIH HHS / CA / U54 CA126540; United States / NCI NIH HHS / CA / R01 CA119125-04; United States / NCI NIH HHS / CA / CA119125-04
  • [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 / Antineoplastic Agents; 0 / CCL2 protein, human; 0 / Chemokine CCL2; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / Taxoids; 15H5577CQD / docetaxel; BZ114NVM5P / Mitoxantrone
  • [Other-IDs] NLM/ NIHMS228122; NLM/ PMC2931415
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99. Altiparmak MR, Bilici A, Kisacik B, Ozguroglu M: Flutamide-induced acute renal failure in a patient with metastatic prostate cancer. Med Oncol; 2002;19(2):117-9
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  • [Title] Flutamide-induced acute renal failure in a patient with metastatic prostate cancer.
  • Androgen blockage, with either orchiectomy or luteinizing hormone releasing hormone (LHRH) analogs combined with an antiandrogen drug, is the standard treatment for metastatic prostate cancer.
  • Flutamide is a non-steroidal antiandrogen drug that is frequently used for total androgen blockage.
  • We report on a 54-yr-old man with metastatic prostate cancer who developed nonoliguric acute renal failure (ARF) during treatment with flutamide.
  • Following discontinuation of flutamide therapy, his renal functions returned to normal limits within 4 wk.
  • His renal function recovered completely after the cessation of the drug for the second time.
  • This observation confirm that ARF may be clearly attributed to flutamide therapy.
  • [MeSH-major] Acute Kidney Injury / chemically induced. Androgen Antagonists / adverse effects. Flutamide / adverse effects. Prostatic Neoplasms / drug therapy

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  • [Cites] J Clin Oncol. 1999 Jul;17(7):2027-38 [10561254.001]
  • [Cites] Br J Urol. 1994 Nov;74(5):642-5 [7827817.001]
  • [Cites] Cancer. 1994 Sep 1;74(5):1612-4 [8062193.001]
  • [Cites] Hum Exp Toxicol. 1999 Mar;18(3):137-40 [10215102.001]
  • [Cites] Am J Clin Oncol. 1997 Aug;20(4):433-4 [9256906.001]
  • [Cites] N Engl J Med. 1989 Aug 17;321(7):419-24 [2503724.001]
  • [Cites] J Clin Oncol. 2001 Jan 1;19(1):62-71 [11134196.001]
  • (PMID = 12180480.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 76W6J0943E / Flutamide
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100. Plotnikov A, Niego B, Ophir R, Korenstein R, Keisari Y: Effective treatment of mouse metastatic prostate cancer by low electric field enhanced chemotherapy. Prostate; 2006 Nov 1;66(15):1620-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effective treatment of mouse metastatic prostate cancer by low electric field enhanced chemotherapy.
  • BACKGROUND: We developed a new anti-cancer treatment, which is a combination of chemotherapeutic agents and low electric field.
  • In the present study we investigated its efficacy against prostate metastatic transgenic adenocarcinoma of mice (TRAMP).
  • METHODS: Mice with 5, 10, and 13 mm in diameter intracutaneous tumors received Low Electric Field Cancer Treatment-Enhanced Chemotherapy (LEFCT-EC) with doxorubicin (10 mg/kg), and monitored for survival, and primary and metastatic tumors growth.
  • In vivo use of LEFCT-EC reduced tumor size, prolonged survival, and cured 36-93% of the animals, dependent on treated tumor size.
  • LEFCT-EC was more effective than surgery with or without chemotherapy.
  • Part of the cured animals developed anti-tumor immunity and immunosuppression, significantly decreased the effectiveness of the treatment.
  • CONCLUSION: Our results suggest that LEFCT-EC is an effective method for the destruction of metastatic prostate tumors.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antibiotics, Antineoplastic / therapeutic use. Doxorubicin / therapeutic use. Electrochemotherapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease Models, Animal. Drug Screening Assays, Antitumor. Electroporation. Male. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Spleen / drug effects. Survival Rate. Treatment Outcome

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  • (PMID = 16941466.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
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