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1. Chauvet B, Villers A, Davin JL, Nahon S: [Update on screening, diagnosis and treatment of cancer of the prostate]. Bull Cancer; 2002 Jan;89(1):37-45
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  • [Title] [Update on screening, diagnosis and treatment of cancer of the prostate].
  • [Transliterated title] Actualités sur le dépistage, le diagnostic et le traitement des cancers de prostate.
  • Recent progress in management of prostate cancer concern screening and treatment.
  • The use of PSA and rectal examination advances the diagnosis by 5 to 10 years and shift the stage at the time of diagnosis toward curative localized intraprostatic disease.
  • However, individual screening explains, at least in part, the decrease of specific mortality due to prostatic cancer, recently observed in USA.
  • PSA and lymphadenectomy have also contributed to a better selection of patients referred for local treatment by prostatectomy or radiotherapy.
  • Recently, dramatic improvement in radiotherapy techniques have been achieved, leading to a better local control by increasing the dose over 70 Gy without additional toxicity.
  • Brachytherapy is also widely used for good prognosis localized disease.
  • Recent randomized trials have demonstrated a benefit of early hormonal therapy concurrent with radiotherapy for patients with poor prognosis localized disease.
  • For hormonoresistant metastatic disease, chemotherapy has been used with limited palliative benefit.
  • New drugs are currently evaluated.
  • [MeSH-major] Prostatic Neoplasms / therapy
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Humans. Lymphatic Metastasis. Male. Mass Screening. Palpation. Patient Education as Topic. Prostate-Specific Antigen / blood. Prostatectomy. Radiotherapy / methods

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  • (PMID = 11847025.001).
  • [ISSN] 0007-4551
  • [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 / Androgen Antagonists; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 78
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2. 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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  • [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.
  • 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.
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  • (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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3. de Wit R: Chemotherapy in hormone-refractory prostate cancer. BJU Int; 2008 Mar;101 Suppl 2:11-5
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  • [Title] Chemotherapy in hormone-refractory prostate cancer.
  • The results of the TAX 327 and SWOG 99-16 trials for the first time showed an improvement in overall survival (OS) with docetaxel-based chemotherapy in patients with metastatic hormone-refractory prostate cancer.
  • As such, 3-weekly (q3w) docetaxel plus low-dose prednisone is widely considered to be the treatment of choice for these patients.
  • Multivariate analysis has shown that prostate-specific antigen (PSA) concentrations and kinetics (pre-treatment PSA doubling time; PSADT) are independent prognostic factors for survival in the TAX 327 cohort, along with pain, number of metastatic sites and measurable disease.
  • A PSA decline of > or 1=30% within 3 months' therapy with docetaxel is also a surrogate of OS.
  • Measurements such as these, and the use of predictive nomograms, can assist the physician in identifying patients at high risk of disease progression who may benefit from earlier treatment with chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasms, Hormone-Dependent / drug therapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Clinical Trials, Phase III as Topic. Disease Progression. Humans. Male. Multivariate Analysis. Neoplasm Metastasis. Nomograms. Predictive Value of Tests. Prednisone / administration & dosage. Prostate-Specific Antigen / blood. Risk Factors. Survival Analysis. Taxoids / administration & dosage

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  • (PMID = 18307687.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; EC 3.4.21.77 / Prostate-Specific Antigen; VB0R961HZT / Prednisone
  • [Number-of-references] 17
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4. Melisi D, Caputo R, Damiano V, Bianco R, Veneziani BM, Bianco AR, De Placido S, Ciardiello F, Tortora G: Zoledronic acid cooperates with a cyclooxygenase-2 inhibitor and gefitinib in inhibiting breast and prostate cancer. Endocr Relat Cancer; 2005 Dec;12(4):1051-8
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  • [Title] Zoledronic acid cooperates with a cyclooxygenase-2 inhibitor and gefitinib in inhibiting breast and prostate cancer.
  • Biphosphonates (BPs) are widely used to inhibit osteoclastic activity in malignant diseases such as bone metastatic breast and prostate carcinoma.
  • The enzyme cyclooxygenase-2 (COX-2) and the epidermal growth factor receptor (EGFR) play an important role in the control of cancer cell growth and inhibitors of COX-2 and EGFR have shown antitumor activity in vitro and in vivo in several tumor types.
  • In the present study we have evaluated the combined effect of zoledronic acid, the most potent nitrogen-containing BP, with the COX-2 inhibitor SC-236 and the selective EGFR-tyrosine kinase inhibitor gefitinib, on breast and prostate cancer models in vitro and in xenografted nude mice.
  • Since studies are ongoing to explore the antitumor effect of zoledronic acid, our results provide new insights into the mechanism of action of these agents and a novel rationale to translate this feasible combination treatment strategy into a clinical setting.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Cyclooxygenase 2 Inhibitors / therapeutic use. Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Prostatic Neoplasms / drug therapy. Pyrazoles / therapeutic use. Quinazolines / therapeutic use. Sulfonamides / therapeutic use
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Female. Humans. Male. Mice. Mice, Nude. Proteins / metabolism. Signal Transduction / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 16322342.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide; 0 / Cyclooxygenase 2 Inhibitors; 0 / Diphosphonates; 0 / Imidazoles; 0 / Proteins; 0 / Pyrazoles; 0 / Quinazolines; 0 / Sulfonamides; 6XC1PAD3KF / zoledronic acid; S65743JHBS / gefitinib
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5. Boccon-Gibod L, Richaud P, Coloby P, Coulange C, Culine S, Davin JL, Soulié M, Zerbib M: [First line indications for hormonal therapy in prostate cancer]. Prog Urol; 2010 Feb;20(2):109-15
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  • [Title] [First line indications for hormonal therapy in prostate cancer].
  • [Transliterated title] Cancer de la prostate et hormonothérapie: indications thérapeutiques de première ligne.
  • The utilization of androgen deprivation therapy in prostate cancer has evolved over time.
  • Unquestionably considered first line treatment in metastatic cancers or in case of lymph node involvement, it is increasingly used in locally advanced and high-risk cancers, combined with radiation therapy.
  • However, the practical modalities of treatment are still controversial (neoadjuvant, concomitant/adjuvant) and should be discussed on a case-by-case basis, taking into account tumor stage and risk level, which depends mainly on Gleason score and PSA levels and kinetics.
  • Hormone therapy is also indicated in case of systemic relapse, especially if PSA doubling time is less than 12 months.
  • LHRH agonists have become the standard care; antiandrogens can be added at the beginning of the LHRH agonist therapy to obtain a complete androgen blockade.
  • Intermittent androgen deprivation therapy has recently proved efficacious and might be more widely used in the future, provided that strict prescription and follow-up recommendations are clearly established.
  • [MeSH-major] Gonadotropin-Releasing Hormone / agonists. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Combined Modality Therapy. Follow-Up Studies. Humans. Lymphatic Metastasis. Male. Neoplasm Staging. Prostate-Specific Antigen / blood. Prostatectomy. Survival Rate. Time Factors

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  • [Copyright] (c) 2009 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20142051.001).
  • [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; 33515-09-2 / Gonadotropin-Releasing Hormone; EC 3.4.21.77 / Prostate-Specific Antigen
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6. Pitchakarn P, Ogawa K, Suzuki S, Takahashi S, Asamoto M, Chewonarin T, Limtrakul P, Shirai T: Momordica charantia leaf extract suppresses rat prostate cancer progression in vitro and in vivo. Cancer Sci; 2010 Oct;101(10):2234-40
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  • [Title] Momordica charantia leaf extract suppresses rat prostate cancer progression in vitro and in vivo.
  • Cancer metastasis is a major cause of death in cancer patients, with invasion as a first step greatly contributing to the failure of clinical treatments.
  • Momordica charantia (bitter melon) is widely consumed as a vegetable and especially as a folk medicine in Asia.
  • Here, we investigated the anti-invasive effects of bitter melon leaf extract (BMLE) on a rat prostate cancer cell line (PLS10) in vitro and in vivo.
  • Real-time RT-PCR revealed that BMLE not only significantly decreased gene expression of MMP-2 and MMP-9, but also markedly increased the mRNA level of TIMP-2, known to have inhibitory effects on the activity of MMP-2.
  • An EnzChek gelatinase/collagenase assay showed that collagenase type IV activity was partially inhibited by BMLE.
  • The incidence of lung metastasis did not show any difference, but the percentage lung area occupied by metastatic lesions was slightly decreased in the 0.1% BMLE treatment group and significantly decreased with 1% BMLE treatment as compared with the control.
  • Thus, the results indicate for the first time an anti-metastatic effect of BMLE both in vitro and in vivo.
  • [MeSH-major] Momordica charantia. Plant Extracts / therapeutic use. Prostatic Neoplasms / drug therapy

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  • [Copyright] © 2010 Japanese Cancer Association.
  • (PMID = 20731662.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Plant Extracts; 0 / Transforming Growth Factor beta; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
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7. Heidenreich A, Albers P, Classen J, Graefen M, Gschwend J, Kotzerke J, Krege S, Lehmann J, Rohde D, Schmidberger H, Uder M, Zeeb H, Association of Urologic Oncology of the German Cancer Society: Imaging studies in metastatic urogenital cancer patients undergoing systemic therapy: recommendations of a multidisciplinary consensus meeting of the Association of Urological Oncology of the German Cancer Society. Urol Int; 2010;85(1):1-10
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  • [Title] Imaging studies in metastatic urogenital cancer patients undergoing systemic therapy: recommendations of a multidisciplinary consensus meeting of the Association of Urological Oncology of the German Cancer Society.
  • INTRODUCTION: Imaging studies are an integral and important diagnostic modality to stage, to monitor and follow-up patients with metastatic urogenital cancer.
  • The currently available guidelines on diagnosis and treatment of urogenital cancer do not provide the clinician with evidence-based recommendations for daily practice.
  • OBJECTIVES: To develop scientifically valid recommendations with regard to the most appropriate imaging technique and the most useful time interval in metastatic urogenital cancer patients undergoing systemic therapy.
  • METHODS: A systematic literature review was performed searching MedLine, Embase and Web of Science databases using the terms prostate, renal cell, bladder and testis cancer in combination with the variables lymph node, lung, liver, bone metastases, chemotherapy and molecular therapy, and the search terms computed tomography, magnetic resonance imaging and positron emission tomography were applied.
  • CONCLUSIONS: Contrast-enhanced computed tomography remains the standard imaging technique for monitoring of pulmonary, hepatic and lymph node metastases.
  • Bone scintigraphy is still the most widely used imaging technique for the detection and follow-up of osseous lesions.
  • Response assessment for patients treated with cytotoxic regime is best performed by the RECIST/WHO criteria; treatment response to molecular triggered therapy is best assessed by CT evaluating decrease in tumor size and density.
  • Cross-sectional imaging studies for response assessment might be obtained after each 2 cycles of systemic therapy to early stratify responders from non-responders.
  • [MeSH-minor] Evidence-Based Medicine. Female. Humans. Male. Neoplasm Staging. Predictive Value of Tests. Treatment Outcome

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  • [Copyright] Copyright (c) 2010 S. Karger AG, Basel.
  • (PMID = 20693823.001).
  • [ISSN] 1423-0399
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Consensus Development Conference; Journal Article; Practice Guideline; Review
  • [Publication-country] Switzerland
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8. Sethi R, Sanfilippo N: Six-month depot formulation of leuprorelin acetate in the treatment of prostate cancer. Clin Interv Aging; 2009;4:259-67
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  • [Title] Six-month depot formulation of leuprorelin acetate in the treatment of prostate cancer.
  • Hormonal deprivation therapy is well established for the treatment of locally advanced and metastatic prostate cancer, as well as the adjuvant treatment of some patients with localized disease.
  • Long-acting gonadotropin releasing hormone (GnRH) agonists have become a mainstay of androgen deprivation therapy, due to their efficacy, tolerability, and convenience of use.
  • One-month, 3-month, and 4-month depot leuprorelin formulations are well established and widely used to this end.
  • Recently, a 6-month depot leuprorelin has been approved for use in advanced and metastatic prostate cancer patients.
  • With similar efficacy and side effect profiles to earlier formulations, 6-month depot leuprorelin is a convenient treatment option for these patients.
  • This review will highlight the role of GnRH agonists in the treatment of prostate cancer with a focus on the clinical efficacy, pharmacology, and patient-focused outcomes of the newer 6-month 45 mg depot leuprorelin formulation in comparison to available shorter-acting products.
  • [MeSH-major] Antineoplastic Agents, Hormonal / administration & dosage. Leuprolide / administration & dosage. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Delayed-Action Preparations. Dose-Response Relationship, Drug. Humans. Male. United States

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  • (PMID = 19554097.001).
  • [ISSN] 1178-1998
  • [Journal-full-title] Clinical interventions in aging
  • [ISO-abbreviation] Clin Interv Aging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Delayed-Action Preparations; EFY6W0M8TG / Leuprolide
  • [Number-of-references] 56
  • [Other-IDs] NLM/ PMC2697591
  • [Keywords] NOTNLM ; hormonal deprivation therapy / leuprorelin / prostate cancer
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9. James ND, Bloomfield D, Luscombe C: The changing pattern of management for hormone-refractory, metastatic prostate cancer. Prostate Cancer Prostatic Dis; 2006;9(3):221-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The changing pattern of management for hormone-refractory, metastatic prostate cancer.
  • Prostate cancer responds initially to hormonal manipulation by androgen withdrawal and peripheral androgen blockade.
  • The inevitable progression to a hormone-refractory state is accompanied by an exacerbation of local symptoms and metastatic spread, principally to the bones, which has a considerable impact on quality of life and survival.
  • Treatment of hormone-refractory prostate cancer is palliative, and surgery and radiotherapy are used for the relief of lower urinary tract symptoms and localized painful bony metastases.
  • Systemic treatments are not widely accepted in this setting, but clinical trials have demonstrated the potential for bone targeting agents such as strontium-89 and the bisphosphonates to palliate painful bone metastases and to delay progression in certain settings.
  • Chemotherapy with mitozantrone in combination with steroids has previously been shown to have palliative benefits and to delay progression.
  • The additional costs incurred by the use of chemotherapy or bone-targeting therapies may be offset by gains in overall care with fewer in-patient admissions compared with steroid monotherapy.
  • Future studies investigating the timing of chemotherapy, combinations with existing treatments or other novel therapies are underway.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Prostatic Neoplasms / therapy
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / secondary. Bone Neoplasms / therapy. Clinical Trials as Topic. Combined Modality Therapy / methods. Diphosphonates / therapeutic use. Drug Resistance, Neoplasm. Humans. Male. Mitoxantrone / therapeutic use. Neoplasm Metastasis / therapy. Palliative Care / methods. Prednisolone / therapeutic use. Spinal Cord Compression / drug therapy. Spinal Cord Compression / etiology. Spinal Cord Compression / surgery. Taxoids / therapeutic use. Urologic Diseases / etiology. Urologic Diseases / surgery

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  • (PMID = 16801939.001).
  • [ISSN] 1365-7852
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Diphosphonates; 0 / Taxoids; 15H5577CQD / docetaxel; 9PHQ9Y1OLM / Prednisolone; BZ114NVM5P / Mitoxantrone
  • [Number-of-references] 64
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10. 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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11. Gaston KE, Ornstein DK: Pharmacotherapy for biochemical recurrences after therapy for localised prostate cancer. Expert Opin Pharmacother; 2002 Jun;3(6):657-69
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  • [Title] Pharmacotherapy for biochemical recurrences after therapy for localised prostate cancer.
  • Prostate-specific antigen (PSA) has revolutionised screening for and monitoring of prostate cancer (CaP).
  • Currently, most men failing potentially curative CaP therapies develop biochemical evidence of recurrent disease (defined by detectable PSA levels) long before the onset of clinical symptoms.
  • Androgen deprivation therapy (ADT) remains the gold standard for the treatment of metastatic CaP.
  • Although widely studied, the optimal timing to begin ADT remains an important and unanswered question.
  • Future advances in gene therapy and immunotherapy hold the greatest promise to provide effective treatments against recurrent CaP while minimising morbidity.
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Androgens / physiology. Clinical Trials as Topic. Cyclooxygenase 2. Drug Administration Schedule. Genetic Therapy. Humans. Isoenzymes / antagonists & inhibitors. Male. Membrane Proteins. Prostaglandin-Endoperoxide Synthases

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  • (PMID = 12036405.001).
  • [ISSN] 1465-6566
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / Isoenzymes; 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Number-of-references] 117
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12. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


13. Benimetskaya L, Stein CA: Antisense therapy: recent advances and relevance to prostate cancer. Clin Prostate Cancer; 2002 Jun;1(1):20-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antisense therapy: recent advances and relevance to prostate cancer.
  • Currently employed treatment options for patients with advanced and metastatic cancer such as surgery, radiation, hormone therapy, and chemotherapy are limited.
  • In particular, the well known limitations of chemotherapy are at least in part due to a lack of specificity.
  • The activation of dominant oncogenes and inactivation of tumor suppressor genes may represent novel targets for cancer therapy.
  • Antisense therapy has been widely used to specifically and selectively inhibit the expression of selected genes at the messenger RNA level.
  • Combinations of antisense oligonucleotides with chemotherapeutic agents may offer important advantages in cancer treatment.
  • Several antisense drugs, especially oblimersen (G3139), have shown interesting results in experiments in animals, and have entered clinical trials.
  • This review summarizes the advantages and limitations of antisense therapy and its use in the treatment of androgen-independent prostate cancer.
  • [MeSH-major] Gene Expression / drug effects. Oligonucleotides, Antisense / therapeutic use. Prostatic Neoplasms / drug therapy. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Clinical Trials as Topic. Humans. Male. Structure-Activity Relationship

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  • (PMID = 15046709.001).
  • [ISSN] 1540-0352
  • [Journal-full-title] Clinical prostate cancer
  • [ISO-abbreviation] Clin Prostate Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2
  • [Number-of-references] 155
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14. Rolfes N, Lümmen G: [The value of biphosphonates in the therapy of prostate cancer]. Urologe A; 2009 Sep;48(9):990, 992, 994-6
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  • [Title] [The value of biphosphonates in the therapy of prostate cancer].
  • [Transliterated title] Der Stellenwert von Bisphosphonaten in der Therapie des Prostatakarzinoms.
  • Skeletal complications of bone metastases or secondary osteoporosis are a frequent event in patients with prostate cancer.
  • Bisphosphonates have been widely used for both indications because of their capacity to prevent bone loss, to reduce pain and to inhibit metastatic growth.
  • Therefore, the risks and benefits of therapy should be considered and informed consent obtained from the patient.
  • Given current evidence the guidelines only allow a recommendation for use in patients with metastatic prostate cancer.
  • [MeSH-major] Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Carcinoma / drug therapy. Carcinoma / secondary. Diphosphonates / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Bone Density Conservation Agents / therapeutic use. Humans. Male

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  • (PMID = 19705098.001).
  • [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 / Antineoplastic Agents; 0 / Bone Density Conservation Agents; 0 / Diphosphonates
  • [Number-of-references] 26
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15. Randall M, Rini B, Ryan C, Rosenberg J, Garcia J, Bubley G, Small EJ: The addition of imatinib mesylate to estramustine/docetaxel (E/D) for the treatment of hormone refractory prostate cancer (HRPC) patients: Results of a phase I trial. J Clin Oncol; 2004 Jul 15;22(14_suppl):4617

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The addition of imatinib mesylate to estramustine/docetaxel (E/D) for the treatment of hormone refractory prostate cancer (HRPC) patients: Results of a phase I trial.
  • : 4617 Background: The E/D combination is used widely to treat metastatic HRPC.
  • METHODS: Metastatic HRPC patients with progressive disease by Consensus Criteria and no prior chemotherapy or investigational therapy were treated in a standard phase I design.
  • All patients received therapy every 21 days consisting of fixed doses of estramustine phosphate, (280 mg po tid D 1-5) dexamethasone (8 mg po bid D 1-3), warfarin (2 mg po qd) and imatinib (400 mg po qd D 1-21).
  • On dose level 3 (400 mg qd imatinib, 70 mg/m2 docetaxel), 2 patients experienced grade 3 elevated prothrombin times attributed to the interaction between imatinib and warfarin, so an additional 3 patients were treated at an intermediate level utilizing 300 mg qd imatinib and 60 mg/m2 docetaxel.

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  • (PMID = 28015756.001).
  • [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. Kaliks-Guendelmann R, Santi P, Cardoso A, Del Giglio A: Complete androgen blockade as second-line hormone manipulation and delay of chemotherapy in metastatic prostate cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e16141

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete androgen blockade as second-line hormone manipulation and delay of chemotherapy in metastatic prostate cancer.
  • : e16141 Background: Complete androgen blockade (CAB) after failure of castration or androgen receptor blocker (ARB) has not shown to prolong survival in patients with metastatic prostate cancer, unlike docetaxel-based chemotherapy.
  • The widely variable clinical benefit seen with CAB as second-line hormone manipulation still justifies the identification of the patients to whom it should be offered.
  • METHODS: We performed a retrospective analysis of all patients with metastatic prostate cancer treated with CAB as second-line hormone manipulation in a single institution after September 2005.
  • We identified 78 patients and evaluated correlations of prostate specific antigen (PSA), Gleason scores, age, type and length of first-line hormone manipulation with OS and PFS during CAB.
  • Forty-four patients received chemotherapy after failing CAB.
  • We did not find any correlation of PFS with type of first-line hormone manipulation (castration vs ARB, p = 0.10), age group (≤70 or >70 years old, p = 0.10), level of PSA at diagnosis (≤50 or >50 ng/mL, p = 0.17) or length of first-line hormone manipulation (≤14m vs >14 m, p = 0.78).
  • Median OS for patients on CAB after failing castration was 36 months (CI 24-48), and median OS of patients on chemotherapy was not reached at 9.5 months follow-up.
  • CONCLUSIONS: Based on a PFS of 12 months, OS of 36 months and good patient tolerance, we believe CAB should still be used in CRPC, prior to initiation of chemotherapy.

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  • (PMID = 27963432.001).
  • [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. Schostak M, Miller K, Schrader M: Hormone therapy for prostate cancer - immediate initiation. Front Radiat Ther Oncol; 2008;41:49-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hormone therapy for prostate cancer - immediate initiation.
  • Although hormone therapy is widely used in the management of prostate cancer, the optimal timing of its initiation remains a matter of debate.
  • Many studies of the last decades have reported a small but significant survival benefit and a clear delay in the development of clinical symptoms after early initiation of therapy.
  • Patients who have localized or locally advanced prostate cancer and are not suitable for curative options like radical prostatectomy or radiotherapy can best be managed by hormone therapy alone, which has already been recognized as the optimal treatment for metastatic disease.
  • On the other hand, long-term hormone treatment will expose the patient to the risk of substantial adverse effects, including muscle wasting, chronic fatigue and osteoporosis.
  • Prognostic and quality-of-life factors also have an impact on the treatment decision, particularly in patients most likely to profit from an extension of the remaining life span.
  • Based on available evidence, early hormone therapy may be recommended for men with poorly differentiated tumors or advanced disease and for those infrequently seen by their physicians.
  • This management can prevent prostate cancer from migrating to the bones, where treatment becomes extremely difficult and cure or even longterm control of the disease is an exception.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents / therapeutic use. Neoplasms, Hormone-Dependent / drug therapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Clinical Trials as Topic. Humans. Male. Prostate-Specific Antigen / blood. Time

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  • (PMID = 18544985.001).
  • [ISSN] 0071-9676
  • [Journal-full-title] Frontiers of radiation therapy and oncology
  • [ISO-abbreviation] Front Radiat Ther Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 40
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18. Akaza H, Chodak GW, Hirao Y: [Usefulness and positioning of MAB therapy for prostate cancer]. Gan To Kagaku Ryoho; 2005 Oct;32(10):1507-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Usefulness and positioning of MAB therapy for prostate cancer].
  • Prostate cancer is a relatively slow-growing disease compared to other cancers, and the patients tend to be older.
  • Taking into consideration therefore life expectancy of the patients and risks of recurrence and progression, conservative treatments (mainly hormonal therapy) are often applied for early cases, as well as radical treatments (total prostatectomy and radiotherapy).
  • Particularly in Japan, many patients start treatment with hormonal therapy alone, in both early and advanced cases.
  • Hence, Maximal Androgen Blockade (MAB) therapy, in which surgical or medical castration (such as LH-RH agonist treatment) and anti-androgen treatment are combined, is widely exercised with the hope to enhance treatment effects.
  • The usefulness of MAB therapy has been assessed in a number of randomized comparative studies, covering mainly metastatic cases.
  • The efficacy of the therapy with the use of flutamide as non-steroidal anti-androgen has been confirmed in some of the studies, although the magnitude of the efficacy cannot be said major.
  • In Phase III clinical studies of MAB therapy with bicalutamide being conducted in Japan for patients in Stages C and D, however, the patient group treated with MAB therapy demonstrated more favorable results compared to the group treated with LH-RH agonist alone, particularly in terms of time to progression (TTP) of the patients in Stage C.
  • These are relatively new findings on the usefulness and adaptability of MAB therapy.
  • In this Panel Discussion, views and experiences are exchanged on a wide variety of topics covering the real usefulness of MAB therapy, its adaptability, possible outcomes of hormonal therapy in early cases, and the future of MAB therapy, taking into account the prevailing opinions and current practices on prostate cancer in both the United States and Japan.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Gonadotropin-Releasing Hormone / agonists. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Anilides / administration & dosage. Clinical Trials as Topic. Clinical Trials, Phase III as Topic. Cost-Benefit Analysis. Drug Administration Schedule. Flutamide / administration & dosage. Humans. Male. Nitriles. Quality of Life. Survival Analysis. Survival Rate. Tosyl Compounds

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  • (PMID = 16227758.001).
  • [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] 19
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19. Aranha O, Vaishampayan U: PSA relapse prostate cancer: the importance of tailored therapy. Urol Oncol; 2004 Jan-Feb;22(1):62-9
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  • [Title] PSA relapse prostate cancer: the importance of tailored therapy.
  • Prostate specific antigen (PSA) is an invaluable tumor marker in the detection of early prostate cancer as well as a predictor of recurrence after treatment of localized disease.
  • Current practice entails the use of factors such as pretherapy grade, stage and PSA, PSA doubling time, nature of previous therapy and patient age and functional status for a treatment recommendation.
  • For a PSA relapse post radical prostatectomy, radiation therapy to the prostatic fossa is a primary therapeutic consideration.
  • For patients with radiation therapy as the primary treatment for their prostate cancer, salvage prostatectomy can be considered, but is rarely feasible.
  • Systemic therapy with hormones is standard if patients are not candidates for the above mentioned salvage local therapies or if they relapse after exhaustive local therapies.
  • Unfortunately androgen suppressive therapy is unlikely to induce cure, or prolonged remissions in PSA relapse prostate cancer.
  • The strategy of addition of chemotherapy or biologic therapy to androgen suppressive therapy is under active investigation.
  • The goal of this therapy is to make an impact on the time to progression to metastatic prostate cancer and correspondingly decrease prostate cancer related mortality.
  • Preliminary results of studies incorporating early chemotherapy in combination with androgen suppressive therapy are encouraging, with improvement in time to progression and overall survival.
  • This is very important to make therapy widely applicable and to enable prolonged administration especially in a disease such as prostate cancer with a relatively long natural history.
  • Strategies of adjuvant and neoadjuvant therapy in locally advanced prostate cancer are exploring the possibility of reducing the chance of PSA relapse by treating micrometastatic disease.
  • This review discusses the current practices in risk stratification and management of PSA relapse prostate cancer.
  • [MeSH-major] Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / therapy. Salvage Therapy


20. Sikes RA, Walls AM, Brennen WN, Anderson JD, Choudhury-Mukherjee I, Schenck HA, Brown ML: Therapeutic approaches targeting prostate cancer progression using novel voltage-gated ion channel blockers. Clin Prostate Cancer; 2003 Dec;2(3):181-7
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  • [Title] Therapeutic approaches targeting prostate cancer progression using novel voltage-gated ion channel blockers.
  • The early detection and treatment of prostate cancer have increased survival and improved clinical outcomes.
  • The development of prostate cancer the time from tumor initiation and progression to invasive carcinoma often begins in men in the fourth or fifth decades of life and extends across decades.
  • This prolonged window highlights the tremendous clinical impact that early intervention with therapeutic agents that selectively target the invasive and metastatic potential of the prostate cancer cell could have on patient survival and quality of life.
  • The expression of voltage-gated sodium channels (VGSCs) was recently associated with the metastatic behavior of prostate cancer cells.
  • In these studies, VGSC blockers altered prostate cancer cell morphology and arrested prostate cancer cell migration.
  • Clinically, one of the most widely used sodium channel blockers is phenytoin.
  • We have used rational drug design based on the phenytoin binding site in a VGSC to make novel sodium channel blockers with enhanced activity and minimal acute toxicity.
  • Our initial studies in vitro demonstrate enhanced binding of the compounds to the sodium channel and increased inhibition of prostate cancer cell growth in culture and in soft agarose compared with phenytoin.
  • These derivatives are currently being tested for their antitumor activity in human prostate cancer xenografts.
  • [MeSH-major] Adenocarcinoma / therapy. Prostatic Neoplasms / therapy. Sodium Channel Blockers / therapeutic use
  • [MeSH-minor] Drug Design. Humans. Ion Channel Gating / drug effects. Ion Channel Gating / physiology. Male. Sodium Channels / physiology

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  • [CommentIn] Clin Prostate Cancer. 2003 Dec;2(3):188-9 [15040864.001]
  • (PMID = 15040863.001).
  • [ISSN] 1540-0352
  • [Journal-full-title] Clinical prostate cancer
  • [ISO-abbreviation] Clin Prostate Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Sodium Channel Blockers; 0 / Sodium Channels
  • [Number-of-references] 73
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21. Persad R: Leuprorelin acetate in prostate cancer: a European update. Int J Clin Pract; 2002 Jun;56(5):389-96
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  • [Title] Leuprorelin acetate in prostate cancer: a European update.
  • This review provides an update on leuprorelin acetate, the world's most widely prescribed depot luteinising hormone-releasing hormone analogue.
  • Leuprorelin acetate has been in clinical use in the palliative treatment of prostate cancer for more than 20 years, but advances continue to be made in terms of convenience and flexibility of administration, and in the incorporation of leuprorelin acetate into novel treatment regimens.
  • The drug is administered in the form of a depot injection containing leuprorelin acetate microspheres, and is at least as effective in suppressing testosterone secretion as orchiectomy.
  • In patients with prostate cancer, serum testosterone levels are reduced to castrate levels (< or = 50 ng/dl) within 2-3 weeks of the first one-month depot injection of 3.75 mg or three-month depot injection of 11.25 mg.
  • Both the one-month and three-month formulations are effective in delaying tumour progression and alleviating symptoms of locally advanced and metastatic prostate cancer.
  • Recent studies have investigated the place of leuprorelin acetate as part of continuous or intermittent maximal androgen blockade (MAB) and in neoadjuvant therapy (i.e. to reduce the size of the prostate and downsize the tumour before radiotherapy).
  • Additional formulations and presentations are in development, including a six-month injection, with the aim of adding to the clinical flexibility and patient acceptability of this important palliative treatment for prostate cancer.
  • [MeSH-major] Antineoplastic Agents, Hormonal / administration & dosage. Leuprolide / administration & dosage. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Humans. Injections. Male. Patient Satisfaction. Testosterone / metabolism. Treatment Outcome

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  • (PMID = 12137449.001).
  • [ISSN] 1368-5031
  • [Journal-full-title] International journal of clinical practice
  • [ISO-abbreviation] Int. J. Clin. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 3XMK78S47O / Testosterone; EFY6W0M8TG / Leuprolide
  • [Number-of-references] 91
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22. Olson KB, Hellie CM, Pienta KJ: Osteonecrosis of jaw in patient with hormone-refractory prostate cancer treated with zoledronic acid. Urology; 2005 Sep;66(3):658
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  • [Title] Osteonecrosis of jaw in patient with hormone-refractory prostate cancer treated with zoledronic acid.
  • Intravenous bisphosphonates are widely used in the management of metastatic bone disease, as well as osteoporosis.
  • Recent published reports have documented a possible link between treatment with intravenous bisphosphonates and osteonecrosis of the jaw.
  • We report a case of osteonecrosis of the jaw in 1 patient with prostate cancer receiving both chemotherapy and intravenous zoledronic acid (Zometa).
  • [MeSH-major] Adenocarcinoma / drug therapy. Bone Density Conservation Agents / adverse effects. Diphosphonates / adverse effects. Imidazoles / adverse effects. Jaw Diseases / chemically induced. Osteonecrosis / chemically induced. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Humans. Male. Middle Aged. Treatment Failure

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  • (PMID = 16140106.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
  • [Number-of-references] 15
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23. DeGroot LJ, Zhang R: Viral mediated gene therapy for the management of metastatic thyroid carcinoma. Curr Drug Targets Immune Endocr Metabol Disord; 2004 Sep;4(3):235-44
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  • [Title] Viral mediated gene therapy for the management of metastatic thyroid carcinoma.
  • Thyroid cancers are of special interest in gene therapy, since it is possible to direct gene expression specifically to the thyroid derived cells by using promoters with limited expression, and secondly, because destruction of the normal tissue by introduction of a toxic gene would have no important adverse effect.
  • Adenovirus is a well studied and widely used vector and is useful for targeting genes because it infects many cell types, including differentiated thyroid cancer and medullary thyroid cancer cells.
  • Combinations of vectors expressing thymidine kinase and IL-12 under control of a strong but non-tissue specific CMV promoter effectively destroy a model anaplastic thyroid tumor in Wistar rats.
  • Medullary thyroid cancer provides a target much like differentiated thyroid cancer because it is possible to address gene expression specifically to the medullary thyroid cells by the use of a modified calcitonin promoter.
  • In the latter system, treatment with adenoviruses expressing genes under control of the modified calcitonin promoter and expressing thymidine kinase or IL-12 leads to destruction of growing medullary thyroid cancer tumors, destroy distant tumors after injection in one tumor, and cause induction of long lasting immunity to subsequent tumor development in the animals.
  • There are many ongoing studies of gene therapy in humans using various genes such as thymidine kinase, IL-2, and now IL-12.
  • Although none of these trials to date shows complete eradication of metastatic tumors in humans, there are reports showing distinctly that the viral mediated gene therapy approach can effectively destroy human tumors after in vivo administration.
  • Tumors that have been treated include melanomas, glioblastomas, breast tumors, and prostate carcinomas.
  • Gene therapy using the adenoviral vectors appears to be safe in studies reported so far.
  • New genes and new vectors under development will certainly lead to the established use of these methods in the therapy of human thyroid carcinomas in the near future.
  • [MeSH-major] Adenoviridae / genetics. Carcinoma / drug therapy. Carcinoma / virology. Genetic Therapy / methods. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / virology


24. Morgan C, Wagstaff J: Is there a role for ibandronate in the treatment of prostate cancer patients with bony metastases? Acta Oncol; 2009;48(6):882-9
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  • [Title] Is there a role for ibandronate in the treatment of prostate cancer patients with bony metastases?
  • PURPOSE: Zoledronic acid is widely accepted as the treatment of choice for a number of cancers which metastasise to bone and is the only bisphosphonate licensed for the treatment of prostate cancer.
  • However, drug related nephrotoxicity, although rare, does pose a significant complication when using zoledronic acid.
  • Prostate cancer patients are generally older than 65 years of age and already exhibit some form of impaired renal function.
  • Thus, for prostate cancer patients who are unable to tolerate zoledronic acid there is a need for an alternative bisphosphonate.
  • METHODS: This article reviews the current published literature regarding the use of ibandronate in the treatment of metastatic prostate cancer.
  • RESULTS: Preliminary data emerging from small Phase II studies suggests ibandronate may provide a therapeutic alternative for the treatment of metastatic prostate cancer when zoledronic acid is deemed unsuitable.
  • CONCLUSION: Further in vivo research with ibandronate in prostate cancer is urgently needed in order to elucidate whether this bisphosphonate may play a role in the treatment and palliative management of metastatic prostate cancer.
  • [MeSH-major] Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / drug therapy. Diphosphonates / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Humans. Male. Treatment Outcome

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  • (PMID = 19925378.001).
  • [ISSN] 1651-226X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 114084-78-5 / ibandronic acid
  • [Number-of-references] 56
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25. Saad F: Treatment of bone complications in advanced prostate cancer: rationale for bisphosphonate use and results of a phase III trial with zoledronic acid. Semin Oncol; 2002 Dec;29(6 Suppl 21):19-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of bone complications in advanced prostate cancer: rationale for bisphosphonate use and results of a phase III trial with zoledronic acid.
  • Prostate cancer often metastasizes to bone during disease progression.
  • Bisphosphonate therapy is widely used for the prevention of skeletal complications in patients with bone lesions from multiple myeloma and breast cancer.
  • Until recently, however, no bisphosphonate had ever shown objective clinical benefit in patients with prostate cancer and osteoblastic bone lesions.
  • A recent multicenter, randomized, placebo-controlled trial found zoledronic acid (4 mg) to be a safe and effective therapy in patients with bone metastases from hormone-refractory prostate cancer.
  • Zoledronic acid significantly reduced the proportion of patients who experienced skeletal complications and extended the time to first skeletal complication.
  • Further, zoledronic acid significantly reduced the risk of skeletal complications over this 15-month study and provided consistent reductions in bone pain that were significant at the 3- and 9-month time points compared with placebo.
  • These results suggest that zoledronic acid may become an important advancement in the care of patients with prostate cancer metastatic to bone.
  • The role of zoledronic acid in the treatment of patients with prostate cancer continues to evolve.
  • [MeSH-major] Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Bone Resorption / drug therapy. Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology

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  • [Copyright] Copyright 2002, Elsevier Science (USA). All rights reserved.
  • (PMID = 12584691.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
  • [Number-of-references] 61
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26. Rubin MA, Mucci NR, Figurski J, Fecko A, Pienta KJ, Day ML: E-cadherin expression in prostate cancer: a broad survey using high-density tissue microarray technology. Hum Pathol; 2001 Jul;32(7):690-7
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  • [Title] E-cadherin expression in prostate cancer: a broad survey using high-density tissue microarray technology.
  • Aberrant or decreased expression has been reported to be associated with prostate carcinoma progression.
  • The degree of E-cadherin expression in prostate cancer remains controversial.
  • To address these variations, we undertook a study to systematically evaluate E-cadherin expression in a broad range of prostate tissue.
  • Benign prostate, clinically localized prostate cancer, and hormone-refractory metastatic prostate cancer were analyzed under uniform conditions using high-density tissue microarrays (TMA).
  • Formalin-fixed, paraffin-embedded prostate carcinoma from men with clinically localized prostate carcinoma and autopsy material from men who died of widely metastatic, hormone-refractory prostate carcinoma were arrayed into 6 high-density TMA blocks.
  • Benign and atrophic prostate tissue and high-grade prostatic intraepithelial neoplasia (PIN) were also included from the clinically localized cases.
  • A total of 1,220 prostate TMA samples were analyzed.
  • High (normal) E-cadherin expression was seen in 87% of 757 benign, 80% of 41 high-grade PIN, 82% of 325 prostate carcinoma and 90% of 97 hormone-refractory prostate carcinoma TMA samples.
  • Mean E-cadherin expression was determined for each of the 128 clinically localized prostate cancer cases.
  • Aberrant E-cadherin expression showed a statistical trend toward an association with positive surgical margins (P =.012), higher Gleason score (P =.18), and prostate-specific antigen (PSA) failure (Kaplan-Meier analysis, log-rank P =.09).
  • The current study shows a broad-spectrum approach to evaluating E-cadherin protein expression in prostate carcinoma.
  • Clinically localized prostate tumors, treated with surgery alone, show a high level of E-cadherin expression.
  • In the metastatic hormone-refractory prostate tumors, E-cadherin expression was vastly expressed, and only rare cases had aberrant expression.
  • Therefore, the findings of this study are most consistent with a transient down-regulation of E-cadherin in localized prostate cancer.
  • Metastatic prostate cancer shows strong E-cadherin expression as determined by anti-E-cadherin antibody HECD-1.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Drug Resistance, Neoplasm. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Metastasis / drug therapy. Neoplasm Metastasis / pathology


27. Chan TY, Epstein JI: Radiation or chemotherapy cystitis with "pseudocarcinomatous" features. Am J Surg Pathol; 2004 Jul;28(7):909-13
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  • [Title] Radiation or chemotherapy cystitis with "pseudocarcinomatous" features.
  • BACKGROUND: The features of radiation or chemotherapy cystitis mimicking invasive urothelial cancer are not widely known.
  • DESIGN: A search of the consultation files from our institution between January 1996 and September 2003 identified 20 patients with bladder biopsies showing cystitis mimicking invasive urothelial cancer.
  • Seventeen patients had a history of pelvic irradiation (15 prostate cancer and 2 endometrial cancer).
  • Two patients had systemic chemotherapy (1 metastatic colon cancer and 1 mixed connective tissue disease).
  • The mean time from radiation and/or chemotherapy to presentation was 27 months (range, 0-84 months).
  • All cases showed epithelial proliferation that mimicked invasive cancer within the lamina propria, with marked proliferation seen in 45% of cases.
  • Seventeen patients were followed for a mean of 9 months (range, 0.25-37 months), and none developed bladder cancer.
  • CONCLUSIONS: Radiation or chemotherapy cystitis can show epithelial proliferations that may be confused with invasive urothelial carcinomas.
  • Other findings characteristic of radiation or chemotherapy cystitis, such as hemorrhage, fibrin, and vascular changes, are often seen in association with the epithelial proliferations and are helpful in distinguishing it from invasive cancer.
  • Pathologists must be aware that these changes may be seen with a remote radiation or chemotherapy history, where this information may not be provided or known at the time of the biopsy evaluation.
  • [MeSH-major] Cystitis / etiology. Cystitis / pathology. Urinary Bladder / drug effects. Urinary Bladder / radiation effects
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Colonic Neoplasms / drug therapy. Diagnosis, Differential. Endometrial Neoplasms / radiotherapy. Epithelium / pathology. Female. Fibrin / analysis. Follow-Up Studies. Hemorrhage / pathology. Histocytochemistry. Humans. Male. Middle Aged. Mixed Connective Tissue Disease / drug therapy. Prostatic Neoplasms / radiotherapy. Radiation Injuries / diagnosis. Radiotherapy / adverse effects. Thrombosis / pathology. Time Factors. Urinary Bladder Neoplasms / pathology

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  • (PMID = 15223961.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 9001-31-4 / Fibrin
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28. Vijayababu MR, Arunkumar A, Kanagaraj P, Venkataraman P, Krishnamoorthy G, Arunakaran J: Quercetin downregulates matrix metalloproteinases 2 and 9 proteins expression in prostate cancer cells (PC-3). Mol Cell Biochem; 2006 Jul;287(1-2):109-16
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  • [Title] Quercetin downregulates matrix metalloproteinases 2 and 9 proteins expression in prostate cancer cells (PC-3).
  • BACKGROUND: Cancer metastasis, involving multiple processes and various cytophysiological changes, is a primary cause of cancer death and may complicate the clinical management, even lead to death.
  • Quercetin is a flavonoid and widely used as an antioxidant and recent studies have revealed its pleiotropic anticancer and antiproliferative capabilities.
  • RESULTS: The results showed that quercetin treatment decreased the expressions of MMP-2 and MMP-9 in dose-dependent manner.
  • CONCLUSION: Hence, we speculated that inhibition of metastasis-specific MMPs in cancer cells may be one of the targets for anticancer function of quercetin, and thus provides the molecular basis for the development of quercetin as a novel chemopreventive agent for metastatic prostate cancer.
  • [MeSH-major] Down-Regulation / drug effects. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 9 / genetics. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / enzymology. Quercetin / pharmacology
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Chemoprevention. Dose-Response Relationship, Drug. Humans. Male. Matrix Metalloproteinase Inhibitors

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  • (PMID = 16645725.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Matrix Metalloproteinase Inhibitors; 9IKM0I5T1E / Quercetin; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
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29. Kostarelos K, Emfietzoglou D, Papakostas A, Yang WH, Ballangrud AM, Sgouros G: Engineering lipid vesicles of enhanced intratumoral transport capabilities: correlating liposome characteristics with penetration into human prostate tumor spheroids. J Liposome Res; 2005;15(1-2):15-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Engineering lipid vesicles of enhanced intratumoral transport capabilities: correlating liposome characteristics with penetration into human prostate tumor spheroids.
  • Liposomes have been widely used delivery systems, particularly relevant to the development of cancer therapeutics.
  • Numerous liposome-based drugs are in the clinic or in clinical trials today against multiple tumor types; however, systematic studies of liposome interactions with solid or metastatic tumor nodules are scarce.
  • This study is describing the in vitro interaction between liposomes and avascular human prostate (LNCaP-LN3) tumor spheroids.
  • Polymer-coated (sterically stabilised) liposomes exhibited almost no interaction with the spheroid, indicating that their limited diffusion within avascular tissues may be a limiting step for their use against micrometastases.
  • This study illustrates that interactions between liposomes and other drug delivery systems with multicellular tumor spheroids can offer critically important information with respect to optimizing solid or micrometastatic tumor delivery and targeting strategies.
  • [MeSH-major] Liposomes. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Spheroids, Cellular

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  • (PMID = 16194925.001).
  • [ISSN] 0898-2104
  • [Journal-full-title] Journal of liposome research
  • [ISO-abbreviation] J Liposome Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipid Bilayers; 0 / Liposomes; 0 / Phospholipids
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30. Feng T, Yohannan J, Allaf ME: Nonseminomatous germ cell tumor of the testes metastatic to the corpus cavernosum of the penis. Urology; 2010 Feb;75(2):255-6
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  • [Title] Nonseminomatous germ cell tumor of the testes metastatic to the corpus cavernosum of the penis.
  • Within the genitourinary tract, advanced prostate cancer is the most common culprit.
  • These cases typically represent widely disseminated disease and are associated with a poor prognosis.
  • The patient received chemotherapy and experienced a complete response.

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 19931126.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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31. Singh A, Singh P, Sahni K, Shukla P, Shukla V, Pant NK: Non-small cell lung cancer presenting with choroidal metastasis as first sign and showing good response to chemotherapy alone: a case report. J Med Case Rep; 2010;4:185

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Non-small cell lung cancer presenting with choroidal metastasis as first sign and showing good response to chemotherapy alone: a case report.
  • INTRODUCTION: Metastatic tumors are the most common intra-ocular malignancies and choroid is by far the most common site for intra-ocular malignancies.
  • The primary sites for choroidal metastasis in decreasing order and by gender are: breast, lung, unknown primary, gastrointestinal and pancreas, skin melanoma and other rare sources in females, and lung, unknown primary, gastrointestinal and pancreas, prostate, kidney, skin melanoma and other rare sources in males.
  • Available treatment options are external beam radiotherapy and plaque radiotherapy, while new methods like surgical resection, transpupillary thermotherapy and intravitreal chemotherapy offer promises for the future.
  • The use of chemotherapy alone for choroidal metastases is not widely reported.
  • He was administered chemotherapy based on gemcitabine and carboplatin.
  • He had significant progressive subjective and objective improvement since his first chemotherapy.
  • His current best corrected visual acuity is 20/60 after three cycles of chemotherapy.
  • CONCLUSIONS: Chemotherapy alone can be used as an effective mode of treatment in patients who have primary tumors that respond to chemotherapy.

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  • [Cites] Arch Ophthalmol. 1973 Feb;89(2):97-9 [4683617.001]
  • [Cites] Arch Ophthalmol. 1974 Oct;92(4):276-86 [4412321.001]
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  • (PMID = 20565905.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2916915
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32. Zucker S, Cao J, Chen WT: Critical appraisal of the use of matrix metalloproteinase inhibitors in cancer treatment. Oncogene; 2000 Dec 27;19(56):6642-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Critical appraisal of the use of matrix metalloproteinase inhibitors in cancer treatment.
  • Experimental studies performed prior to 1990 led to the widely held belief that matrix metalloproteinases (MMPs) produced by cancer cells are of critical importance in tumor invasion and metastasis.
  • Based on this evidence, the pharmaceutical industry produced several well tolerated, orally active MMP inhibitors (MMPIs) which demonstrated efficacy in mouse cancer models.
  • Phase III clinical trials initiated in 1997-98 using marimastat, prinomastat (AG3340), and BAY 12-9566 alone or in combination with standard chemotherapy in patients with advanced cancers (lung, prostate, pancreas, brain, GI tract) have recently been reported; no clinical efficacy was demonstrated.
  • Bayer and Agouron have discontinued their ongoing Phase III drug trials of MMPIs in advanced cancer.
  • In retrospect, the failure of MMPIs to alter disease progression in metastatic cancer might have been anticipated since MMPs appear to be important in early aspects of cancer progression (local invasion and micrometastasis) and may no longer be required once metastases have been established.
  • Our understanding of MMP pathophysiology in cancer has expanded considerably in the past 10 years.
  • (2) cancer cells induce stromal cells to synthesize MMPs using extracellular matrix metalloproteinase inducer (EMMPRIN) and cytokine stimulatory mechanisms; and (3) MMPs promote cell migration and the release of growth factors sequestered in the extracellular matrix.
  • In spite of considerable recent progress in identifying multiple roles of MMPs in disease, our understanding of MMP function in cancer is far from complete (see Table 1).
  • (1) patients with early stage cancer;.
  • (2) the use of MMPIs along with chemotherapy;.
  • (3) the measurement of MMPs in tumor tissue and blood as a means of identifying patients who are more likely to respond to MMPI therapy; and (4) identification of biomarkers that reflect activation or inhibition of MMPs in vivo.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Matrix Metalloproteinase Inhibitors. Neoplasms / drug therapy
  • [MeSH-minor] Animals. Clinical Trials as Topic. Drug Design. Drug Evaluation, Preclinical. Humans. Matrix Metalloproteinases / chemistry. Matrix Metalloproteinases / physiology. Mice. Models, Biological. Neoplasm Metastasis. Neovascularization, Pathologic. Stromal Cells / enzymology

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  • (PMID = 11426650.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Matrix Metalloproteinase Inhibitors; EC 3.4.24.- / Matrix Metalloproteinases
  • [Number-of-references] 75
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33. Dobrovolskaia MA, Kozlov SV: Inflammation and cancer: when NF-kappaB amalgamates the perilous partnership. Curr Cancer Drug Targets; 2005 Aug;5(5):325-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inflammation and cancer: when NF-kappaB amalgamates the perilous partnership.
  • Chronic inflammation has long been suggested to constitute a risk factor for a variety of epithelial cancers such as malignancies of prostate, cervix, esophagus, stomach, liver, colon, pancreas, and bladder.
  • Cytokines and growth factors can further promote tumor growth by stimulating cell proliferation, adhesion, vascularization, and metastatic potential of later stage tumors.
  • Nuclear factor kappa B (NF-kappaB) is a family of ubiquitously expressed transcription factors that are widely believed to trigger both the onset and the resolution of inflammation.
  • Recent data have expanded the concept of inflammation as a critical component in carcinogenesis suggesting new anti-inflammatory therapies for a complementary approach in treating a variety of tumor types.
  • These observations highlighted the NF-kappaB pathway as an attractive avenue for drug discovery and development.
  • The present review will outline recent advances in our understanding of NF-kappaB function in the inflammatory processes and its input in tumor initiation/promotion, as well as summarize the development of animal and cell culture models for validating drug candidates with NF-kappaB-modulating activities, and applications of the latter in cancer therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Inflammation / etiology. NF-kappa B / metabolism. Neoplasms / drug therapy. Neoplasms / etiology
  • [MeSH-minor] Animals. Cytokines / metabolism. Drug Design. Free Radicals / metabolism. Gene Expression Regulation. Humans. Membrane Glycoproteins / metabolism. Receptors, Cell Surface / metabolism. Receptors, Tumor Necrosis Factor, Type II / metabolism. Signal Transduction / drug effects. Toll-Like Receptors. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16101381.001).
  • [ISSN] 1568-0096
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines; 0 / Free Radicals; 0 / Membrane Glycoproteins; 0 / NF-kappa B; 0 / Receptors, Cell Surface; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Toll-Like Receptors; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 242
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34. Kondo M, Sakuta K, Noguchi A, Ariyoshi N, Sato K, Sato S, Sato K, Hosoi A, Nakajima J, Yoshida Y, Shiraishi K, Nakagawa K, Kakimi K: Zoledronate facilitates large-scale ex vivo expansion of functional gammadelta T cells from cancer patients for use in adoptive immunotherapy. Cytotherapy; 2008;10(8):842-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Zoledronate facilitates large-scale ex vivo expansion of functional gammadelta T cells from cancer patients for use in adoptive immunotherapy.
  • Because they can kill tumor cells in a major histocompatibility complex (MHC)-unrestricted manner, adoptive transfer of activated gammadelta T cells may represent a novel cancer immunotherapy.
  • We tested whether gammadelta T cells from advanced cancer patients can be expanded by zoledronate.
  • METHODS: Peripheral blood mononuclear cells from healthy donors and patients with advanced non-small cell lung cancer, bone metastatic breast or prostate cancer, or lung metastatic colorectal cancer, were stimulated with zoledronate (5 microM) and interleukin (IL)-2 (1000 IU/mL) for 14 days.
  • The phenotype and function of the expanded gammadelta T-cell populations from healthy donors and cancer patients were compared.
  • RESULTS: Gammadelta T cells from cancer patients and healthy donors responded to zoledronate equally well in terms of both phenotype and function. gammadelta T cells grew rapidly in vitro and expression of effector molecules, such as interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, perforin, granzyme B, FasL and TRAIL, increased over time.
  • Cytotoxicity peaked on days 12-14, and proliferation continued up to 14 days, during which time>1x10(9) gammadelta T cells could be obtained from a starting sample of 45-70 mL peripheral blood.
  • DISCUSSION: Using the agent zoledronate, already widely used in the clinic, we have established that efficient large-scale ex vivo expansion of gammadelta T cells from cancer patients is possible.
  • These cells exert potent cytotoxicity and may be used for autologous cellular immunotherapy of cancer.
  • [MeSH-major] Bone Neoplasms / therapy. Breast Neoplasms / therapy. Carcinoma, Non-Small-Cell Lung / therapy. Cell Proliferation / drug effects. Colorectal Neoplasms / therapy. Cytokines / metabolism. Cytotoxicity, Immunologic / drug effects. Diphosphonates / pharmacology. Imidazoles / pharmacology. Immunotherapy, Adoptive. Lung Neoplasms / therapy. Prostatic Neoplasms / therapy. Receptors, Antigen, T-Cell, gamma-delta / metabolism. T-Lymphocytes / pathology

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  • (PMID = 19016372.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Diphosphonates; 0 / Imidazoles; 0 / Receptors, Antigen, T-Cell, gamma-delta; 63231-63-0 / RNA; 6XC1PAD3KF / zoledronic acid
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35. Stein WD, Litman T, Fojo T, Bates SE: A Serial Analysis of Gene Expression (SAGE) database analysis of chemosensitivity: comparing solid tumors with cell lines and comparing solid tumors from different tissue origins. Cancer Res; 2004 Apr 15;64(8):2805-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A Serial Analysis of Gene Expression (SAGE) database analysis of chemosensitivity: comparing solid tumors with cell lines and comparing solid tumors from different tissue origins.
  • Drug sensitivity and resistance has been most extensively studied in cell lines carried in tissue culture.
  • Furthermore, cell lines have been widely used in testing new anticancer agents, despite the widely recognized observation that cell lines are more sensitive to cytotoxic drugs than are their corresponding solid tumors.
  • We used the Serial Analysis of Gene Expression (SAGE) database to identify differences between solid tumors and cell lines, hoping to detect genes that could potentially explain differences in drug sensitivity.
  • SAGE libraries were available for both solid tumors and cell lines from breast, colon, ovarian, pancreatic, and prostate carcinomas and from gliomas and medulloblastomas.
  • We next used the SAGE database to identify genetic differences between tumor types that convey a broad range of survival to the patients that bear them as distant metastases.
  • SAGE gene expression data were correlated with 5-year survivals documented in the SEER (Surveillance, Epidemiology and End-Results) database for patients diagnosed with "distant" or metastatic cancers.
  • These are unlikely to be amenable to surgical resection; therefore, survival here reflects, to some extent, sensitivity to systemic therapy, i.e., chemotherapy.
  • Using survival data as a surrogate of chemotherapy sensitivity, a spectrum can be generated, with testicular cancer at one end and pancreatic cancer at the other.
  • Poor 5-year survival correlates with expression of cell adhesion, cytoskeletal, and ECM genes, a pattern similar to that found to distinguish solid tumors from the more cytotoxin-sensitive cancer cell lines.
  • One interpretation is that resistance to chemotherapy may arise, in part, from the adherent, relatively inert condition (i.e., low in protein synthesis potential) of refractory cancers.
  • Thus, attachment or ECM genes could be targets for anticancer therapy.
  • [MeSH-major] Cell Line, Tumor / drug effects. Neoplasms / drug therapy. Neoplasms / genetics
  • [MeSH-minor] Databases, Genetic. Drug Screening Assays, Antitumor. Gene Expression Profiling. Humans

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  • (PMID = 15087397.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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36. Rocha-Lima CM, Soares HP, Raez LE, Singal R: EGFR targeting of solid tumors. Cancer Control; 2007 Jul;14(3):295-304
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Recent clinical trials suggest that epidermal growth factor receptor (EGFR)-targeted agents could benefit many patients with cancer.
  • METHODS: We review the current status of several EGFR-targeted therapies in cancer patients and address the efficacy of theses drugs as monotherapy or in combination with other drugs and/or treatments.
  • RESULTS: Cetuximab is the most widely studied anti-EGFR monoclonal antibody.
  • All of these agents have been studied for the treatment of colorectal, lung, breast, pancreatic, renal, head and neck, gynecologic, and prostate cancer.
  • Currently, cetuximab and panitumumab are FDA approved for the treatment of metastatic colorectal cancer.
  • Additionally, cetuximab is approved for head and neck cancer.
  • Erlotinib is FDA approved for advanced/metastatic lung cancer.
  • Erlotinib in combination with gemcitabine is approved for advanced/metastatic pancreatic cancer treatment.
  • Researchers are continuously investigating additional cancer types and combined treatment modalities that could also benefit from the use of EGFR-targeted agents.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Neoplasms / drug therapy. Pancreatic Neoplasms / drug therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Cetuximab. Colorectal Neoplasms / drug therapy. Humans. Lung Neoplasms / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • (PMID = 17615536.001).
  • [ISSN] 1073-2748
  • [Journal-full-title] Cancer control : journal of the Moffitt Cancer Center
  • [ISO-abbreviation] Cancer Control
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab
  • [Number-of-references] 72
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37. Korsisaari N, Kasman IM, Forrest WF, Pal N, Bai W, Fuh G, Peale FV, Smits R, Ferrara N: Inhibition of VEGF-A prevents the angiogenic switch and results in increased survival of Apc+/min mice. Proc Natl Acad Sci U S A; 2007 Jun 19;104(25):10625-30
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  • Anti-VEGF-A monoclonal antibodies, in combination with chemotherapy, result in a survival benefit in patients with metastatic colorectal and non-small cell lung cancer, but little is known regarding the impact of anti-VEGF-A therapy on benign or premalignant tumors.
  • The Apc+/min mice have been widely used as a model recapitulating early intestinal adenoma formation.
  • Short-term (3 or 6 weeks) treatment with anti-VEGF-A Mab G6-31 resulted in a nearly complete suppression of adenoma growth throughout the small intestine.
  • Long-term (up to 52 weeks) treatment with Mab G6-31 led to a substantial increase in median survival.
  • [MeSH-minor] Adenoma / blood supply. Adenoma / genetics. Adenoma / immunology. Adenoma / therapy. Animals. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / pharmacology. Gene Deletion. In Situ Hybridization. Intestinal Neoplasms / blood supply. Intestinal Neoplasms / genetics. Intestinal Neoplasms / immunology. Intestinal Neoplasms / therapy. Mice. Mice, Inbred C57BL. Signal Transduction / immunology. Survival Analysis. Time Factors

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  • (PMID = 17553957.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ PMC1888576
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38. Spieth ME, Lin YG, Nguyen TT: Diagnosing and treating small-cell carcinomas of prostatic origin. Clin Nucl Med; 2002 Jan;27(1):11-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Small-cell carcinoma is very aggressive, metastasizes early and often, and does not respond to most chemotherapy regimens.
  • In approximately 50% of cases of prostate cancer, tumors are a combination of small-cell carcinoma and androgen-sensitive adenocarcinoma.
  • It is widely believed that no successful treatment exists for androgen-independent prostate cancer.
  • METHODS: A 67-year-old man had undergone androgen ablation therapy and radical prostatectomy for prostate cancer followed by bilateral orchiectomy, limited radiation therapy, and unsuccessful chemotherapy for pain-causing metastatic bone disease.
  • Biopsy and immunohistochemical analysis revealed neuroendocrine differentiation of the cancer.
  • The full extent of metastatic disease was assessed successfully using In-111, a somatostatin derivative.
  • RESULTS: In-111 OctreoScan scintigraphy was more sensitive in the diagnostic demonstration of metastatic foci than was bone scanning.
  • Therapy with the cold somatostatin derivative resulted in a rapid and significant relief of pain with significant tumor shrinkage.
  • CONCLUSIONS: Somatostatin analogs and their radionuclide and cytotoxic derivatives are recommended as adjuvant treatments for prostate carcinoma, especially in those patients who are at high risk for carcinoma recurrence after radical prostatectomy and who have advanced prostate carcinoma at the time of relapse.
  • Because small-cell carcinomas of the prostate and lung are identical, these analogs may be useful in the detection and treatment of these tumors as well.
  • [MeSH-major] Carcinoma, Small Cell / diagnosis. Carcinoma, Small Cell / therapy. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Follow-Up Studies. Humans. Lung Neoplasms / diagnosis. Lung Neoplasms / secondary. Lung Neoplasms / therapy. Magnetic Resonance Imaging. Male. Prostatectomy. Radiotherapy, Adjuvant. Somatostatin / administration & dosage. Somatostatin / analogs & derivatives. Treatment Outcome

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  • (PMID = 11805477.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 51110-01-1 / Somatostatin
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39. Lee KL, Terris MK: Luteinizing hormone-releasing hormone agonists and meningioma: a treatment dilemma. Urology; 2003 Aug;62(2):351
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Luteinizing hormone-releasing hormone agonists and meningioma: a treatment dilemma.
  • The relative contraindication of hormonal therapy for patients with prostate cancer and a history of meningioma has not been widely emphasized.
  • Using immunohistochemistry to determine the presence of hormone receptors in meningioma specimens proved potentially valuable in 2 patients with biochemical recurrence after prostatectomy who were being considered for androgen deprivation therapy.
  • These cases also highlight the need for caution against assuming that skull-based intracranial growths in patients receiving hormonal therapy for prostate cancer are metastatic lesions rather than hormonally induced primary tumors.
  • [MeSH-minor] Aged. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / chemically induced. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / radiotherapy. Neoplasm Recurrence, Local / surgery. Neoplasms, Second Primary / chemically induced. Prostatectomy. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / radiotherapy. Prostatic Neoplasms / surgery

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  • (PMID = 12893358.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 33515-09-2 / Gonadotropin-Releasing Hormone
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40. Coleman RE: Optimising treatment of bone metastases by Aredia(TM) and Zometa(TM). Breast Cancer; 2000;7(4):361-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Optimising treatment of bone metastases by Aredia(TM) and Zometa(TM).
  • Metastatic bone disease develops as a result of the many interactions between tumour cells and bone cells.
  • This leads to disruption of normal bone metabolism, with the increased osteoclast activity seen in most, if not all, tumor types providing a rational target for treatment.
  • The clinical course of metastatic bone disease in multiple myeloma, breast and prostate cancers is relatively long, with patients experiencing sequential skeletal complications over a period of several years.
  • External beam radiotherapy and systemic endocrine and cytotoxic treatments are the mainstay of treatment in advanced cancers.
  • However, it is now clear that the bisphosphonates provide an additional treatment strategy, which reduces both the symptoms and complications of bone involvement.
  • Pamidronate (Aredia(TM)) is the most widely evaluated bisphosphonate and is recommended for most patients with multiple myeloma or breast cancer with bone metastases.
  • Clinical studies in treatment of hypercalcemia of malignancy have been completed, as have Phase I and II trials in patients with cancer and pre-existing bone metastases.
  • Three randomized, double-blind, controlled Phase III trials are now ongoing to establish the efficacy and safety of Zometa in treatment of bone metastases in patients with osteolytic and osteoblastic lesions.
  • Additionally, new specific molecules such as osteoprotogerin have been developed that are based on our improved understanding of the cellular signalling mechanisms involved in cancer induced bone disease.
  • Ongoing research is aimed at trying to define the optimum route, dose, schedule and type of bisphosphonate in metastatic bone disease and their use in the prevention and treatment of osteoporosis in cancer patients.
  • In vitro suggestions of direct anti-cancer activity and some promising clinical data in early breast cancer have resulted in considerable interest in the possible adjuvant use of bisphosphonates to inhibit the development of bone metastases.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Breast Neoplasms / drug therapy. Diphosphonates / therapeutic use. Imidazoles / therapeutic use
  • [MeSH-minor] Female. Humans. Hypercalcemia / drug therapy. Male. Osteoclasts / drug effects. Osteoporosis / prevention & control. Prostatic Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
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  • (PMID = 11114866.001).
  • [ISSN] 1340-6868
  • [Journal-full-title] Breast cancer (Tokyo, Japan)
  • [ISO-abbreviation] Breast Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid; OYY3447OMC / pamidronate
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41. Rayman S, Almas K, Dincer E: Bisphosphonate-related jaw necrosis: a team approach management and prevention. Int J Dent Hyg; 2009 May;7(2):90-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bisphosphonates (BPs) are becoming recognized increasingly as having a significant impact on dental treatments.
  • BPs are the most widely used class of anti-resorptive drugs.
  • They prevent bone resorption through osteoclast inhibition and are considered the standard of care for the management of metastatic bone disease.
  • BPs are used for the treatment of skeletal disorders such as osteoporosis, hypercalcaemia of malignancy, osteolytic lesions arising from solid tumours and Paget's disease, breast cancer or prostate cancer.
  • [MeSH-minor] Bone Diseases / drug therapy. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Dental Hygienists. Dentists. Humans. Injections, Intravenous. Osteoclasts / drug effects

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  • MedlinePlus Health Information. consumer health - Osteonecrosis.
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  • [CommentIn] Int J Dent Hyg. 2010 May;8(2):154 [20522142.001]
  • (PMID = 19422147.001).
  • [ISSN] 1601-5037
  • [Journal-full-title] International journal of dental hygiene
  • [ISO-abbreviation] Int J Dent Hyg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates
  • [Number-of-references] 18
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