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1. Van Brussel JP, Jan Van Steenbrugge G, Van Krimpen C, Bogdanowicz JF, Van Der Kwast TH, Schröder FH, Mickisch GH: Expression of multidrug resistance related proteins and proliferative activity is increased in advanced clinical prostate cancer. J Urol; 2001 Jan;165(1):130-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of multidrug resistance related proteins and proliferative activity is increased in advanced clinical prostate cancer.
  • PURPOSE: Advanced disseminated prostate cancer is highly resistant to cytotoxic chemotherapy.
  • We identified proteins that may be involved in multidrug resistance in clinical prostate cancer.
  • MATERIALS AND METHODS: Paraffin embedded, formalin fixed prostate cancer specimens from archival sources of 3 distinct patient groups were examined.
  • These groups were clearly distinct with regard to pathological stage and responsiveness to antihormonal therapy.
  • Group 1 consisted of patients with organ confined prostate cancer treated with radical prostatectomy (early pathological stage T2N0M0).
  • Group 2 patients had disseminated, early advanced prostate cancer and were treated with transurethral prostatic resection for urinary obstruction before receiving antihormonal therapy.
  • Group 3 patients had disseminated prostate cancer with relapse despite antihormonal treatment (late advanced prostate cancer) and they underwent transurethral prostatic resection to relieve the symptoms of urinary obstruction.
  • The number of cases expressing multidrug resistance associated protein, lung resistance protein, glutathione-S-transferase pi, p53, Bcl-2, topoisomerase IIalpha and Ki-67 was significantly increased in the group with advanced disseminated prostate cancer.
  • Topoisomerase I and IIbeta were homogeneously and highly expressed at all stages of prostate cancer progression, while P-glycoprotein was not expressed in any tumors regardless of the patient group.
  • CONCLUSIONS: Up-regulation of the expression of the drug transporters multidrug resistance associated protein and lung resistance protein, detoxifying enzyme glutathione-S-transferase pi, and apoptosis inhibiting proteins Bcl-2 and p53 may be an explanation of the resistance of disseminated progressive prostate cancer to chemotherapy.
  • As shown by the up-regulation of Ki-67 and topoisomerase IIalpha, increased proliferation reflects the aggressiveness of metastatic prostate cancer.
  • Research on agents that counteract multidrug resistance mechanisms and may sensitize prostate carcinoma to cytotoxic chemotherapy may possibly lead to more effective treatment of progressive disseminated prostate cancer.
  • [MeSH-minor] Aged. Case-Control Studies. Cell Division. Drug Resistance, Multiple. Humans. Immunohistochemistry. Male. Middle Aged. Multidrug Resistance-Associated Proteins. Up-Regulation


2. Gillitzer R, Hampel C, Wiesner C, Hadaschik B, Thüroff J: Single-institution experience with primary tumours of the male urethra. BJU Int; 2008 Apr;101(8):964-8
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  • RESULTS: Three patients had tumours of the prostatic urethra, two of which had proliferating focal inflammation and one a low-grade, superficial urothelial cancer.
  • Six patients had carcinoma of the bulbar or penile urethra, including two with previous local percutaneous radiotherapy for prostate cancer.
  • One patient had adjuvant chemotherapy after surgery.
  • CONCLUSION: Primary carcinoma of the male urethra is a rare entity.
  • Local surgical tumour control is essential for long-term survival, but the extent of surgery depends on tumour location and stage.
  • Multimodal therapy might be required to obtain an optimum oncological outcome.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Carcinoma, Transitional Cell / pathology. Urethral Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Combined Modality Therapy. Epidemiologic Methods. Humans. Lymphatic Metastasis. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local. Prognosis

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  • (PMID = 18070169.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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3. Yan Y, Mahotka C, Heikaus S, Shibata T, Wethkamp N, Liebmann J, Suschek CV, Guo Y, Gabbert HE, Gerharz CD, Ramp U: Disturbed balance of expression between XIAP and Smac/DIABLO during tumour progression in renal cell carcinomas. Br J Cancer; 2004 Oct 4;91(7):1349-57
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  • Dysregulation of apoptosis plays an important role in tumour progression and resistance to chemotherapy.
  • To explore the relevance of antiapoptotic XIAP and proapoptotic Smac/DIABLO for tumour progression in renal cell carcinomas (RCCs), we analysed XIAP and Smac/DIABLO mRNA and protein expression in the primary tumour tissue from 66 RCCs of all major histological types by quantitative real-time PCR, Western blot and ELISA.
  • Western blot analysis confirmed the tumour stage-dependent increase of XIAP expression on the protein level.
  • [MeSH-major] Apoptosis / genetics. Carcinoma, Renal Cell / genetics. Carcinoma, Renal Cell / pathology. Carrier Proteins / biosynthesis. Gene Expression Profiling. Kidney Neoplasms / genetics. Kidney Neoplasms / pathology. Mitochondrial Proteins / biosynthesis. Protein Biosynthesis. Proteins

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  • (PMID = 15328523.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DIABLO protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Mitochondrial Proteins; 0 / Proteins; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human
  • [Other-IDs] NLM/ PMC2409908
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4. Ramalingam SS, Harvey RD, Saba N, Owonikoko TK, Kauh J, Shin DM, Sun SY, Strychor S, Tighiouart M, Egorin MJ, Fu H, Khuri FR: Phase 1 and pharmacokinetic study of everolimus, a mammalian target of rapamycin inhibitor, in combination with docetaxel for recurrent/refractory nonsmall cell lung cancer. Cancer; 2010 Aug 15;116(16):3903-9
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  • [Title] Phase 1 and pharmacokinetic study of everolimus, a mammalian target of rapamycin inhibitor, in combination with docetaxel for recurrent/refractory nonsmall cell lung cancer.
  • BACKGROUND: Everolimus is a novel inhibitor of the mammalian target of rapamycin pathway, which is aberrantly activated in nonsmall cell lung cancer (NSCLC).
  • METHODS: Patients with advanced stage NSCLC and progression after prior platinum-based chemotherapy were eligible.
  • Everolimus area under the concentration time curve (AUC) was not different with 60 or 75 mg/m2 docetaxel.
  • CONCLUSIONS: The recommended phase 2 doses of docetaxel and everolimus for combination therapy are 60 mg/m2 and 5 mg orally daily, respectively.

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  • [Copyright] Copyright (c) 2010 American Cancer Society.
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  • (PMID = 20564143.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA116676; United States / NCI NIH HHS / CA / P01 CA116676-03; United States / NCI NIH HHS / CA / 5 P01 CA116676-03
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; 9HW64Q8G6G / Everolimus; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS189772; NLM/ PMC2940062
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5. Fozing T, Scheuer C, Samnick S: Synthesis and initial tumor affinity testing of iodine-123 labelled EGFR-affine agents as potential imaging probes for hormone-refractory prostate cancer. Eur J Med Chem; 2010 Sep;45(9):3780-6
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  • [Title] Synthesis and initial tumor affinity testing of iodine-123 labelled EGFR-affine agents as potential imaging probes for hormone-refractory prostate cancer.
  • The epidermal growth factor receptor (EGFR) is over-expressed in a variety of human cancers, including in hormone-refractory prostate carcinomas, in which the EGFR has been associated with advanced disease stage, resistance to standard treatment and poor prognosis.
  • Therefore, the EGFR is considered to be a promising molecular target for molecular imaging and therapy for hormone-refractory prostate cancer.
  • This work describes the synthesis and initial tumor affinity testing of the EGFR antagonist (123)I-mAb425 and the EGF receptor tyrosine kinase (EGFR-TK) inhibitor (123)I-PD153035 as potential imaging probes for studying EGFR-expressing prostate cancer using single photon emission tomography.
  • The potential of (123)I-mAb425 and (123)I-PD153035 to target EGFR-positive prostate carcinoma was tested on androgen-insensitive PC-3 and DU-145 prostate carcinoma cell lines, and on the androgen-sensitive LNCaP prostate cancer cell line for comparison.
  • In vivo, the capability of (123)I-mAb425 and (123)I-PD153035 to target hormone-refractory prostate cancer was assessed in RNU rats or nu/nu mice bearing human PC3 prostate cancer xenografts.
  • RESULTS: (123)I-mAb425 was obtained in >90% radiochemical yield using the IODO-GEN method. (123)I-PD153035 was synthesized by a non-isotopic [(123)I]iodo-debromination of PD153035 in 50-60% radiochemical yield in a total synthesis time including HPLC separation of 70 min.
  • In vitro (123)I-mAb425 and (123)I-PD153035 accumulated highly in human PC-3 and DU-145 prostate cancer cells.
  • In comparison, the uptake of the EGFR-affine probes into LNCaP prostate carcinoma cells was significantly low (105 +/- 25 cpm/1000 cells).
  • Inhibition experiments revealed that (123)I-mAb425 is taken up into tumor cells via the same pathway as the naturally occurring epidermal growth factor (EGF), while (123)I-PD153035 accumulation in prostate cancer cells occurs presumably via the same pathway as the selective EGFR-Tyrosine kinase antagonist AG1418.
  • In vivo, the human prostate cancer xenografts in mouse war accurately visualized after i.v. administration of (123)I-mAb425 by a gamma camera.
  • CONCLUSION: These data suggest that (123)I-mAb425 and (123)I-PD153035 are promising candidates as imaging probes for EGFR-positive prostate cancer and warrant further in vivo validations to ascertain their potential as imaging agents for clinical used.
  • [MeSH-major] Antibodies, Monoclonal / analysis. Drug Resistance, Neoplasm. Hormones / pharmacology. Molecular Imaging / methods. Prostatic Neoplasms / metabolism. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Animals. Biological Transport. Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Humans. Iodine Radioisotopes. Male. Mice. Protein Kinase Inhibitors / metabolism. Protein Kinase Inhibitors / pharmacology. Quinazolines / metabolism. Quinazolines / pharmacology. Rats. Tomography. Xenograft Model Antitumor Assays

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  • [Copyright] 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20538380.001).
  • [ISSN] 1768-3254
  • [Journal-full-title] European journal of medicinal chemistry
  • [ISO-abbreviation] Eur J Med Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / 4-((3-bromophenyl)amino)-6,7-dimethoxyquinazoline; 0 / Antibodies, Monoclonal; 0 / Hormones; 0 / Iodine Radioisotopes; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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6. Szende B, Romics I, Minik K, Szabó J, Torda I, Lovász S, Szomor L, Tóth L, Bély M, Kerényi T, Bartók K, Végh A: Repeated biopsies in evaluation of therapeutic effects in prostate carcinoma. Prostate; 2001 Oct 1;49(2):93-100
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  • [Title] Repeated biopsies in evaluation of therapeutic effects in prostate carcinoma.
  • METHODS: At the time of diagnosis by needle biopsy TNM stage, serum PSA, Gleason's grade, apoptotic and mitotic index, Ki67, p53, and bcl(2) expression were investigated in 60 prostate carcinoma patients.
  • Antiandrogen therapy supplemented with surgical or chemical castration was administered.
  • Serum PSA-test and needle biopsy were repeated 13-14 weeks after starting the therapy, simultaneously with determination of the apoptotic and mitotic index, Ki67, p53, and bcl(2) expression.
  • Decrease in mitotic, increase in apoptotic index predicted favourable long-term response to antiandrogen therapy.
  • Lower Ki67 and (mutant) p53 expression in the first and also in the second biopsy pointed to favourable effect of antiandrogen treatment.
  • Since the ratio between Ki67 and apoptotic index strongly decreased in the survivors upon therapy, changes in Ki67/apoptosis ratio is recommended as a histologically detectable predictive factor. bcl(2) expression did not show significant correlation with the outcome of the disease.
  • CONCLUSIONS: Histological evaluation of mitotic and apoptotic index, Ki67, and p53 expression in repeated biopsies contributes to predicting the value of the actual treatment and may be useful to institute alterations in therapy.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma / drug therapy. Carcinoma / pathology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Age Factors. Aged. Apoptosis / drug effects. Biopsy. Humans. Immunohistochemistry. Ki-67 Antigen / biosynthesis. Male. Mitotic Index. Neoplasm Staging. Prostate-Specific Antigen / blood. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Tumor Suppressor Protein p53 / biosynthesis

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  • [Copyright] Copyright 2001 Wiley-Liss, Inc.
  • (PMID = 11582587.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; EC 3.4.21.77 / Prostate-Specific Antigen
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7. Bracarda S, de Cobelli O, Greco C, Prayer-Galetti T, Valdagni R, Gatta G, de Braud F, Bartsch G: Cancer of the prostate. Crit Rev Oncol Hematol; 2005 Dec;56(3):379-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer of the prostate.
  • Prostate carcinoma, with about 190,000 new cases occurring each year (15% of all cancers in men), is the most frequent cancer among men in northern and western Europe.
  • Causes of the disease are essentially unknown, although hormonal factors are involved, and diet may exert an indirect influence; some genes, potentially involved in hereditary prostate cancer (HPC) have been identified.
  • A suspect of prostate cancer may derive from elevated serum prostate-specific antigen (PSA) values and/or a suspicious digital rectal examination (DRE) finding.
  • For a definitive diagnosis, however, a positive prostate biopsy is requested.
  • Treatment strategy is defined according to initial PSA stage, and grade of the disease and age and general conditions of the patient.
  • In localized disease, watchful waiting is indicated as primary option in patients with well or moderately differentiated tumours and a life expectancy <10 years, while radical prostatectomy and radiotherapy (with or without hormone-therapy) could be appropriate choices in the remaining cases.
  • Hormone-therapy is the treatment of choice, combined with radiotherapy, for locally advanced or bulky disease and is effective, but not curative, in 80-85% of the cases of advanced disease.
  • Patients who develop a hormone-refractory prostate cancer disease (HRPC) have to be evaluated for chemotherapy because of the recent demonstration of improved overall survival (2-2.5 months) and quality of life with docetaxel in more than 1,600 cases.
  • [MeSH-minor] Antineoplastic Protocols. Humans. Male. Neoplasm Staging / methods. Postoperative Complications / etiology. Prognosis. Radiotherapy / adverse effects. Treatment Outcome


8. Hatori M, Totuka Y, Yamanaka H: The pharmacokinetics of fosfestrol and diethylstilbestrol in chronic hemodialysis patients with prostate cancer. Int J Urol; 2001 Dec;8(12):681-5
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  • [Title] The pharmacokinetics of fosfestrol and diethylstilbestrol in chronic hemodialysis patients with prostate cancer.
  • BACKGROUND: Fosfestrol drip infusion therapy is an available endocrinotherapy for prostate cancer.
  • We conducted fosfestrol drip infusion therapy as an induction therapy in chronic hemodialysis patients with prostate cancer.
  • One was a 68-year-old man who had been in hemodialysis for 15.7 years and had stage B2 prostate cancer.
  • The other was a 74-year-old man who had been in hemodialysis for 4.4 years and had stage C prostate cancer.
  • The drug was given subcutaneously during 14 consecutive days and a luteinizing hormone-releasing hormone agonist was injected on day 15.
  • RESULTS: Serum fosfestrol levels increased rapidly after the drip infusion was started and remained at high levels during infusion, but fell quickly after the treatment ended.
  • Diethylstilbestrol (DES) was also detected in blood after the infusion was started and its levels peaked when infusion ended.
  • But on the next day, neither fosfestrol nor DES were detected in the blood of the patients.
  • Moreover, neither fosfestrol nor DES was detected in the blood of the two patients before administering fosfestrol on day 15.
  • Fosfestrol was quickly eliminated from the blood after hemodialysis was started, while DES remained in the blood during hemodialysis.
  • CONCLUSIONS: Fosfestrol drip infusion therapy appeared to be safe as an endocrinotherapy for prostate cancer in chronic hemodialysis patients.
  • [MeSH-major] Diethylstilbestrol / analogs & derivatives. Diethylstilbestrol / pharmacokinetics. Kidney Failure, Chronic / blood. Prostatic Neoplasms / drug therapy. Renal Dialysis
  • [MeSH-minor] Aged. Area Under Curve. Humans. Infusions, Intravenous. Male. Treatment Outcome

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  • (PMID = 11851768.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 731DCA35BT / Diethylstilbestrol; A0E0NMA80F / fosfestrol
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9. Ishizu K, Tsushimi M, Shimajiri S, Hamada T, Sasaguri Y, Naito K: [Small cell carcinoma of the prostate successfully treated with combined chemotherapy and radiotherapy: a case report]. Hinyokika Kiyo; 2002 Feb;48(2):97-100
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  • [Title] [Small cell carcinoma of the prostate successfully treated with combined chemotherapy and radiotherapy: a case report].
  • The prostate was enlarged, and the serum level of prostate specific antigen was within the normal range.
  • Under the diagnosis of benign prostatic hypertrophy, transurethral resection of the prostate was performed.
  • Unexpectedly, histopathological examination of the resected tissues revealed pure small cell carcinoma.
  • The cancer was clinically diagnosed as stage C.
  • Pelvic radiotherapy combined with chemotherapy using cisplatin (CDDP) and etoposide (VP-16) was started according to the treatment for limited small cell cancer of the lung.
  • After four months, the prostate was reduced in size without any findings of metastases on computed tomography, and prostate biopsy revealed no viable cancer cells.
  • [MeSH-major] Carcinoma, Small Cell / drug therapy. Carcinoma, Small Cell / radiotherapy. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Combined Modality Therapy. Humans. Male. Middle Aged

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  • (PMID = 11968736.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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10. Daniel KG, Anderson JS, Zhong Q, Kazi A, Gupta P, Dou QP: Association of mitochondrial calpain activation with increased expression and autolysis of calpain small subunit in an early stage of apoptosis. Int J Mol Med; 2003 Aug;12(2):247-52
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  • [Title] Association of mitochondrial calpain activation with increased expression and autolysis of calpain small subunit in an early stage of apoptosis.
  • Various stimuli including anticancer drugs are capable of initiating the apoptotic death program in human tumor cells via activation of caspases.
  • In the current study, we have examined the expression and activation of mitochondrial calpain in Jurkat T leukemia cells, MCF-7 breast carcinoma and LNCaP prostate cancer cells during apoptosis induced by an anticancer drug (VP-16, tamoxifen) or the specific p38 kinase inhibitor PD-169316.
  • Our results suggest that increased expression and autolysis of the mitochondrial calpain small subunit are tightly associated with calpain activation in an early stage of apoptosis.
  • Furthermore, pretreatment with the specific pharmacological calpain inhibitor calpeptin blocked the drug-induced calpain small subunit autolysis and calpain activation in mitochondria and inhibited apoptosis-associated caspase-3 activation, demonstrating that mitochondrial calpain activation through small subunit cleavage is an essential step for inducing tumor cell apoptosis by various anticancer drugs.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Autolysis. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cytochrome c Group / drug effects. Cytochrome c Group / metabolism. Enzyme Activation. Enzyme Inhibitors / pharmacology. Etoposide / pharmacology. Female. Humans. Imidazoles / pharmacology. Jurkat Cells / drug effects. Male. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinases / metabolism. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. Protein Subunits. Tamoxifen / pharmacology. Tumor Cells, Cultured. p38 Mitogen-Activated Protein Kinases

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  • (PMID = 12851726.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytochrome c Group; 0 / Enzyme Inhibitors; 0 / Imidazoles; 0 / PD 169316; 0 / Protein Subunits; 094ZI81Y45 / Tamoxifen; 6PLQ3CP4P3 / Etoposide; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Calpain
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11. Berruti A, Dogliotti L, Mosca A, Bellina M, Mari M, Torta M, Tarabuzzi R, Bollito E, Fontana D, Angeli A: Circulating neuroendocrine markers in patients with prostate carcinoma. Cancer; 2000 Jun 1;88(11):2590-7
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  • [Title] Circulating neuroendocrine markers in patients with prostate carcinoma.
  • BACKGROUND: Circulating neuroendocrine markers were measured in patients with prostate carcinoma (PC), prostatic intraepithelial neoplasia (PIN), and benign prostatic hypertrophy (BPH) with the goal to:.
  • 3) compare values in patients with hormone-naive and hormone-refractory disease; and 4) assess changes after androgen deprivation or chemotherapy.
  • CgA was monitored in 31 patients submitted to androgen deprivation and in 24 patients receiving chemotherapy.
  • RESULTS: Supranormal CgA was observed more frequently in patients with American Urologic Association (AUA) Stage D2 disease (45.5%) compared with those with Stage D1 disease (33.3%), Stage C disease (16.7%), Stage A/B disease (18.8%), PIN (25.9%), and BPH (17.0%) (P < 0.02).
  • Elevated baseline CgA values decreased > 50% in 1 of 12 patients who received luteinizing hormone-releasing hormone analogs and in 2 of 12 patients who underwent chemotherapy.
  • Elevated CgA values correlate with poor prognosis and are scarcely influenced by either endocrine therapy or chemotherapy.
  • [MeSH-major] Biomarkers, Tumor / blood. Carcinoma / blood. Chromogranins / blood. Phosphopyruvate Hydratase / blood. Prostatic Hyperplasia / blood. Prostatic Intraepithelial Neoplasia / blood. Prostatic Neoplasms / blood

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  • [Copyright] Copyright 2000 American Cancer Society.
  • (PMID = 10861438.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Chromogranins; EC 4.2.1.11 / Phosphopyruvate Hydratase
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12. Fine RL, Shah SS, Moulton TA, Yu IR, Fogelman DR, Richardson M, Burris HA, Samuels BL, Assanasen C, Gorroochurn P, Hibshoosh H, Orjuela M, Garvin J, Goldman FD, Dubovsky D, Walterhouse D, Halligan G: Androgen and c-Kit receptors in desmoplastic small round cell tumors resistant to chemotherapy: novel targets for therapy. Cancer Chemother Pharmacol; 2007 Mar;59(4):429-37
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  • [Title] Androgen and c-Kit receptors in desmoplastic small round cell tumors resistant to chemotherapy: novel targets for therapy.
  • PURPOSE: Desmoplastic small round cell tumor (DSRCT) is a highly fatal, mainly peritoneal cell origin cancer which predominantly affects young adult males.
  • METHODS: Slides were prepared from 27 multi-institutional patients all with end-stage DSRCT.
  • Slides were stained for AR, c-Kit, various growth factors, and drug resistance-associated proteins.
  • Six patients with positive AR status were treated solely with combined androgen blockade (CAB) as used for prostate cancer.
  • All patients had failed at least two prior multi-agent chemotherapy regimens and 44% had progressed after autologous stem cell transplant.
  • Six patients with positive AR status were treated with CAB alone and three of six attained clinical benefit (1-PR, 1-MR, 1-SD) in a range of 3-4 months.
  • [MeSH-major] Carcinoma, Small Cell / chemistry. Proto-Oncogene Proteins c-kit / analysis. Receptors, Androgen / analysis. Soft Tissue Neoplasms / chemistry


13. Cesinaro AM, Migaldi M, Ferrari G, Castagnetti G, Dotti A, De Gaetani C, Ferrari P, Trentini GP: Expression of p53 and bcl-2 in clinically localized prostate cancer before and after neo-adjuvant hormonal therapy. Oncol Res; 2000;12(1):43-9
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  • [Title] Expression of p53 and bcl-2 in clinically localized prostate cancer before and after neo-adjuvant hormonal therapy.
  • The prognostic significance of p53 and bcl-2 expression in prostate carcinoma is currently under investigation.
  • The aim of the present study was to analyze their expression in diagnostic biopsies and in prostatectomies performed after neo-adjuvant hormonal therapy to investigate their role in hormone resistance.
  • One hundred and six patients with advanced prostate carcinoma were treated for 3 months with LHRH analogues before radical surgery.
  • The expression of p53 and bcl-2 was analyzed by immunohistochemistry in all cases of prostatectomy and in available biopsies obtained before treatment, and was correlated with clinicopathologic parameters and follow-up.
  • A significant increase in p53 expression was found following hormonal therapy, whereas no changes were observed in the expression of bcl-2.
  • The increase in p53 did not correlate with the presence of therapy-induced morphological changes in prostate cancers, but it did correlate significantly with histologic grade and pathologic stage, biochemical progression of the disease, and short overall survival.
  • At multivariate analysis, only grade and stage proved to be independent predictors of shorter survival.
  • The unfavorable clinical course associated with p53-positive carcinomas suggests that neo-adjuvant hormonal therapy may cause the selection of minor p53 mutated clones, rather than the induction of wild-type p53.
  • In any case, the enhanced expression of p53 could label hormone-resistant cancers for further adjuvant therapy.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Biomarkers, Tumor / metabolism. Gonadotropin-Releasing Hormone / therapeutic use. Prostatic Neoplasms / drug therapy. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Aged. Biopsy, Needle. Drug Resistance, Neoplasm. Humans. Immunoenzyme Techniques. Lymph Nodes / pathology. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Predictive Value of Tests. Prognosis. Sensitivity and Specificity

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  • (PMID = 11061345.001).
  • [ISSN] 0965-0407
  • [Journal-full-title] Oncology research
  • [ISO-abbreviation] Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 33515-09-2 / Gonadotropin-Releasing Hormone
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14. Pinthus JH, Sheffer Y, Nagler A, Fridman E, Mor Y, Genina O, Pines M: Inhibition of Wilms tumor xenograft progression by halofuginone is accompanied by activation of WT-1 gene expression. J Urol; 2005 Oct;174(4 Pt 2):1527-31
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  • Although it is curable with long-term survival, the combination of surgery, chemotherapy and often radiotherapy in some cases results in severe complications in adulthood.
  • Therefore, novel therapeutic strategies that would decrease treatment burden and improve outcome for high risk patients are required.
  • We evaluated the efficacy of halofuginone, an inhibitor of collagen type I synthesis and angiogenesis, to inhibit WT development in xenografts models.
  • RESULTS: Independent of disease stage, tumor location or administration route, halofuginone caused a decrease in angiogenesis that resulted in marked inhibition of tumor development.
  • In culture halofuginone increased the synthesis of WT1 in the human WT cell-line SK-NEP-1 and in other cancer cell lines such as hepatocellular carcinoma and prostate cancer.
  • Because of its unique mode of action, halofuginone may decrease the treatment burden when combined with chemotherapy.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Kidney Neoplasms / drug therapy. Quinazolines / pharmacology. WT1 Proteins / biosynthesis. Wilms Tumor / drug therapy

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  • (PMID = 16148645.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Piperidines; 0 / Quinazolines; 0 / Quinazolinones; 0 / WT1 Proteins; 9007-34-5 / Collagen; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 2.7.10.1 / Receptor, ErbB-2; L31MM1385E / halofuginone
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15. Rinaldo F, Li J, Wang E, Muders M, Datta K: RalA regulates vascular endothelial growth factor-C (VEGF-C) synthesis in prostate cancer cells during androgen ablation. Oncogene; 2007 Mar 15;26(12):1731-8
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  • [Title] RalA regulates vascular endothelial growth factor-C (VEGF-C) synthesis in prostate cancer cells during androgen ablation.
  • Prostate cancer mortality is primarily due to failure to cure patients with metastatic disease.
  • In its early stages, prostate cancer growth is enhanced by androgens.
  • As such, the primary therapy for advanced (locally extensive or metastatic) prostate cancer consists of androgen deprivation therapy by pharmacotherapeutic or surgical means.
  • As the detailed molecular mechanism underlying this transition to a more aggressive phenotype is poorly understood, it has been difficult to develop effective treatments for this advanced stage of the disease.
  • We have previously reported an increase in vascular endothelial growth factor-C (VEGF-C) expression in human prostate cancer cells after androgen withdrawal.
  • In our present study, we show that androgen deprivation of human prostate carcinoma cells activates the small GTPase, RalA, a molecule important for human oncogenesis.
  • We also show that elevated levels of intracellular reactive oxygen species in prostate cancer cells under androgen-ablated conditions is the major inducer of RalA activation and VEGF-C synthesis.

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  • (PMID = 16964283.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / PHS HHS / / 1 PSOCA91956-3
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / DNA Primers; 0 / Reactive Oxygen Species; 0 / Vascular Endothelial Growth Factor C; EC 3.6.1.- / RALA protein, human; EC 3.6.5.2 / ral GTP-Binding Proteins
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16. Dreicer R, Magi-Galluzzi C, Zhou M, Rothaermel J, Reuther A, Ulchaker J, Zippe C, Fergany A, Klein EA: Phase II trial of neoadjuvant docetaxel before radical prostatectomy for locally advanced prostate cancer. Urology; 2004 Jun;63(6):1138-42
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  • [Title] Phase II trial of neoadjuvant docetaxel before radical prostatectomy for locally advanced prostate cancer.
  • OBJECTIVES: To perform a Phase II trial of docetaxel administered on a weekly schedule for 6 weeks before radical prostatectomy (RP) in patients with locally advanced prostate cancer.
  • METHODS: Treatment consisted of six doses of docetaxel 40 mg/m(2) intravenously administered weekly for 6 weeks followed by RP.
  • Eligibility criteria included clinical Stage T2b, prostate-specific antigen (PSA) level 15 ng/mL or greater or Gleason sum 8 or greater, and no evidence of metastatic disease.
  • The primary endpoint was feasibility and drug-related and surgical-related toxicities.
  • Secondary endpoints included pre-RP PSA level, local response, pathologic outcomes, and time to PSA failure.
  • RESULTS: Twenty-nine patients were entered; 80% completed all 6 weeks of therapy and 97% underwent RP.
  • The median PSA level was 12 ng/mL (range 2.5 to 43.3), the median Gleason sum was 8 (range 6 to 9), and all had Stage T2b or greater disease.
  • Pathologic analysis demonstrated residual carcinoma in all cases.
  • At a median follow-up of 23 months (range 1.5 to 36), 20 patients were disease free with no additional therapy.
  • CONCLUSIONS: This trial establishes the baseline effect of short-course high-dose docetaxel alone on locally advanced prostate cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Prostatectomy. Prostatic Neoplasms / therapy. Taxoids / administration & dosage
  • [MeSH-minor] Aged. Biomarkers, Tumor / blood. Chemotherapy, Adjuvant. Dexamethasone / administration & dosage. Humans. Lymph Node Excision. Male. Middle Aged. Premedication. Prostate-Specific Antigen / blood. Treatment Outcome

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  • (PMID = 15183967.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Taxoids; 15H5577CQD / docetaxel; 7S5I7G3JQL / Dexamethasone; EC 3.4.21.77 / Prostate-Specific Antigen
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17. Scifo C, Cardile V, Russo A, Consoli R, Vancheri C, Capasso F, Vanella A, Renis M: Resveratrol and propolis as necrosis or apoptosis inducers in human prostate carcinoma cells. Oncol Res; 2004;14(9):415-26
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  • [Title] Resveratrol and propolis as necrosis or apoptosis inducers in human prostate carcinoma cells.
  • Vegetables and fruit help the prevention and the therapy of several kinds of cancer because they contain micronutrients, a class of substances that have been shown to exhibit chemopreventive and chemotherapeutic activities.
  • In the present study the effects of resveratrol (100 and 200 microM), a phytoalexin found in grapes, and of the ethanolic extract of propolis (50 and 100 microg/ml), a natural honeybee hive product, were tested in androgen-resistant prostate cancer cells (DU145), a cell line resembling the last stage of prostate carcinoma.
  • A comparison between the activity of these micronutrients and vinorelbine bitartrate (Navelbine), a semi-synthetic drug normally used in the therapy of prostate cancer, was conducted.
  • Our results point out the anticancer activity of resveratrol and propolis extract in human prostate cancer, exerting their cytotoxicity through two different types of cell death: necrosis and apoptosis, respectively.
  • The data obtained suggest the possible use of these micronutrients both in alternative to classic chemotherapy, and in combination with very low dosage of vinorelbine (5 microM).
  • [MeSH-major] Apoptosis / drug effects. Propolis / pharmacology. Prostatic Neoplasms / drug therapy. Stilbenes / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / physiology. Humans. Male. Necrosis. Reactive Oxygen Species / metabolism

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  • (PMID = 15490973.001).
  • [ISSN] 0965-0407
  • [Journal-full-title] Oncology research
  • [ISO-abbreviation] Oncol. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 0 / Stilbenes; 9009-62-5 / Propolis; Q369O8926L / resveratrol
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18. Wrasidlo W, Gaedicke G, Guy RK, Renaud J, Pitsinos E, Nicolaou KC, Reisfeld RA, Lode HN: A novel 2'-(N-methylpyridinium acetate) prodrug of paclitaxel induces superior antitumor responses in preclinical cancer models. Bioconjug Chem; 2002 Sep-Oct;13(5):1093-9
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  • [Title] A novel 2'-(N-methylpyridinium acetate) prodrug of paclitaxel induces superior antitumor responses in preclinical cancer models.
  • The development of novel strategies for the treatment of malignancies by successful intervention in advanced stage disease is a major challenge in oncology.
  • Structure/activity profiles of all compounds in tissue culture revealed cytotoxicity effective at picomolar concentrations with a panel of 16 cancer cell lines in contrast to 4 nonmalignant cell lines.
  • Specifically, the 2'-MPA-paclitaxel prodrug induced regression of primary tumors in three xenograft models of nonsmall cell lung carcinoma, ovarian carcinoma and prostate cancer, in contrast to ineffective C-7 derivatives and parental paclitaxel.
  • At the same time, a reduced systemic toxicity of 2'-MPA-paclitaxel was observed in contrast to a far more toxic parental paclitaxel.
  • Taken together, these findings demonstrate that the 2'-MPA-paclitaxel prodrug is a promising new candidate for cancer therapy.
  • [MeSH-minor] Animals. Cattle. Drug Screening Assays, Antitumor. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy. Onium Compounds. Structure-Activity Relationship. Transplantation, Heterologous. Treatment Outcome. Tubulin / drug effects. Tumor Cells, Cultured

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  • (PMID = 12236791.001).
  • [ISSN] 1043-1802
  • [Journal-full-title] Bioconjugate chemistry
  • [ISO-abbreviation] Bioconjug. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Onium Compounds; 0 / Prodrugs; 0 / Tubulin; P88XT4IS4D / Paclitaxel
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19. Clark PE, Peereboom DM, Dreicer R, Levin HS, Clark SB, Klein EA: Phase II trial of neoadjuvant estramustine and etoposide plus radical prostatectomy for locally advanced prostate cancer. Urology; 2001 Feb;57(2):281-5
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  • [Title] Phase II trial of neoadjuvant estramustine and etoposide plus radical prostatectomy for locally advanced prostate cancer.
  • METHODS: Treatment consisted of three cycles of estramustine (10 mg/kg/day) and etoposide (50 mg/m(2)/day) orally on days 1 through 21, repeated every 28 days, followed by radical prostatectomy.
  • The eligibility criteria included locally advanced prostate cancer (clinical Stage T2b/c or T3, prostate-specific antigen [PSA] level of 15 ng/mL or greater, or Gleason score of 8 or higher) without evidence of metastatic disease.
  • The median PSA level was 14 ng/mL (range 5.3 to 50), the median Gleason score was 7 (range 6 to 9), and 44% had Stage T2b/c or T3 disease.
  • The primary endpoint was feasibility of neoadjuvant therapy and radical prostatectomy, including drug and surgery-related toxicities.
  • Secondary endpoints included the pre-prostatectomy PSA level, local response, pathologic outcomes, and time to PSA failure.
  • RESULTS: Eighteen patients were entered and completed all three cycles of therapy, and 16 (89%) underwent radical prostatectomy.
  • A local response occurred in 15 (94%) of 16 patients with palpable tumors, and the serum PSA reached undetectable levels after therapy and before radical prostatectomy in 9 patients (50%).
  • The median operative time was 125 minutes, the mean blood loss was 665 mL, and the mean length of stay was 2.5 nights.
  • The pathologic analysis demonstrated residual carcinoma with squamous metaplasia and androgen deprivation effect in all patients.
  • All patients achieved an undetectable PSA level postoperatively and at a median follow-up of 14 months (range 5 to 20) and without additional therapy, all 14 patients with negative lymph nodes were disease free.
  • CONCLUSIONS: This trial confirms the feasibility of radical prostatectomy with acceptable surgical morbidity after neoadjuvant therapy with estramustine and etoposide in patients with locally advanced prostate cancer.
  • Additional study of this paradigm with other drug regimens is warranted.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Antineoplastic Agents, Phytogenic / therapeutic use. Estramustine / therapeutic use. Etoposide / therapeutic use. Prostatectomy / methods. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / surgery
  • [MeSH-minor] Follow-Up Studies. Humans. Male. Middle Aged. Neoadjuvant Therapy. Prostate-Specific Antigen / blood. Treatment Outcome

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  • (PMID = 11182337.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Antineoplastic Agents, Phytogenic; 35LT29625A / Estramustine; 6PLQ3CP4P3 / Etoposide; EC 3.4.21.77 / Prostate-Specific Antigen
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20. Cellini N, Pompei L, Fortuna G, Ammaturo MV, De Paula U, Luzi S, Mattiucci GC, Morganti AG, Digesù C, Rosetto ME, Palloni T, Petrongari MG, Gentile P, Deodato F, Valentini V: High-dose radiotherapy plus prolonged hormone therapy in CT2-3 prostatic carcinoma: is it useful? Tumori; 2004 Mar-Apr;90(2):201-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-dose radiotherapy plus prolonged hormone therapy in CT2-3 prostatic carcinoma: is it useful?
  • AIMS AND BACKGROUND: Clinical studies published in the last decade have shown the possible improvement in prognosis of patients with prostatic carcinoma undergoing radiation therapy with dose escalation or in combination with hormone therapy.
  • However, in studies on hormone therapy, moderate doses of radiation therapy have been used, whereas in studies with high-dose radiotherapy, hormone therapy usually was not administered.
  • Therefore, it is not clear whether the concomitant use of high doses and prolonged hormone therapy could determine an additional beneficial effect.
  • The aim of the present study was therefore to evaluate the relative prognostic role of different dose levels (< 70 versus > or = 70 Gy) of external beam radiotherapy and of different hormone therapies (neoadjuvant only versus neoadjuvant + adjuvant).
  • METHODS: A total of 426 patients (median age, 71 yrs; range, 51-87 yrs) underwent external beam radiotherapy (70 Gy median dose to prostate volume +/- 45 Gy to pelvic lymph nodes) and neoadjuvant hormone therapy (bicalutamide for 30 days; goserelin, 3.6 mg every 28 days starting two months before radiotherapy and for its entire duration).
  • Dose to the prostate was < 70 Gy in 44.8% of patients and > or = 70 Gy in 55.2%.
  • A total of 244 patients received adjuvant hormonal therapy.
  • The distribution according to the clinical stage was 48.1% T2 and 51.9% T3.
  • The distribution according to pretreatment prostate-specific antigen levels (in ng/mL) was 7.0% for 0-4, 29.3% for 4-10, 30.3% for 10-20, and 33.3% for > 20.
  • At the time of this writing, no patient has died from prostatic carcinoma.
  • At univariate analysis, the radiation dose delivered to the tumor and the administration of adjuvant hormone therapy were shown to be significantly correlated with biochemical disease-free survival.
  • In the subset of patients not treated with adjuvant hormone therapy, there was a significant correlation between radiation dose and biochemical disease-free survival at univariate and multivariate analysis.
  • A similar correlation between adjuvant hormone therapy and biochemical disease-free survival was observed in the subset of stage cT3 patients at univariate and multivariate analysis.
  • In patients undergoing combined treatment without adjuvant hormone therapy, a significant correlation was observed between clinical stage and biochemical disease-free survival, at univariate and at multivariate analysis.
  • CONCLUSIONS: The results of the study confirmed the positive impact of radiotherapy doses > 70 Gy and of adjuvant hormone therapy in patients with locally advanced prostatic carcinoma.
  • Owing to the lack of evidence of a correlation between radiation dose and biochemical outcome in patients undergoing prolonged hormone therapy, the role of further dose escalation in patients undergoing combined hormone and radiation therapy is still unclear.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Actuarial Analysis. Aged. Aged, 80 and over. Analysis of Variance. Anilides / administration & dosage. Chemotherapy, Adjuvant. Disease Progression. Disease-Free Survival. Drug Administration Schedule. Goserelin / administration & dosage. Humans. Male. Middle Aged. Neoadjuvant Therapy. Neoplasm Staging. Nitriles. Patient Selection. Prognosis. Prospective Studies. Prostate-Specific Antigen / blood. Radiotherapy Dosage. Radiotherapy, Adjuvant / adverse effects. Survival Analysis. Tosyl Compounds. Treatment Outcome

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  • (PMID = 15237583.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents, Hormonal; 0 / Nitriles; 0 / Tosyl Compounds; 0F65R8P09N / Goserelin; A0Z3NAU9DP / bicalutamide; EC 3.4.21.77 / Prostate-Specific Antigen
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21. Vargas C, Martínez A, Galalae R, Demanes J, Harsolia A, Schour L, Nuernberg N, Gonzalez J: High-dose radiation employing external beam radiotherapy and high-dose rate brachytherapy with and without neoadjuvant androgen deprivation for prostate cancer patients with intermediate- and high-risk features. Prostate Cancer Prostatic Dis; 2006;9(3):245-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-dose radiation employing external beam radiotherapy and high-dose rate brachytherapy with and without neoadjuvant androgen deprivation for prostate cancer patients with intermediate- and high-risk features.
  • The role of neoadjuvant androgen deprivation (NAD) in high-risk prostate cancer patients receiving high-dose radiotherapy (RT) remains unstudied.
  • Of 1260 prostate cancer patients with high-risk features (pretreatment prostate-specific antigen (PSA) > or =10, Gleason Score (GS) > or =7, or T stage > or =T2b), 560 received no NAD (n=308) or NAD for < or =6 months (n=252).
  • Median dose to the prostate from RT and HDR was 42 and 23 Gy, respectively.
  • Average total biologic equivalent prostate dose was >100 Gy (alpha/beta=1.2).
  • Pretreatment characteristics were similar on chi(2) tables for all 560 patients treated with or without NAD including pretreatment PSA (P=0.11), GS (P=0.4), and clinical T stage (P=0.2).
  • AD given before definitive high-dose RT did not benefit prostate cancer patients with intermediate- and high-risk features.
  • We favor the use of concurrent/adjuvant AD over prolonged NAD for prostate cancer patients for whom AD is clinically indicated.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Brachytherapy / methods. Carcinoma / drug therapy. Carcinoma / radiotherapy. Neoadjuvant Therapy / methods. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Aged. Antineoplastic Agents, Hormonal / therapeutic use. Chemotherapy, Adjuvant. Disease-Free Survival. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Metastasis / drug therapy. Neoplasm Staging. Prostate-Specific Antigen / blood. Radiation Dosage. Radiotherapy Dosage. Retrospective Studies. Risk Assessment. Survival Analysis






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