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1. Bono AV, Mazzucchelli R, Ferrari I, Lopez-Beltran A, Galosi AB, Cheng L, Montironi R: Bicalutamide 50 mg monotherapy in patients with isolated high-grade PIN: findings in repeat biopsies at 6 months. J Clin Pathol; 2007 Apr;60(4):443-6
Hazardous Substances Data Bank. BICALUTAMIDE .

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  • [Title] Bicalutamide 50 mg monotherapy in patients with isolated high-grade PIN: findings in repeat biopsies at 6 months.
  • OBJECTIVES: To evaluate morphological findings in repeat biopsies in patients with isolated high-grade prostatic intraepithelial neoplasia (HGPIN) after a 6-month course of bicalutamide (Casodex) 50 mg/day.
  • METHODS: 20 consecutive patients with isolated HGPIN in prostate biopsies were treated for 6 months with bicalutamide 50 mg/day.
  • After treatment, the patients were resubmitted to prostate biopsy mapping.
  • The control group included 22 untreated consecutive patients with isolated high-grade PIN with repeat biopsies taken 6 months after the initial biopsies.
  • In the repeat biopsies HGPIN was present in 2 patients, monofocal in both, whereas prostate adenocarcinoma (PCa) was discovered in one.
  • Treatment did not affect the incidence of cancer (treated vs control: 5% vs 4.5%).
  • [MeSH-major] Anilides / therapeutic use. Antineoplastic Agents / therapeutic use. Nitriles / therapeutic use. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Neoplasms / drug therapy. Tosyl Compounds / therapeutic use
  • [MeSH-minor] Aged. Biopsy. Follow-Up Studies. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 16822873.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anilides; 0 / Antineoplastic Agents; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide
  • [Other-IDs] NLM/ PMC2001123
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2. Luchman HA, Benediktsson H, Villemaire ML, Peterson AC, Jirik FR: The pace of prostatic intraepithelial neoplasia development is determined by the timing of Pten tumor suppressor gene excision. PLoS One; 2008;3(12):e3940
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  • [Title] The pace of prostatic intraepithelial neoplasia development is determined by the timing of Pten tumor suppressor gene excision.
  • Loss of the PTEN tumor suppressor is a common occurrence in human prostate cancer, particularly in advanced disease.
  • In keeping with its role as a pivotal upstream regulator of the phosphatidylinositol 3-kinase signaling pathway, experimentally-induced deletion of Pten in the murine prostate invariably results in neoplasia.
  • However, and unlike humans where prostate tumorigenesis likely evolves over decades, disease progression in the constitutively Pten deficient mouse prostate is relatively rapid, culminating in invasive cancer within several weeks post-puberty.
  • Given that the prostate undergoes rapid androgen-dependent growth at puberty, and that Pten excisions during this time might be especially tumorigenic, we hypothesized that delaying prostate-specific Pten deletions until immediately after puberty might alter the pace of tumorigenesis.
  • To this end we generated mice with a tamoxifen-inducible Cre recombinase transgene enabling temporal control over prostate-specific gene alterations.
  • Despite evidence of increased Akt/mTOR/S6K axis activity at early time points in Pten-deficient epithelial cells, excisions induced in the post-pubertal (6 wk-old) prostate yielded gradual acquisition of a range of lesions.
  • These progressed from pre-malignant changes (nuclear atypia, focal hyperplasia) and low grade prostatic intraepithelial neoplasia (PIN) at 16-20 wks post-tamoxifen exposure, to overtly malignant lesions by approximately 1 yr of age, characterized by high-grade PIN and microinvasive carcinoma.
  • In contrast, when Pten excisions were triggered in the pre-pubertal (2 week-old) prostate, neoplasia evolved over a more abbreviated time-frame, with a spectrum of premalignant lesions, as well as overt PIN and microinvasive carcinoma by 10-12 wks post-tamoxifen exposure.
  • These results indicate that the developmental stage at which Pten deletions are induced dictates the pace of PIN development.
  • [MeSH-major] Gene Deletion. Genes, Tumor Suppressor. PTEN Phosphohydrolase / genetics. Prostatic Intraepithelial Neoplasia / enzymology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Androgen-Binding Protein / genetics. Animals. Apoptosis. Arrestins / metabolism. Cell Proliferation. Crosses, Genetic. Disease Progression. Epithelium / enzymology. Epithelium / pathology. Female. Humans. Integrases / metabolism. Male. Mice. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / metabolism. Precancerous Conditions / drug therapy. Precancerous Conditions / enzymology. Precancerous Conditions / genetics. Precancerous Conditions / pathology. Rats. Ribosomal Protein S6 / metabolism. Tamoxifen / analogs & derivatives. Tamoxifen / therapeutic use. Time Factors. Up-Regulation

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  • (PMID = 19081794.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen-Binding Protein; 0 / Arrestins; 0 / Ribosomal Protein S6; 0 / beta-arrestin; 094ZI81Y45 / Tamoxifen; 17197F0KYM / afimoxifene; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2597775
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3. Ding Q, Huo L, Yang JY, Xia W, Wei Y, Liao Y, Chang CJ, Yang Y, Lai CC, Lee DF, Yen CJ, Chen YJ, Hsu JM, Kuo HP, Lin CY, Tsai FJ, Li LY, Tsai CH, Hung MC: Down-regulation of myeloid cell leukemia-1 through inhibiting Erk/Pin 1 pathway by sorafenib facilitates chemosensitization in breast cancer. Cancer Res; 2008 Aug 1;68(15):6109-17
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  • [Title] Down-regulation of myeloid cell leukemia-1 through inhibiting Erk/Pin 1 pathway by sorafenib facilitates chemosensitization in breast cancer.
  • Here, we showed that Pin 1 stabilizes Mcl-1, which is required for Mcl-1 posphorylation by Erk.
  • Based on this newly identified mechanism of Mcl-1 stabilization, two strategies were used to overcome Mcl-1-mediated chemoresistance: inhibiting Erk by Sorafenib, an approved clinical anticancer drug, or knocking down Pin1 by using a SiRNA technique.
  • In conclusion, the current report not only unravels a novel mechanism to link Erk/Pin1 pathway and Mcl-1-mediated chemoresistance but also provides a plausible combination therapy, Taxol (Paclitaxel) plus Sorafenib, which was shown to be effective in killing breast cancer cells.

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  • (PMID = 18676833.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109311; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA83639; United States / NCI NIH HHS / CA / CA116199; United States / NCI NIH HHS / CA / CA099031; United States / NCI NIH HHS / CA / P50 CA083639-050003; United States / NCI NIH HHS / CA / CA099031-05; United States / NCI NIH HHS / CA / P01 CA099031-05; United States / NCI NIH HHS / CA / P50 CA116199; United States / NCI NIH HHS / CA / P20 CA101936; United States / NCI NIH HHS / CA / CA109311-05; United States / NCI NIH HHS / CA / CA 16672; United States / NCI NIH HHS / CA / CA109311; United States / NCI NIH HHS / CA / P50 CA083639; United States / NCI NIH HHS / CA / CA083639-050003; United States / NCI NIH HHS / CA / P01 CA099031; United States / NCI NIH HHS / CA / P20 CA101936-010001; United States / NCI NIH HHS / CA / R01 CA109311-05; United States / NCI NIH HHS / CA / CA101936; United States / NCI NIH HHS / CA / CA101936-010001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / NIMA-interacting peptidylprolyl isomerase; 0 / Phenylurea Compounds; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 5.2.1.8 / Peptidylprolyl Isomerase
  • [Other-IDs] NLM/ NIHMS76170; NLM/ PMC2676572
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4. Shinohara N, Harabayashi T, Suzuki S, Nagao K, Seki H, Murakumo M, Mitsuhashi K, Demura T, Nagamori S, Matsuyama H, Naito K, Nonomura K: Salvage chemotherapy with paclitaxel, ifosfamide, and nedaplatin in patients with urothelial cancer who had received prior cisplatin-based therapy. Cancer Chemother Pharmacol; 2006 Sep;58(3):402-7
Hazardous Substances Data Bank. IFOSFAMIDE .

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  • [Title] Salvage chemotherapy with paclitaxel, ifosfamide, and nedaplatin in patients with urothelial cancer who had received prior cisplatin-based therapy.
  • BACKGROUND AND AIMS: The aim of the present phase II study was to evaluate the efficacy of combination chemotherapy of paclitaxel, ifosfamide, and nedaplatin (PIN regimen) in patients with recurrent urothelial cancer who had been treated with cisplatin-based chemotherapy.
  • PATIENTS/METHODS: Eligible patients were those with histologically confirmed urothelial cancer who had progressed or relapsed after cisplatin-based chemotherapy.
  • The PIN regimen consisted of paclitaxel 175 mg/m(2) on day 1; ifosfamide 4.5 g/m2 divided over days 1, 2, and 3; and nedaplatin 70 mg/m(2) on day 1; PIN was given every 28 days.
  • The median time to progression was 8 months (range, 0-50+ months) and the median survival was 22 months (range, 4-52+ months).
  • All patients experienced Grade 3 or 4 neutropenia, while Grade 3 or 4 thrombocytopenia was seen in 8 patients; Grade 3 or 4 anemia was seen in 6 patients; Grade 3 neuropathy was observed in 1 patient, for whom the PIN therapy was discontinued.
  • There were no treatment-related deaths.
  • CONCLUSION: The PIN combination was highly active and tolerable in previously treated patients with urothelial cancer as a second-line treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasm Recurrence, Local / drug therapy. Salvage Therapy. Urologic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Cisplatin / administration & dosage. Cisplatin / adverse effects. Cisplatin / therapeutic use. Disease-Free Survival. Drug Administration Schedule. Female. Humans. Ifosfamide / administration & dosage. Ifosfamide / adverse effects. Ifosfamide / therapeutic use. Male. Middle Aged. Organoplatinum Compounds / administration & dosage. Organoplatinum Compounds / adverse effects. Organoplatinum Compounds / therapeutic use. Paclitaxel / administration & dosage. Paclitaxel / adverse effects. Paclitaxel / therapeutic use. Treatment Outcome

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  • (PMID = 16416335.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; 8UQ3W6JXAN / nedaplatin; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin; UM20QQM95Y / Ifosfamide
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5. Goeman L, Joniau S, Ponette D, Van der Aa F, Roskams T, Oyen R, Van Poppel H: Is low-grade prostatic intraepithelial neoplasia a risk factor for cancer? Prostate Cancer Prostatic Dis; 2003;6(4):305-10
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  • [Title] Is low-grade prostatic intraepithelial neoplasia a risk factor for cancer?
  • INTRODUCTION: High-grade prostatic intraepithelial neoplasia (HGPIN) is generally accepted to be a precursor lesion of prostate cancer.
  • The likely outcome of isolated low-grade PIN (LGPIN) lesions in prostate biopsies remains unclear.
  • MATERIALS AND METHODS: In a 2-y period, 207 men were diagnosed with isolated PIN on standard systematic sextant biopsy of the prostate.
  • No patients had ever received androgen deprivation therapy, chemotherapy or radiation therapy.
  • CONCLUSIONS: These data are intriguing since the risk of finding prostate carcinoma on repeat sextant biopsy in the LGPIN group is 30%.
  • [MeSH-major] Prostatic Intraepithelial Neoplasia / blood. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biopsy, Needle. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Prostate-Specific Antigen / blood. Risk Factors. Selenium / pharmacology. Vitamin E / pharmacology

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  • (PMID = 14663472.001).
  • [ISSN] 1365-7852
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 1406-18-4 / Vitamin E; EC 3.4.21.77 / Prostate-Specific Antigen; H6241UJ22B / Selenium
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6. Golubović Z, Stojiljković P, Macukanović-Golubović L, Milić D, Milenković S, Kadija M, Matović Z, Turković G, Radenković M, Visnjić A, Golubović I, Stojanović S, Vidić G, Mitković M: [External fixation in the treatment of open tibial shaft fractures]. Vojnosanit Pregl; 2008 May;65(5):343-8
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  • [Title] [External fixation in the treatment of open tibial shaft fractures].
  • In 95 of the patients the treatment of open tibia shaft fractures consisted of the surgical treatment of wound and the external fixation of the fractured bone using "Mitkovic" type external fixator with a convergent method of pin applications.
  • One primary amputations had been done in patients with grade IIIC open tibial fracture with large soft tissue defect.
  • There were nine (9.38%) soft tissue pin track infections and six (6.25%) superficial wound infections.
  • The mean time of union was 21 (14-36) week.
  • In one patients (1.04%) deep pin track infection developed.
  • Two patients (2.08%) had below the knee amputation (one primary in patient with type III C open fracture and one secondary after the development of deep infections).
  • CONCLUSION: Surgical treatment of wounds, external fixation, leaving the wounds open and performing necessary debridements, adequate drug therapy administration are essential for obtaining good results in patients with open tibial shaft fractures.

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  • (PMID = 18630126.001).
  • [ISSN] 0042-8450
  • [Journal-full-title] Vojnosanitetski pregled
  • [ISO-abbreviation] Vojnosanit Pregl
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia
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7. Raina K, Blouin MJ, Singh RP, Majeed N, Deep G, Varghese L, Glodé LM, Greenberg NM, Hwang D, Cohen P, Pollak MN, Agarwal R: Dietary feeding of silibinin inhibits prostate tumor growth and progression in transgenic adenocarcinoma of the mouse prostate model. Cancer Res; 2007 Nov 15;67(22):11083-91
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  • [Title] Dietary feeding of silibinin inhibits prostate tumor growth and progression in transgenic adenocarcinoma of the mouse prostate model.
  • Herein, for the first time, we evaluated the chemopreventive efficacy of dietary silibinin against prostate cancer (PCa) growth and progression in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice from two different genetic backgrounds [C57BL/6 (TRAMP) x FVB; C57BL/6 (TRAMP) x C57BL/6].
  • Silibinin-fed groups had a lower tumor grade and higher incidence of prostatic intraepithelial neoplasia (PIN) at the expense of a strong decrease in adenocarcinoma incidence.
  • Prostate tissue showed a 47% (P < 0.001) decrease in proliferating cell nuclear antigen (PCNA)-positive cells and an approximately 7-fold (P < 0.001) increase in apoptotic cells at the highest silibinin dose.
  • As potential mechanisms of silibinin efficacy, an approximately 50% (P < 0.05) decrease in insulin-like growth factor (IGF) receptor type I beta and an approximately 13-fold (P < 0.001) increase in IGF-binding protein 3 (IGFBP-3) protein levels were also observed.
  • Together, these findings suggest that oral silibinin blocks PCa growth and progression at PIN stage in TRAMP mice via modulation of tumor IGF-IGFBP-3 axis and cell cycle regulation, and therefore it has practical and translational potential in suppressing growth and neoplastic conversion of PIN to PCa in humans.
  • [MeSH-major] Adenocarcinoma / prevention & control. Adenocarcinoma / therapy. Prostatic Neoplasms / prevention & control. Prostatic Neoplasms / therapy
  • [MeSH-minor] Animals. Anticarcinogenic Agents / therapeutic use. Antioxidants / therapeutic use. Disease Models, Animal. Disease Progression. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Phosphorylation. Prostate / drug effects. Silymarin / therapeutic use. Species Specificity

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  • (PMID = 18006855.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100938; United States / NCI NIH HHS / CA / R01 CA102514; United States / NCI NIH HHS / CA / R01 CA104286; United States / NCI NIH HHS / CA / R01 CA84296
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Silymarin; 4RKY41TBTF / silybin
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8. Bettuzzi S, Brausi M, Rizzi F, Castagnetti G, Peracchia G, Corti A: Chemoprevention of human prostate cancer by oral administration of green tea catechins in volunteers with high-grade prostate intraepithelial neoplasia: a preliminary report from a one-year proof-of-principle study. Cancer Res; 2006 Jan 15;66(2):1234-40
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  • [Title] Chemoprevention of human prostate cancer by oral administration of green tea catechins in volunteers with high-grade prostate intraepithelial neoplasia: a preliminary report from a one-year proof-of-principle study.
  • Recent studies showed that 30% of men with high-grade prostate intraepithelial neoplasia (HG-PIN) would develop prostate cancer (CaP) within 1 year after repeated biopsy.
  • This prompted us to do a proof-of-principle clinical trial to assess the safety and efficacy of GTCs for the chemoprevention of CaP in HG-PIN volunteers.
  • Sixty volunteers with HG-PIN, who were made aware of the study details, agreed to sign an informed consent form and were enrolled in this double-blind, placebo-controlled study.
  • Daily treatment consisted of three GTCs capsules, 200 mg each (total 600 mg/d).
  • Total prostate-specific antigen did not change significantly between the two arms, but GTCs-treated men showed values constantly lower with respect to placebo-treated ones.
  • International Prostate Symptom Score and quality of life scores of GTCs-treated men with coexistent benign prostate hyperplasia improved, reaching statistical significance in the case of International Prostate Symptom Scores.
  • As a secondary observation, administration of GTCs also reduced lower urinary tract symptoms, suggesting that these compounds might also be of help for treating the symptoms of benign prostate hyperplasia.
  • [MeSH-major] Catechin / therapeutic use. Prostatic Hyperplasia / drug therapy. Prostatic Neoplasms / prevention & control. Tea
  • [MeSH-minor] Administration, Oral. Aged. Chemoprevention. Double-Blind Method. Humans. Male. Middle Aged. Placebos. Prostate-Specific Antigen / blood. Quality of Life


9. Montironi R, Mazzucchelli R: HER-2 expression and gene amplification in high-grade PIN and prostate cancer. Arch Ital Urol Androl; 2006 Dec;78(4):135-9
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  • [Title] HER-2 expression and gene amplification in high-grade PIN and prostate cancer.
  • The aim of the current study was to analyze HER-2 expression and gene amplification in prostate cancer and HGPIN incidentally detected in cystoprostatectomies.
  • Eighty prostate cases were used.
  • Group 1 (incidental): nineteen cystoprostatectomy specimens with prostate cancer and HGPIN and no residual urothelial carcinoma in the prostate.
  • Group 2 (untreated): twenty-five radical prostatectomy specimens with prostate cancer Group 3 (hormonally treated): nineteen radical prostatectomy specimens with prostate cancer.
  • All the patients were under total androgen ablation therapy for three months before surgery.
  • Group 4 (hormone-independent): nine TURP specimens with locally recurrent androgen independent prostate cancer Group 5 (normal reference): eight cystoprostatectomy specimens without HGPIN and without prostate cancer, and no residual urothelial carcinoma.
  • None of the patients belonging to Groups 1, 2, and 5 had received chemotherapy, hormone therapy, or radiation therapy before surgery.
  • Weak to moderate HER-2 membrane immunoreactivity was observed in most of the basal cells but not in the secretory cells of normal prostatic ducts and acini both in the cystoprostatectomies and in the radicals of the untreated patients.
  • High-grade PIN.
  • Prostate cancer HER-2 overexpression was seen in 16% of cases in the CyP group, 36% in the untreated group and 47.5% in the treated group.

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  • (PMID = 17269616.001).
  • [ISSN] 1124-3562
  • [Journal-full-title] Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica
  • [ISO-abbreviation] Arch Ital Urol Androl
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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10. Mazzucchelli R, Montironi R, Santinelli A, Lucarini G, Pugnaloni A, Biagini G: Vascular endothelial growth factor expression and capillary architecture in high-grade PIN and prostate cancer in untreated and androgen-ablated patients. Prostate; 2000 Sep 15;45(1):72-9
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  • [Title] Vascular endothelial growth factor expression and capillary architecture in high-grade PIN and prostate cancer in untreated and androgen-ablated patients.
  • BACKGROUND: Recent studies have demonstrated that angiogenesis is a potent prognostic indicator for patients with prostate cancer (PCa) and have pointed out that the evaluation of vascular endothelial growth factor (VEGF) is useful in assessing the angiogenic phenotype in PCa.
  • The aim of the study was to investigate immunohistochemically the expression of VEGF and its correlation with the pattern of capillary architecture in prostate cancer and high-grade prostatic intraepithelial neoplasia (PIN), in untreated and androgen-ablated patients.
  • METHODS: Forty-five patients who underwent radical prostatectomy (RP) for localized prostate carcinoma were recruited for this study.
  • The study population included two groups: 35 patients who did not receive chemo-, hormone, or radiation therapy before surgery, and 10 patients who were under complete androgen blockade (CAB) for 3 months at time of surgery.
  • VEGF was examined by immunohistochemistry, and its tissue expression was compared with the pattern of capillary architecture evaluated by immunostaining the endothelial antigen CD34.
  • RESULTS: In normal tissue, the intensity of the VEGF immunoreactivity in the cytoplasm of secretory cells ranged from negative to low.
  • All prostate cancer specimens stained positively, the intensity of the immunoreaction ranging from low to strong and being correlated with the Gleason score.
  • Two discrete immunostaining patterns were observed in high-grade PIN.
  • VEGF expression of low-to-moderate intensity was defined as pattern A.
  • The capillary architecture in high-grade PIN with pattern A was similar to the orderly vascular network seen in normal prostates, whereas in the pattern B it had the characteristics of microvessels usually seen in PCa.
  • CONCLUSIONS: Our immunohistochemical results indicate that significant levels of VEGF are present in prostate cancer and in a population of PIN lesions, expression being highest in association with NE cells.
  • [MeSH-major] Adenocarcinoma / blood supply. Androgen Antagonists / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Endothelial Growth Factors / biosynthesis. Lymphokines / biosynthesis. Neovascularization, Pathologic / physiopathology. Prostatic Intraepithelial Neoplasia / blood supply. Prostatic Neoplasms / blood supply
  • [MeSH-minor] Aged. Anilides / administration & dosage. Capillaries / anatomy & histology. Capillaries / drug effects. Capillaries / physiopathology. Goserelin / administration & dosage. Humans. Immunohistochemistry. Male. Middle Aged. Nitriles. Prostatectomy. Tosyl Compounds. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10960845.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Nitriles; 0 / Tosyl Compounds; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 0F65R8P09N / Goserelin; A0Z3NAU9DP / bicalutamide
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11. Gordon JE, Kelly-Hahn J, Carpenter CJ, Schoenecker PL: Pin site care during external fixation in children: results of a nihilistic approach. J Pediatr Orthop; 2000 Mar-Apr;20(2):163-5
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  • [Title] Pin site care during external fixation in children: results of a nihilistic approach.
  • A simple pin care system with no physical pin cleansing except that provided by daily showers was used.
  • Children with inflamed or infected pin sites were placed on an oral antibiotic (cephalexin) for 10 days.
  • Pin sites were graded according to the system of Dahl et al. on a 0 to 5 scale.
  • Patients developed 178 pin tract infections (4.0% per observation), with 151 (85%) grade 1 and 27 (15%) grade 2 infections.
  • No pin was removed because of infection.
  • Diaphyseal half pin sites were less commonly infected (1.6%) than periarticular wire or half pin sites (4.5%).
  • We recommend only showering without other physical pin cleaning procedures in children undergoing external fixation procedures.
  • [MeSH-major] Antibiotic Prophylaxis / methods. Cephalexin / administration & dosage. External Fixators / microbiology. Ilizarov Technique / instrumentation. Leg Length Inequality / surgery. Surgical Wound Infection / drug therapy

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  • (PMID = 10739275.001).
  • [ISSN] 0271-6798
  • [Journal-full-title] Journal of pediatric orthopedics
  • [ISO-abbreviation] J Pediatr Orthop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] OBN7UDS42Y / Cephalexin
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12. Steiner MS, Pound CR: Phase IIA clinical trial to test the efficacy and safety of Toremifene in men with high-grade prostatic intraepithelial neoplasia. Clin Prostate Cancer; 2003 Jun;2(1):24-31
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  • [Title] Phase IIA clinical trial to test the efficacy and safety of Toremifene in men with high-grade prostatic intraepithelial neoplasia.
  • Men with high-grade prostatic intraepithelial neoplasia (PIN) evident on prostate biopsy are at high risk for the eventual development of prostate cancer.
  • The ability to reverse high-grade PIN may reduce the incidence or delay the development of prostate cancer.
  • Toremifene (GTx-006, Acapodene trade mark ) is a selective estrogen receptor modulator that has been shown in the transgenic mouse model of prostate cancer to eliminate high-grade PIN and reduce the incidence of prostate cancer.
  • This study was aimed at the evaluation of the safety and efficacy of toremifene in men diagnosed with high-grade PIN.
  • This was an open-label, phase IIA clinical trial that enrolled 21 men (mean age, 64.7 years) with evidence of high-grade PIN on biopsy within 6 months of entry into the study.
  • Eighteen of these men (86%) completed toremifene treatment (60 mg/day orally for 4 months) and then underwent follow-up prostate biopsy (8 cores) to determine high-grade PIN status.
  • The effect of the drug on serum prostate-specific antigen (PSA), percentage of free PSA, testosterone, estradiol, and quality of life was also measured.
  • After toremifene treatment, 72% of these 18 men (vs. 17.9% of historical controls) had no high-grade PIN on subsequent prostate biopsies.
  • Quality of life was not significantly affected by treatment.
  • Toremifene appeared to reduce high-grade PIN in this small, exploratory trial.
  • The drug was well tolerated.
  • A double-blind, dose-finding, randomized, placebo-controlled phase IIB/III study is currently open to further study toremifene's activity against high-grade PIN and prostate cancer incidence.
  • [MeSH-major] Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Toremifene / administration & dosage
  • [MeSH-minor] Administration, Oral. Aged. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Hormonal / adverse effects. Biopsy, Needle. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Humans. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Staging. Prognosis. Quality of Life. Risk Assessment. Survival Analysis. Treatment Outcome

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  • [CommentIn] Clin Prostate Cancer. 2003 Jun;2(1):32-3 [15046681.001]
  • (PMID = 15046680.001).
  • [ISSN] 1540-0352
  • [Journal-full-title] Clinical prostate cancer
  • [ISO-abbreviation] Clin Prostate Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 7NFE54O27T / Toremifene
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13. Lim IK: TIS21 (/BTG2/PC3) as a link between ageing and cancer: cell cycle regulator and endogenous cell death molecule. J Cancer Res Clin Oncol; 2006 Jul;132(7):417-26
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  • On the other hand, it has lately been found that the expression of TIS21 is constitutive and high in thymus, lung alveolar epithelium, proximal tubule of kidney and basal cell layer of prostate acini.
  • (1) TIS21 inhibits early phase of carcinogenesis in its high expressers such as kidney, prostate, breast and thymus: Loss of constitutive and high expression of TIS21 was observed in the precancerous lesions as well as tumor tissues.
  • As an endogenous cell death molecule, TIS21 may be involved in translocation of Pin-1 to cytoplasm.
  • Pin-1 subsequently interacts with Serine(147) residue in TIS21 protein, resulting in mitochondrial depolarization. (2) TIS21 regulates transition of cell cycle at G1/S and G2/M phases in cancer cells with inactive pRB and/or p53, as well as in normal cells by regulating pRB/p16(INK4a) pathway.
  • Based on the previous report that the expression of TIS21 is involved in the induction of senescence after chemotherapy of cancer cells, which can be a mechanism to resist carcinogenesis, TIS21(/BTG2/PC3), the endogenous cell death molecule and pan-cell cycle regulator, might be a link between cellular senescence and carcinogenesis.

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  • (PMID = 16456675.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Immediate-Early Proteins; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 141490-22-4 / BTG2 protein, human
  • [Number-of-references] 65
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14. Segev Y, Nativ O: [Nutrition and pharmacological treatment for prevention of prostate cancer]. Harefuah; 2006 Jan;145(1):47-51, 76-7
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  • [Title] [Nutrition and pharmacological treatment for prevention of prostate cancer].
  • Prostate cancer is the most common neoplasm and the second cause of cancer death.
  • Well-established risk factors for prostate cancer include African-American race, older age and family history.
  • Since high grade prostatic intraepithelial neoplasia (PIN) is an early predictor of prostate cancer, preventive strategies focusing on men with high grade PIN are being explored.
  • It was demonstrated that finasteride could significantly reduce prostate cancer in asymptomatic men with normal PSA and no abnormalities on rectal examination.
  • Elevated prostaglandin levels, and upregulation of cyclooxygenase-2 (COX-2) are found in prostate cancer cell lines.
  • There is some epidemiologic evidence that regular use of NSAIDs, which inhibit COX-2, may be associated with a lower risk of prostate cancer.
  • In the field of nutrition, data from prospective large-scale studies demonstrated that increased consumption of lycopene-rich tomato-based foods referred to a reduction in the risk for prostate cancer.
  • Vitamin E was also found to reduce prostate cancer risk.
  • Prospective data showed that vitamin D has an inhibitory effect on prostate cancer development while increased calcium consumption, independent from dietary intake, might increase the risk.
  • Dietary fat intake, particularly from animal sources, may also increase the risk for prostate cancer.
  • Further study will hopefully help to establish a core set of nutritional and dietary factors that can positively or negatively affect prostate cancer development, as well as a set of pharmacologic agents that can reduce the risk of prostate cancer development and/or progression in selected patients.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Nutritional Physiological Phenomena. Prostatic Neoplasms / prevention & control

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  • (PMID = 16450727.001).
  • [ISSN] 0017-7768
  • [Journal-full-title] Harefuah
  • [ISO-abbreviation] Harefuah
  • [Language] heb
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Israel
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents
  • [Number-of-references] 40
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15. Rhoden EL, Morgentaler A: Testosterone replacement therapy in hypogonadal men at high risk for prostate cancer: results of 1 year of treatment in men with prostatic intraepithelial neoplasia. J Urol; 2003 Dec;170(6 Pt 1):2348-51
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  • [Title] Testosterone replacement therapy in hypogonadal men at high risk for prostate cancer: results of 1 year of treatment in men with prostatic intraepithelial neoplasia.
  • PURPOSE: One of the greatest concerns among clinicians regarding testosterone replacement therapy (TRT) is the fear of causing or promoting prostate cancer.
  • We evaluated prostatic changes in hypogonadal men with and without high grade prostatic intraepithelial neoplasia (PIN), which is considered a prostatic precancerous lesion, after 1 year of TRT.
  • All underwent prostate biopsy prior to initiating treatment.
  • Of the men 55 had benign prostate biopsies (PIN-) and 20 had PIN without frank cancer (PIN+).
  • All men with PIN underwent repeat biopsy to exclude cancer prior to the initiation of testosterone treatment.
  • Prostate specific antigen (PSA), and total and free testosterone were determined prior to treatment and at 1 year.
  • RESULTS: PSA was similar at baseline in men with and without PIN (1.49 +/- 1.1 and 1.53 +/- 1.6 ng/dl, p >0.05) and after 12 months of TRT (1.82 +/- 1.1 and 1.78 +/- 1.6 ng/dl, respectively, p >0.05).
  • A slight, similar increase in mean PSA was noted in the PIN- and PIN+ groups (0.25 +/- 0.6 and 0.33 +/- 0.6 ng/dl, p >0.05).
  • One man in the PIN+ group had cancer after biopsy was performed due to abnormal digital rectal examination.
  • Four additional men in the PIN- group and 2 in the PIN+ group underwent re-biopsy for elevated PSA and none had cancer.
  • No differences were noted between the PIN- and PIN+ groups with regard to total and free testosterone at baseline and at 1 year (p = 0.267).
  • CONCLUSIONS: After 1 year of TRT men with PIN do not have a greater increase in PSA or a significantly increased risk of cancer than men without PIN.
  • These results indicate that TRT is not contraindicated in men with a history of PIN.
  • [MeSH-major] Hormone Replacement Therapy. Hypogonadism / drug therapy. Prostatic Intraepithelial Neoplasia / complications. Prostatic Neoplasms / chemically induced. Testosterone / therapeutic use
  • [MeSH-minor] Adult. Aged. Humans. Male. Middle Aged. Prostate-Specific Antigen / blood. Risk Factors


16. Bostwick DG, Qian J: Effect of androgen deprivation therapy on prostatic intraepithelial neoplasia. Urology; 2001 Aug;58(2 Suppl 1):91-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of androgen deprivation therapy on prostatic intraepithelial neoplasia.
  • There is a marked decrease in the prevalence and extent of high-grade prostatic intraepithelial neoplasia (PIN) in men with prostate cancer after androgen deprivation therapy (ADT) when compared with untreated cases.
  • These findings indicate that the benign and dysplastic prostatic epithelium is androgen dependent.
  • In the normal prostatic epithelium, luminal secretory cells are more sensitive to the absence of androgen than basal cells, and the proliferative cells of high-grade PIN share this androgen sensitivity.
  • Remarkably little is known about the comparative effect of different forms of chemical ADT on PIN and cancer, although there appears to be a limited and consistent repertoire of morphologic responses to all forms of this therapy.
  • Conversely, blockade of 5alpha-reductase with finasteride has little or no effect on PIN (or benign epithelium and cancer), unlike other forms of ADT.
  • A recent international consensus conference sponsored by the World Health Organization concluded that identification of high-grade PIN offered the possibility of chemoprevention with hormonal therapy to block the development of clinical cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Prostatic Intraepithelial Neoplasia / drug therapy
  • [MeSH-minor] Chemoprevention / methods. Chemoprevention / trends. Drug Administration Schedule. Humans. Male. Precancerous Conditions / drug therapy. Precancerous Conditions / pathology. Prostate / pathology

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  • (PMID = 11502458.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 30
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17. Sperling H, Rossi R, Lümmen G, Rübben H: [Testosterone and the prostate]. Urologe A; 2004 Sep;43(9):1092-6
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  • [Title] [Testosterone and the prostate].
  • [Transliterated title] Testosteron und Prostata.
  • Testosterone has a distinct role in benign and malignant diseases of the prostate.
  • Therefore, knowledge about the physiological interactions between testosterone and the prostate and the special circumstances under testosterone substitution are of great impact for urologists.PSA value and prostate volume do not show significant changes under testosterone substitution therapy.
  • Even if there are no long-term studies in men under substitution due to decreased testosterone, the therapy seems to be safe under regular control of the prostate with PSA and sonography, and the risk for prostate carcinoma is not increased.
  • In hypogonadal men with high-grade PIN under testosterone substitution, 1 in 20 cases with suspicious rectal examination exhibited a carcinoma; the PSA values did not show a difference between men with or without PIN.Nevertheless, it remains unclear whether men after successful radical prostatectomy should receive testosterone substitution.
  • [MeSH-major] Hormone Replacement Therapy / methods. Hypogonadism / blood. Hypogonadism / drug therapy. Prostate-Specific Antigen / blood. Prostatic Neoplasms / chemically induced. Testosterone / administration & dosage. Testosterone / deficiency
  • [MeSH-minor] Aged. Aged, 80 and over. Aging / blood. Humans. Male. Prostate / drug effects. Prostate / metabolism. Risk Assessment / methods. Risk Factors

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  • (PMID = 15368045.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 29
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18. Barve A, Khor TO, Hao X, Keum YS, Yang CS, Reddy B, Kong AN: Murine prostate cancer inhibition by dietary phytochemicals--curcumin and phenyethylisothiocyanate. Pharm Res; 2008 Sep;25(9):2181-9
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  • [Title] Murine prostate cancer inhibition by dietary phytochemicals--curcumin and phenyethylisothiocyanate.
  • PURPOSE: Prior studies from our laboratory have demonstrated the efficacy of a combined treatment of low doses of dietary agents curcumin and phenylethylisothiocyanate in effectively suppressing prostate cancer in vitro in human prostate cancer PC3 cells as well as in vivo in immunodeficient mice implanted with PC3 cells.
  • Hence, this study was undertaken to examine the potential chemopreventive properties of the two agents against transgenic adenocarcinoma of the mouse prostate.
  • MATERIALS AND METHODS: The efficacy of AIN-76A diet supplemented with 2% curcumin or 0.05% PEITC or a combination of 1% curcumin and 0.025% PEITC for periods of 10 and 16 weeks was tested against adenocarcinoma of the mouse prostate.
  • RESULTS: Supplementing AIN-76A diet with dietary phytochemicals curcumin or PEITC either alone or in combination, significantly decreased incidence of prostate tumor formation (P = 0.0064).
  • Immunohistochemistry revealed a significant inhibition of high-grade PIN (P = 0.0006, 0.000069, 0.00029 for a treatment period of 10 weeks and P = 0.02582, 0.022179, 0.0317 for a treatment period of 16 weeks) along with decreased proliferation and increased apoptotic index in the curcumin, PEITC or curcumin and PEITC treated animals, respectively.
  • Furthermore, Western blot analysis revealed that downregulation of the Akt signaling pathway may in part play a role in decreasing cell proliferation ultimately retarding prostate tumor formation.
  • CONCLUSION: Our data lucidly evidence the chemopreventive merits of dietary phytochemicals curcumin and PEITC in suppressing prostate adenocarcinoma.

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  • (PMID = 18437538.001).
  • [ISSN] 0724-8741
  • [Journal-full-title] Pharmaceutical research
  • [ISO-abbreviation] Pharm. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA094828; United States / NCI NIH HHS / CA / R01-CA118947; United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NCI NIH HHS / CA / R01 CA094828-07; United States / NCI NIH HHS / CA / R01 CA118947-03; United States / NCI NIH HHS / CA / CA118947-03; United States / NCI NIH HHS / CA / R01-CA094828; United States / NCI NIH HHS / CA / R01 CA118947; United States / NCI NIH HHS / CA / CA094828-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Bad protein, mouse; 0 / Forkhead Transcription Factors; 0 / Foxo1 protein, mouse; 0 / Isothiocyanates; 0 / bcl-Associated Death Protein; 6U7TFK75KV / phenethyl isothiocyanate; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.2 / pyruvate dehydrogenase (acetyl-transferring) kinase; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ NIHMS221201; NLM/ PMC3465714
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19. Matsuyama M, Hayama T, Funao K, Kawahito Y, Sano H, Takemoto Y, Nakatani T, Yoshimura R: Overexpression of cysteinyl LT1 receptor in prostate cancer and CysLT1R antagonist inhibits prostate cancer cell growth through apoptosis. Oncol Rep; 2007 Jul;18(1):99-104
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  • [Title] Overexpression of cysteinyl LT1 receptor in prostate cancer and CysLT1R antagonist inhibits prostate cancer cell growth through apoptosis.
  • We investigated LTD4 receptor (cysteinyl LT1 receptor: CysLT1R) expression in prostate cancer (PC), as well as the effects of CysLT1R antagonist on cell proliferation in PC cell lines.
  • CysLT1R expression in PC patients, prostatic intraepithelial neoplasia (PIN), benign prostatic hyperplasia (BPH), and normal prostate (NP) tissues were examined.
  • Initially, only slight CysLT1R expression was detected in BPH and NP tissues and marked CysLT1R expression was detected in PIN and PC tissues.
  • CysLT1R expression was higher in high-grade cancer than in low-grade cancer.
  • Furthermore, CysLT1R antagonist caused marked inhibition of PC cells in a concentration- and time-dependent manner through early apoptosis.
  • Thus, the target of CysLT1R may become a new therapy in the treatment of PC.
  • [MeSH-major] Acetates / pharmacology. Apoptosis / drug effects. Cell Proliferation / drug effects. Leukotriene Antagonists / pharmacology. Membrane Proteins / metabolism. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / pathology. Quinolines / pharmacology. Receptors, Leukotriene / metabolism
  • [MeSH-minor] Aged. Disease Progression. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. Immunoenzyme Techniques. Male. Middle Aged. Prostate / metabolism. Prostate / pathology. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial Neoplasia / metabolism. Prostatic Intraepithelial Neoplasia / pathology. Tumor Cells, Cultured / drug effects


20. Willman JH, Holden JA: Immunohistochemical staining for DNA topoisomerase II-alpha in benign, premalignant, and malignant lesions of the prostate. Prostate; 2000 Mar 1;42(4):280-6
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  • [Title] Immunohistochemical staining for DNA topoisomerase II-alpha in benign, premalignant, and malignant lesions of the prostate.
  • BACKGROUND: The DNA topoisomerase II-alpha (topo II-alpha)-targeting drug etoposide was recently shown to be an active agent in the combined chemotherapy of hormone-insensitive prostatic carcinoma.
  • Much experimental data indicate that cells sensitive to topo II-targeting chemotherapeutic drugs are rapidly proliferating and show elevated topo II expression.
  • There is little information concerning topo II expression in lesions of the prostate.
  • METHODS: Paraffin blocks from cases of invasive prostatic carcinoma, prostatic intraepithelial neoplasia, and prostatic nodular hyperplasia were retrieved from the surgical pathology files at the University of Utah Health Sciences Center.
  • Using a new immunohistochemical stain, specific for the alpha isoform of DNA topo II, enzyme expression was evaluated in 54 prostatic adenocarcinomas, 22 lesions of high-grade prostatic intraepithelial neoplasia (PIN), and 10 cases of benign prostatic nodular hyperplasia.
  • RESULTS: The average topo II-alpha index for well-differentiated prostatic adenocarcinomas (Gleason scores 2-4) was 1.5 +/- 0.9; for moderately differentiated tumors (Gleason scores 5-7), 3.1 +/- 2.4; and for poorly differentiated tumors (Gleason scores 8-10), 6.7 +/- 5.5.
  • The average topo II-alpha index for all invasive prostatic adenocarcinomas was 4.0 (range, 0-19.0).
  • Benign prostatic nodular hyperplasia had the lowest average topo II-alpha index, of 0.54 (range, 0.2-1.0).
  • The average topo II-alpha index of 2.3 (range, 0-8.6) for high-grade prostatic intraepithelial neoplasia was intermediate between the invasive tumors and benign prostate.
  • CONCLUSIONS: Topo II-alpha expression in carcinoma of the prostate correlates with Gleason score.
  • Prostatic nodular hyperplasia shows little expression of topo II-alpha.
  • Prostatic intraepithelial neoplasia has an average topo II-alpha index intermediate between nodular hyperplasia and carcinoma.
  • [MeSH-major] Adenocarcinoma / enzymology. DNA Topoisomerases, Type II / analysis. Isoenzymes / analysis. Prostate / enzymology. Prostatic Hyperplasia / enzymology. Prostatic Intraepithelial Neoplasia / enzymology. Prostatic Neoplasms / enzymology

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10679757.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / Isoenzymes; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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21. 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.
  • Membranous staining was recorded as low (aberrant) or high (normal).
  • 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-major] Adenocarcinoma / metabolism. Cadherins / metabolism. Prostatic Neoplasms / metabolism
  • [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


22. Chang SS, Reuter VE, Heston WD, Hutchinson B, Grauer LS, Gaudin PB: Short term neoadjuvant androgen deprivation therapy does not affect prostate specific membrane antigen expression in prostate tissues. Cancer; 2000 Jan 15;88(2):407-15
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  • [Title] Short term neoadjuvant androgen deprivation therapy does not affect prostate specific membrane antigen expression in prostate tissues.
  • BACKGROUND: Prostate specific membrane antigen (PSMA) is a transmembrane glycoprotein highly expressed in benign prostate secretory-acinar epithelium and prostate carcinoma.
  • The results of several studies suggest that PSMA expression is increased in prostate carcinoma cell lines subjected to androgen deprivation and in androgen-independent tumors.
  • The authors studied the effects of short term (3-month) androgen deprivation on PSMA expression in prostate carcinoma specimens using two anti-PSMA monoclonal antibodies (mAbs), 7E11 and PM2J004.5.
  • METHODS: The study included patients with clinically localized prostate carcinoma who were prospectively randomized into 1 of 2 treatment groups: 3 months of neoadjuvant androgen deprivation therapy followed by radical prostatectomy (ADT/RP), or radical prostatectomy (RP) alone.
  • Representative formalin fixed, paraffin embedded prostate sections were immunostained with the anti-PSMA mAbs 7E11 and PM2J004.5 by the streptavidin-biotin method.
  • The authors recorded the staining intensity and the percentage of positive cells stained in benign epithelium, high grade prostatic intraepithelial neoplasia (PIN), and prostate carcinoma.
  • They compared the results of 7E11 with those of PM2J004.5 in benign epithelium, high grade prostate, and carcinoma and also compared the results between the two treatment groups (ADT/RP vs. RP alone).
  • RESULTS: Both anti-PSMA mAbs stained benign secretory-acinar epithelium, high grade PIN, and prostate carcinoma.
  • In both treatment groups, PM2J004.5 reacted with a significantly greater percentage of cells (P < 0.001) and with significantly greater intensity (P < 0.001) compared with 7E11 in benign epithelium and prostate carcinoma.
  • With both anti-PSMA mAbs, the percentage of cells stained and the intensity of staining in high grade PIN was similar to that in prostate carcinoma.
  • In the group that received RP alone, the percentage of cells stained and the intensity of staining with 7E11 were significantly greater in high grade PIN and prostate carcinoma compared with benign epithelium (P < 0.001), and the intensity of staining with the PM2J004.5 was significantly greater in high grade PIN and prostate carcinoma compared with benign epithelium (P < 0.001).
  • In the ADT/RP group, the percentage of cells stained and the intensity of staining with 7E11 and PM2J004.5 were significantly greater in prostate carcinoma compared with benign epithelium (P < 0.006).
  • PSMA staining did not correlate with either Gleason score (in the group that received RP alone) or pathologic stage (in both the RP-alone and ADT/RP groups) and did not differ between the two treatment groups.
  • CONCLUSIONS: Short term neoadjuvant ADT does not affect PSMA expression in benign prostate secretory-acinar epithelium, high grade PIN, or prostate carcinoma.
  • Prostate carcinoma and high grade PIN express significantly higher levels of PSMA than benign prostate secretory-acinar epithelium.
  • Compared with 7E11, the PM2J004.5 anti-PSMA mAb is a more sensitive immunohistochemical marker of prostate carcinoma in formalin fixed, paraffin embedded tissue.
  • [MeSH-major] Androgen Antagonists / pharmacology. Antigens, Surface. Carboxypeptidases / biosynthesis. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal. Glutamate Carboxypeptidase II. Humans. Immunohistochemistry. Male. Middle Aged. Neoadjuvant Therapy. Prostatectomy. Sensitivity and Specificity

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  • [Copyright] Copyright 2000 American Cancer Society.
  • (PMID = 10640975.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 47650
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antibodies, Monoclonal; 0 / Antigens, Surface; EC 3.4.- / Carboxypeptidases; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
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23. Comstock TL, Paterno MR, Usner DW, Pichichero ME: Efficacy and safety of besifloxacin ophthalmic suspension 0.6% in children and adolescents with bacterial conjunctivitis: a post hoc, subgroup analysis of three randomized, double-masked, parallel-group, multicenter clinical trials. Paediatr Drugs; 2010 Apr 01;12(2):105-12
MedlinePlus Health Information. consumer health - Antibiotics.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Acute conjunctivitis is the most frequent eye disorder seen by primary care physicians and one that often affects children.
  • Besifloxacin is a new topical fluoroquinolone, the first chlorofluoroquinolone, for the treatment of bacterial conjunctivitis.
  • METHODS: This was a post hoc analysis of a subgroup of pediatric patients aged 1-17 years who had participated in three previously reported, randomized, double-masked, parallel-group, multicenter, clinical trials evaluating the safety and efficacy of besifloxacin in the treatment of bacterial conjunctivitis.
  • All three clinical trials included children (aged > or = 1 year) with a clinical diagnosis of bacterial conjunctivitis in at least one eye, based on the presence at baseline of grade 1 or greater purulent conjunctival discharge and conjunctival injection, and pin-hole visual acuity of at least 20/200 in both eyes for verbal patients.
  • In all studies, besifloxacin ophthalmic suspension 0.6% was administered as one drop in the affected eye(s) three times daily, at approximately 6-hourly intervals, for 5 days.
  • CONCLUSION: Besifloxacin ophthalmic suspension 0.6% was shown to be safe and effective for the treatment of bacterial conjunctivitis in children and adolescents aged 1-17 years.
  • [MeSH-major] Anti-Bacterial Agents / therapeutic use. Azepines / therapeutic use. Conjunctivitis, Bacterial / drug therapy. Fluoroquinolones / therapeutic use
  • [MeSH-minor] Administration, Topical. Adolescent. Aza Compounds / adverse effects. Aza Compounds / therapeutic use. Child. Child, Preschool. Double-Blind Method. Female. Humans. Infant. Male. Ophthalmic Solutions. Quinolines / adverse effects. Quinolines / therapeutic use. Randomized Controlled Trials as Topic. Treatment Outcome

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  • (PMID = 20218747.001).
  • [ISSN] 1179-2019
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Grant] United States / NIDCD NIH HHS / DC / R01 DC008671
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Aza Compounds; 0 / Azepines; 0 / Fluoroquinolones; 0 / Ophthalmic Solutions; 0 / Quinolines; BFE2NBZ7NX / 7-(3-aminohexahydro-1H-azepin-1-yl)-8-chloro-1-cyclopropyl-6-fluoro-1,4-dihydro-4-oxo-3-quinolinecarboxylic acid; U188XYD42P / moxifloxacin
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24. Gupta A, Axelsson K, Thörn SE, Matthiessen P, Larsson LG, Holmström B, Wattwil M: Low-dose bupivacaine plus fentanyl for spinal anesthesia during ambulatory inguinal herniorrhaphy: a comparison between 6 mg and 7. 5 mg of bupivacaine. Acta Anaesthesiol Scand; 2003 Jan;47(1):13-9
Hazardous Substances Data Bank. FENTANYL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low-dose bupivacaine plus fentanyl for spinal anesthesia during ambulatory inguinal herniorrhaphy: a comparison between 6 mg and 7. 5 mg of bupivacaine.
  • BACKGROUND: Inguinal herniorrhaphy is commonly performed as an outpatient procedure.
  • The sensory block was measured by 'pin-prick' and the motor block was evaluated by a modified Bromage scale.
  • The return of the modified Bromage scale to grade 0 was earlier in Group L than in Group H (P<0.05) but the time to mobilization and discharge was similar.
  • Times to home discharge (median) were 350 and 445 min, respectively, in Groups L and H.
  • In Group H, 95% of the patients and in Group L 85% would have the same anesthetic again if operated upon for a similar procedure.
  • However, the long discharge times and risk for urinary retention restrict its routine use in all patients.
  • [MeSH-minor] Adult. Aged. Conscious Sedation. Female. Follow-Up Studies. Humans. Male. Middle Aged. Pain Measurement / drug effects. Pain, Postoperative / drug therapy. Pain, Postoperative / epidemiology. Postoperative Period

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  • [CommentIn] Acta Anaesthesiol Scand. 2003 Jan;47(1):1-2 [12492789.001]
  • (PMID = 12492791.001).
  • [ISSN] 0001-5172
  • [Journal-full-title] Acta anaesthesiologica Scandinavica
  • [ISO-abbreviation] Acta Anaesthesiol Scand
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anesthetics, Intravenous; 0 / Anesthetics, Local; UF599785JZ / Fentanyl; Y8335394RO / Bupivacaine
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