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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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2. 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


3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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4. 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
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  • [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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5. 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


6. 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
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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).
  • The 1- and 2-year overall survival rates were 53.7 and 42.9%, respectively.
  • 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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7. 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


8. Bostwick DG, Qian J: Effect of androgen deprivation therapy on prostatic intraepithelial neoplasia. Urology; 2001 Aug;58(2 Suppl 1):91-3
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  • [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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9. 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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10. 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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11. 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


12. 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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13. 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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14. 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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15. Pamir MN, Ozduman K, Dinçer A, Yildiz E, Peker S, Ozek MM: First intraoperative, shared-resource, ultrahigh-field 3-Tesla magnetic resonance imaging system and its application in low-grade glioma resection. J Neurosurg; 2010 Jan;112(1):57-69
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  • [Title] First intraoperative, shared-resource, ultrahigh-field 3-Tesla magnetic resonance imaging system and its application in low-grade glioma resection.
  • OBJECT: The authors describe the first shared-resource, 3-T intraoperative MR (ioMR) imaging system and analyze its impact on low-grade glioma (LGG) resection with an emphasis on the use of intraoperative proton MR spectroscopy.
  • A new 5-pin headrest-head coil combination and floating transfer table were specifically designed for this system.
  • Intraoperative proton MR spectroscopy and diffusion weighted MR imaging were used to differentiate residual tumor tissue from peritumoral parenchymal changes.
  • No infections or other procedure-related complications were encountered.
  • [MeSH-minor] Adolescent. Adult. Brain / metabolism. Brain / pathology. Brain / surgery. Child. Diffusion Magnetic Resonance Imaging / economics. Diffusion Magnetic Resonance Imaging / methods. Facility Design and Construction / economics. Female. Humans. Magnetic Resonance Spectroscopy / economics. Magnetic Resonance Spectroscopy / methods. Male. Middle Aged. Neoplasm Staging. Time Factors. Ultrasonography / economics. Ultrasonography / methods. Young Adult


16. 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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17. Hull D, Bostwick DG: Androgen deprivation therapy for precancerous lesions of the prostate. Best Pract Res Clin Endocrinol Metab; 2008 Apr;22(2):285-91
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  • [Title] Androgen deprivation therapy for precancerous lesions of the prostate.
  • Androgen deprivation therapy has become well-established in the treatment of prostate cancer.
  • Luteinizing-hormone-releasing hormone (LHRH) agonists, anti-androgens, orchiectomy, and combination hormonal therapy are treatment options offered to select patients.
  • The prospect of intervention prior to the development of adenocarcinoma is appealing, and high-grade prostate intra-epithelial neoplasia (PIN), the only known precursor, is the best possible target.
  • There is a decrease in the incidence of high-grade PIN in patients treated with combination androgen deprivation therapy (LHRH agonist and anti-androgen).
  • Treatment with the 5alpha-reductase inhibitor finasteride results in a significant decrease in the incidence of high-grade PIN.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Humans. Male. Models, Biological. Neoplasm Staging. Neoplasms, Hormone-Dependent / drug therapy. Precancerous Conditions / drug therapy. Prostate / drug effects. Prostate / pathology. Selective Estrogen Receptor Modulators / therapeutic use

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  • (PMID = 18471786.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Selective Estrogen Receptor Modulators
  • [Number-of-references] 42
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18. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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