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1. Ayyathurai R, Civantos F, Soloway MS, Manoharan M: Basal cell carcinoma of the prostate: current concepts. BJU Int; 2007 Jun;99(6):1345-9
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  • [Title] Basal cell carcinoma of the prostate: current concepts.
  • [MeSH-major] Carcinoma, Adenoid Cystic / pathology. Carcinoma, Basal Cell / pathology. Prostatectomy / methods. Prostatic Neoplasms / pathology

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  • (PMID = 17419700.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 36
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2. Montironi R, Mazzucchelli R, Stramazzotti D, Scarpelli M, López Beltran A, Bostwick DG: Basal cell hyperplasia and basal cell carcinoma of the prostate: a comprehensive review and discussion of a case with c-erbB-2 expression. J Clin Pathol; 2005 Mar;58(3):290-6
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  • [Title] Basal cell hyperplasia and basal cell carcinoma of the prostate: a comprehensive review and discussion of a case with c-erbB-2 expression.
  • Prostatic basal cell proliferations range from ordinary basal cell hyperplasia (BCH) to florid basal cell hyperplasia to basal cell carcinoma.
  • The distinction between these forms of BCH, including the variant with prominent nucleoli (formerly called atypical BCH), and basal cell carcinoma depends on morphological and immunohistochemical criteria and, in particular, on the degree of cell proliferation.
  • In florid BCH, the proliferation index is intermediate between ordinary BCH and basal cell carcinoma.
  • Immunohistochemistry is also useful for identifying the cell composition of the basal cell proliferations, including the basal cell nature of the cells, their myoepithelial differentiation, and c-erbB-2 oncoprotein expression.
  • Based on the information derived from the literature and on the appearance and follow up of the case presented here, florid BCH might represent a lesion with an intermediate position between ordinary BCH and basal cell carcinoma.
  • In general, basal cell carcinoma is seen as a low grade carcinoma.
  • [MeSH-major] Carcinoma, Basal Cell / diagnosis. Prostatic Hyperplasia / diagnosis. Prostatic Neoplasms / diagnosis. Receptor, ErbB-2 / metabolism
  • [MeSH-minor] Aged. Cell Proliferation. Diagnosis, Differential. Humans. Immunoenzyme Techniques. Male. Prostatectomy

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  • [Cites] Am J Surg Pathol. 2002 Feb;26(2):237-43 [11812946.001]
  • [Cites] Hum Pathol. 2003 May;34(5):462-70 [12792920.001]
  • [Cites] Am J Surg Pathol. 2003 Dec;27(12):1523-9 [14657711.001]
  • [Cites] Virchows Arch. 2003 Dec;443(6):787-91 [14756145.001]
  • [Cites] Am J Surg Pathol. 2004 Oct;28(10):1289-98 [15371944.001]
  • [Cites] Am J Surg Pathol. 1984 Sep;8(9):699-704 [6206734.001]
  • [Cites] Hum Pathol. 1998 Dec;29(12):1447-50 [9865831.001]
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  • [Cites] Histopathology. 1992 Feb;20(2):151-5 [1559669.001]
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  • (PMID = 15735163.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC1770600
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3. Segawa N, Tsuji M, Nishida T, Takahara K, Azuma H, Katsuoka Y: Basal cell carcinoma of the prostate: report of a case and review of the published reports. Int J Urol; 2008 Jun;15(6):557-9
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  • [Title] Basal cell carcinoma of the prostate: report of a case and review of the published reports.
  • Prostatic basal cell carcinoma (BCC), a distinctive variant of adenocarcinoma, is rare.
  • Digital rectal examination disclosed a stony hard prostate.
  • Serum prostate-specific antigen and prostatic acid phosphatase were within the normal range.
  • Transrectal needle biopsy of the prostate was followed by transurethral resection as symptomatic treatment.
  • [MeSH-major] Carcinoma, Basal Cell. Prostatic Neoplasms

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  • (PMID = 18489650.001).
  • [ISSN] 1442-2042
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 10
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4. Begnami MD, Quezado M, Pinto P, Linehan WM, Merino M: Adenoid cystic/basal cell carcinoma of the prostate: review and update. Arch Pathol Lab Med; 2007 Apr;131(4):637-40
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  • [Title] Adenoid cystic/basal cell carcinoma of the prostate: review and update.
  • CONTEXT: Although most prostate carcinomas are of the conventional acinar type, unusual variants have been reported.
  • Adenoid cystic/basal cell carcinoma of the prostate is a rare tumor with distinctive histopathologic features.
  • OBJECTIVE: To review current literature together with the clinical, pathologic, and immunohistochemical features of adenoid cystic/basal cell carcinoma of the prostate and offer a practical approach to the diagnosis--including the differential diagnosis--of this neoplasm in surgical pathologic specimens.
  • DATA SOURCES: Adenoid cystic/basal cell carcinoma of the prostate is composed of infiltrating basaloid cells forming dilated acinar and cribriform spaces with luminal basementlike material.
  • Differentiation of adenoid cystic/basal cell carcinoma from basal cell hyperplasia and cribriform pattern of acinar adenocarcinoma may be difficult.
  • The use of cytokeratin 34betaE12 and prostate-specific antigen can help in difficult cases.
  • CONCLUSIONS: Various histologic and immunohistochemical features are helpful in recognizing adenoid cystic/basal cell carcinoma of the prostate.
  • This is a rare subtype of prostate cancer and correct diagnosis is important because of the unique clinical and biological features and the implications for treatment and prognosis.
  • [MeSH-major] Carcinoma, Adenoid Cystic / pathology. Carcinoma, Basal Cell / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 17425398.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 30
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5. Halat SK, MacLennan GT: Adenoid cystic/basal cell carcinoma of the prostate. J Urol; 2008 Apr;179(4):1576
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  • [Title] Adenoid cystic/basal cell carcinoma of the prostate.
  • [MeSH-major] Carcinoma, Adenoid Cystic / pathology. Carcinoma, Basal Cell / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 18295260.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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6. Micke P, Kappert K, Ohshima M, Sundquist C, Scheidl S, Lindahl P, Heldin CH, Botling J, Ponten F, Ostman A: In situ identification of genes regulated specifically in fibroblasts of human basal cell carcinoma. J Invest Dermatol; 2007 Jun;127(6):1516-23
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  • [Title] In situ identification of genes regulated specifically in fibroblasts of human basal cell carcinoma.
  • Basal cell carcinoma (BCC) is characterized by slow growth, virtual absence of metastases, and strong stroma-dependency.
  • Analyses of CAFs from squamous cell cancer, prostate cancer, and colon cancer did not indicate that these genes were upregulated in these cancers.
  • [MeSH-major] Carcinoma, Basal Cell / genetics. Fibroblasts / physiology. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Skin Neoplasms / genetics

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  • (PMID = 17273163.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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7. Iczkowski KA, Montironi R: Adenoid cystic/basal cell carcinoma of the prostate strongly expresses HER-2/neu. J Clin Pathol; 2006 Dec;59(12):1327-30
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  • [Title] Adenoid cystic/basal cell carcinoma of the prostate strongly expresses HER-2/neu.
  • Adenoid cystic/basal cell carcinoma (ACBCC) is a rare neoplasm in the prostate.
  • Protein and mRNA expression were 2+ to 3+ (of 3+) in all patients with ACBCC, compared to a breast cancer control with strong reactivity, whereas protein expression was noted in only one acinar carcinoma and mRNA expression was absent in all acinar carcinomas.
  • Benign acini expressed HER-2/neu only in the basal layer.
  • [MeSH-major] Carcinoma, Adenoid Cystic / metabolism. Carcinoma, Basal Cell / metabolism. Mixed Tumor, Malignant / metabolism. Prostatic Neoplasms / metabolism. Receptor, ErbB-2 / metabolism


8. Kuzmanov A, Hayrabedyan S, Karaivanov M, Todorova K: Basal cell subpopulation as putative human prostate carcinoma stem cells. Folia Histochem Cytobiol; 2007;45(2):75-80
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  • [Title] Basal cell subpopulation as putative human prostate carcinoma stem cells.
  • The present study examines the expression of p63, glutathione S-transferase-pi (GSTP1) and alpha-methylacyl-CoAracemase (AMACR) in serial slices in proliferative inflammatory atrophy (PIA) in order to implicate that some of the basal cells are probably the putative human prostate carcinoma stem cells (PHPCSC).
  • Quantitative immunohistochemistry analysis (QIHC) of the studied antigen expression levels revealed that there are two populations of p63 basal cells.
  • Type I basal cells had high AMACR, low GSTP1 and p63 expression.
  • Type II basal cells had low AMACR, high GSTP1 and p63 expression.
  • Therefore, we propose that the putative human prostate carcinoma stem cells probably reside within the population of type I basal cells.

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  • (PMID = 17597019.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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9. Tonini G, Rosini R, Teppa A, Aulenti V, Kalantary F, Tosana M, Bianchi D, Zorzi F: [Adenoid cystic/basal cell carcinoma of the prostate:case report]. Urologia; 2008 Oct-Dec;75(4):245-8
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  • [Title] [Adenoid cystic/basal cell carcinoma of the prostate:case report].
  • Although most prostate carcinomas belong to the conventional acinar type, unusual variants have been reported.
  • The adenoid cystic/basal cell carcinoma of the prostate is a rare tumor with distinctive histopathologic features.
  • METHODS. A 71-year-old man had an increased PSA value (5.11 ng/dL); the prostatic biopsy examination was positive for adenoid cystic/basal cell carcinoma.
  • The histology examination showed an acinar conventional carcinoma and adenoid cystic/basal cell carcinoma.
  • CONCLUSIONS. Various histologic and immunohistochemical features are helpful in recognizing the adenoid cystic/basal cell carcinoma of the prostate.

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  • (PMID = 21086341.001).
  • [ISSN] 0391-5603
  • [Journal-full-title] Urologia
  • [ISO-abbreviation] Urologia
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
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10. Ali TZ, Epstein JI: Basal cell carcinoma of the prostate: a clinicopathologic study of 29 cases. Am J Surg Pathol; 2007 May;31(5):697-705
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  • [Title] Basal cell carcinoma of the prostate: a clinicopathologic study of 29 cases.
  • We studied 29 cases of basal cell carcinoma of the prostate including what others call adenoid cystic carcinoma of the prostate.
  • Other patterns included: basal cell hyperplasialike in 9 cases (32%); small tubules occasionally lined by a hyaline rim in 9 cases (32%), with 4 of these cases also demonstrating intermingling cords of cells; and large solid nests in 8 cases (28.5%), 5 of which had central necrosis.
  • Perineural and vascular invasion was seen in 2 basal cell carcinomas with large basaloid nests.
  • Basal cell markers (HMWCK, p63) either:.
  • Basal cell carcinomas are rare tumors with a broad morphologic spectrum.
  • The most common morphology among those with an aggressive behavior is large solid nests more often with central necrosis, high Ki67%, and less staining with basal cell markers.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Biopsy, Needle. Combined Modality Therapy. Humans. Male. Middle Aged. Mitosis. Neoplasm Recurrence, Local. Retrospective Studies. Transurethral Resection of Prostate

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  • (PMID = 17460452.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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11. Bohn OL, Rios-Luna NP, Navarro L, Duran-Peña A, Sanchez-Sosa S: Basal cell carcinoma of the prostate gland: a case report and brief review of the basal cell proliferations of the prostate gland. Ann Diagn Pathol; 2010 Oct;14(5):365-8
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  • [Title] Basal cell carcinoma of the prostate gland: a case report and brief review of the basal cell proliferations of the prostate gland.
  • Basal cell proliferations within the prostate gland encompass a group of benign and malignant entities.
  • Although basal cell hyperplasia is a common finding, basal cell carcinoma of the prostate gland is a rare tumor that can be mistaken by a benign condition and represents a diagnostic problem in genitourinary pathology.
  • We report a case of basal cell carcinoma in a previously healthy 65-year-old man with urinary symptoms and low prostate-specific antigen.
  • The microscopic findings are presented and the use of immunohistochemical markers classifying basal cell lesions of the prostate discussed.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Basal Cell / diagnosis. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Humans. Male. Prostate / metabolism. Prostate / pathology. Prostate-Specific Antigen / analysis. Prostate-Specific Antigen / metabolism. Sensitivity and Specificity

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20850702.001).
  • [ISSN] 1532-8198
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
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12. Komura K, Inamoto T, Tsuji M, Ibuki N, Koyama K, Ubai T, Azuma H, Katsuoka Y: Basal cell carcinoma of the prostate: unusual subtype of prostatic carcinoma. Int J Clin Oncol; 2010 Dec;15(6):594-600
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  • [Title] Basal cell carcinoma of the prostate: unusual subtype of prostatic carcinoma.
  • Basal cell carcinoma of the prostate, which has been generally considered to be indolent, is an unusual histological type of prostatic carcinoma and is extremely rare.
  • This tumor has been classified according to the prevalent pattern of growth as adenoid cystic carcinoma or basaloid cell carcinoma (BCC), with the former growth pattern being considered to be the main feature of this entity.
  • His prostate was slightly enlarged, stony hard, and with a rough surface on digital rectal examination, while serum prostate-specific antigen and prostatic acid phosphatase concentrations were within the normal ranges (0.007 and 0.9 ng/mL, respectively).
  • Specimens obtained by prostatic needle biopsy showed immunohistochemical reactivity for cytokeratin 34βE12 and P63, findings that were identical to those seen in basal cell carcinoma.
  • Basal cell carcinoma of the prostate is a rare tumor, reported in 56 cases so far, and among all these, the pure form of BCC is extremely rare.
  • Our findings reveal that tumors with a basaloid cell-predominant pattern have significant potential for a poor prognosis, in contrast with the conventional understanding regarding this neoplasm.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / blood. Fluorodeoxyglucose F18. Humans. Immunoenzyme Techniques. Male. Positron-Emission Tomography. Prognosis. Prostate-Specific Antigen / blood. Radiopharmaceuticals. Tomography, X-Ray Computed

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  • [Cites] Int J Urol. 2001 Aug;8(8):S41-4 [11555019.001]
  • [Cites] Int J Urol. 2008 Jun;15(6):557-9 [18489650.001]
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  • (PMID = 20422244.001).
  • [ISSN] 1437-7772
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; EC 3.4.21.77 / Prostate-Specific Antigen
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13. Teglund S, Toftgård R: Hedgehog beyond medulloblastoma and basal cell carcinoma. Biochim Biophys Acta; 2010 Apr;1805(2):181-208
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  • [Title] Hedgehog beyond medulloblastoma and basal cell carcinoma.
  • The Hedgehog (Hh) signaling pathway is of central importance during embryo development in metazoans and governs a diverse array of processes including cell proliferation, differentiation, and tissue patterning.
  • In normal adult physiology, the pathway is implicated in stem cell maintenance, tissue repair and regeneration.
  • However, the pathway's darker side is its involvement in several types of human cancer, to which it confers growth promoting and/or survival capabilities to the cancer cell to varying degrees, and by different mechanisms.
  • The Hh pathway is firmly linked to the etiology of basal cell carcinoma and to at least a subset of medulloblastoma.
  • There is increasing evidence that other sporadic cancers, including those in pancreas, prostate, lung, and breast, could also be dependent on Hh pathway activity.
  • [MeSH-major] Brain Neoplasms / metabolism. Carcinoma, Basal Cell / metabolism. Hedgehog Proteins / metabolism. Medulloblastoma / metabolism. Signal Transduction / physiology. Skin Neoplasms / metabolism


14. Rukin NJ, Zeegers MP, Ramachandran S, Luscombe CJ, Liu S, Saxby M, Lear J, Strange RC: A comparison of sunlight exposure in men with prostate cancer and basal cell carcinoma. Br J Cancer; 2007 Feb 12;96(3):523-8
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  • [Title] A comparison of sunlight exposure in men with prostate cancer and basal cell carcinoma.
  • Ultraviolet radiation exposure increases basal cell carcinoma (BCC) risk, but may be protective against prostate cancer.
  • We attempted to identify exposure patterns that confer reduced prostate cancer risk without increasing that of BCC.
  • We used a questionnaire to assess exposure in 528 prostate cancer patients and 442 men with basal cell carcinoma, using 365 benign prostatic hypertrophy patients as controls.
  • Skin type 1 (odds ratio (OR)=0.47, 95% CI=0.26-0.86), childhood sunburning (OR=0.38, 95% CI=0.26-0.57), occasional/frequent sunbathing (OR=0.21, 95% CI=0.14-0.31), lifetime weekday (OR=0.85, 95% CI=0.80-0.91) and weekend exposure (OR=0.79, 95% CI=0.73-0.86) were associated with reduced prostate cancer risk.
  • Combinations of one or two parameters were associated with a progressive decrease in the ORs for prostate cancer risk (OR=0.54-0.25) with correspondingly increased BCC risk (OR=1.60-2.54).
  • Our data do not define exposure patterns that reduce prostate cancer risk without increasing BCC risk.
  • [MeSH-major] Carcinoma, Basal Cell / etiology. Prostatic Neoplasms / etiology. Sunlight / adverse effects

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  • (PMID = 17262085.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2360028
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15. Bauer R: Cylindroma of the prostate. Am J Surg Pathol; 2007 Aug;31(8):1288-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cylindroma of the prostate.
  • A sporadic prostate tumor morphologically and immunophenotypically identical to dermal cylindroma is reported for the first time.
  • The patient was a 78-year-old man with normal prostate-specific antigen serum level.
  • The only obvious difference from typical dermal cylindroma was a lack of intratumoral Langerhans cells in the prostate neoplasm.
  • Differentiation from all hitherto known variants of basal cell proliferative lesions of the prostate was straightforward.
  • However, focal cylindromalike features have been reported in rare cases of otherwise typical basaloid proliferations of the prostate.
  • [MeSH-major] Carcinoma, Adenoid Cystic / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Disease-Free Survival. Fluorescent Antibody Technique, Direct. Humans. Male. Transurethral Resection of Prostate. Treatment Outcome

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  • (PMID = 17667556.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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16. Luebke AM, Schlomm T, Gunawan B, Bonkhoff H, Füzesi L, Erbersdobler A: Simultaneous tumour-like, atypical basal cell hyperplasia and acinar adenocarcinoma of the prostate: a comparative morphological and genetic approach. Virchows Arch; 2005 Mar;446(3):338-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Simultaneous tumour-like, atypical basal cell hyperplasia and acinar adenocarcinoma of the prostate: a comparative morphological and genetic approach.
  • Basal cell tumours of the prostatic gland are rare, and the classification is difficult.
  • However, there were no definite criteria for a malignant behaviour of the basal cell tumour.
  • Comparative genomic hybridisation from microdissected tumour cells yielded losses at the short arms of chromosomes 8 and 12 in the conventional adenocarcinoma and a normal karyotype in the basal cell tumour.
  • The pathological findings favoured the diagnosis of an atypical basal cell hyperplasia.
  • [MeSH-major] Carcinoma, Acinar Cell / complications. Carcinoma, Acinar Cell / pathology. Prostatic Hyperplasia / complications. Prostatic Hyperplasia / pathology. Prostatic Neoplasms / complications. Prostatic Neoplasms / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasms, Basal Cell / genetics. Neoplasms, Basal Cell / pathology. Nucleic Acid Hybridization

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  • (PMID = 15726402.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Germany
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17. Fomperoza-Torres A, Valero A, González-Berjón J, Arista-Nasr J: [Frequency of focal prostatic carcinoma and atypical glandular proliferations in 1,000 needle prostatic biopsies]. Rev Invest Clin; 2008 Mar-Apr;60(2):87-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Frequency of focal prostatic carcinoma and atypical glandular proliferations in 1,000 needle prostatic biopsies].
  • [Transliterated title] Frecuencia de carcinoma focal y proliferaciones glandulares atípicas en 1,000 biopsias prostáticas por punción.
  • The recognition of these lesions is important since many of them correspond to potentially curable cancers or to benign lesions that mimic carcinoma.
  • Immunohistochemical studies and the analysis of additional histologic sections allowed the classification of 17 cases of AGP into specific categories (prostatic adenosis, atrophy, atypical basal cell hyperplasia and seminiferous ducts).
  • Of the 29 AGP, additional biopsies were taken in four cases and in one of them prostatic carcinoma was the final diagnosis.
  • The frequency of focal carcinoma and AGP in our material was similar to other series; however in many of the AGP cases additional biopsies were not performed despite its high predictive value for carcinoma.
  • [MeSH-major] Prostate / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 18637566.001).
  • [ISSN] 0034-8376
  • [Journal-full-title] Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición
  • [ISO-abbreviation] Rev. Invest. Clin.
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Mexico
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18. Han B, Suleman K, Wang L, Siddiqui J, Sercia L, Magi-Galluzzi C, Palanisamy N, Chinnaiyan AM, Zhou M, Shah RB: ETS gene aberrations in atypical cribriform lesions of the prostate: Implications for the distinction between intraductal carcinoma of the prostate and cribriform high-grade prostatic intraepithelial neoplasia. Am J Surg Pathol; 2010 Apr;34(4):478-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ETS gene aberrations in atypical cribriform lesions of the prostate: Implications for the distinction between intraductal carcinoma of the prostate and cribriform high-grade prostatic intraepithelial neoplasia.
  • BACKGROUND: Atypical cribriform lesions (ACLs) of the prostate consist of cribriform glands lined with cytologically malignant cells with partial or complete basal cell lining.
  • It may represent cribriform "high-grade prostatic intraepithelial neoplasia" (HGPIN) or "intraductal carcinoma of the prostate" (IDC-P), which is almost always associated with clinically aggressive prostate carcinoma (PCa).
  • METHODS: To better understand the biologic and molecular basis of distinction between cribriform HGPIN and IDC, we used break-apart fluorescence in-situ hybridization assay to assess ETS gene aberrations, a specific and commonest molecular alteration involving PCa, in a cohort of 16 isolated ACL, presumed to be an isolated cribriform HGPIN, and 45 carcinoma-associated ACL (ACL-PCa) on radical prostatectomy specimens, presumed to be spectrum of IDC-P.
  • Hundred percent (34 of 34) of the IDC-P showed concordance of ERG rearrangement status with adjacent invasive carcinoma.
  • [MeSH-major] Carcinoma, Ductal / pathology. Chromosome Aberrations. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology. Proto-Oncogene Proteins c-ets / genetics

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  • (PMID = 20220513.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / R01 CA102872; United States / NCI NIH HHS / CA / UO1 CA111275-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins c-ets
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19. Shah RB, Magi-Galluzzi C, Han B, Zhou M: Atypical cribriform lesions of the prostate: relationship to prostatic carcinoma and implication for diagnosis in prostate biopsies. Am J Surg Pathol; 2010 Apr;34(4):470-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical cribriform lesions of the prostate: relationship to prostatic carcinoma and implication for diagnosis in prostate biopsies.
  • Atypical cribriform lesions of the prostate (ACL) are cribriform glands lined by cytologically malignant cells with partial or complete basal cell lining.
  • They represent cribriform high-grade PIN (cribriform HGPIN), which can be an isolated finding not associated with PCa (isolated ACL), or "intraductal carcinoma (IDC-P)" that is almost always associated with infiltrative high-grade prostate carcinoma (PCa) (cancer-associated ACL, ACL-PCa).
  • We report the incidence, topographic relation to cancer, and morphologic differences of these 2 lesions in radical prostatectomy and discuss the potential biologic basis and implication for diagnosis in prostate biopsy.
  • ACL was defined as cribriform glands comprising cytologically malignant cells that spanned the entire glandular lumens with partial or complete basal cell lining confirmed by basal cell immunostaining.
  • These histologic features of ACL were reviewed: number of ACL/prostate gland, size, glandular contour (round, irregular, branching), architectural pattern (dense cribriform, irregular cribriform, solid), comedonecrosis, and nuclear features (round and uniform, round with varying sizes, pleomorphic, giant nuclei [6x adjacent nuclei]).
  • The mean number of ACL per prostate was 23.8 for ACL-PCa and 2.4 for isolated ACL (P=0.008).
  • [MeSH-major] Adenocarcinoma / pathology. Prostate / pathology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 20182345.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Kanner WA, Galgano MT, Atkins KA: Podoplanin expression in basal and myoepithelial cells: utility and potential pitfalls. Appl Immunohistochem Mol Morphol; 2010 May;18(3):226-30

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Podoplanin expression in basal and myoepithelial cells: utility and potential pitfalls.
  • We evaluated the expression of D2-40 in breast, salivary gland, skin, and mucosa, all organs rich in myoepithelial cells and basal cells.
  • This study assessed the utility of using D2-40 to highlight basal/myoepithelial cells and to identify potential pitfalls in misinterpretation of lymphatic invasion.
  • Our results showed that myoepithelial cells in breast and salivary gland and basal cells in prostate consistently demonstrate D2-40 immunoreactivity, but typically less intensely than lymphatics.
  • Cutaneous and mucosal-based basal cells also have D2-40 expression, but often in a patchy, focal manner.
  • In addition, many salivary gland tumors and squamous cell carcinomas had strong D2-40 expression, sometimes making distinction of lymphatics versus tumor edge staining difficult.
  • D2-40 is excellent for assessing lymphatic invasion in breast, prostate, and cervix as long as the pathologist is aware of the expression in myoepithelial cells/basal cells to avoid misinterpretation of ductal carcinoma in situ or normal prostate glands or tumor stroma retraction as tumor lymphatic invasion.
  • Given the patchy positivity in basal cells of skin and mucosa and the reactivity in squamous cell carcinoma, D2-40 was not helpful in assessing for microinvasion of squamous cell carcinoma.

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  • (PMID = 20042851.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Membrane Glycoproteins; 0 / PDPN protein, human
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21. Rouet V, Bogorad RL, Kayser C, Kessal K, Genestie C, Bardier A, Grattan DR, Kelder B, Kopchick JJ, Kelly PA, Goffin V: Local prolactin is a target to prevent expansion of basal/stem cells in prostate tumors. Proc Natl Acad Sci U S A; 2010 Aug 24;107(34):15199-204
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  • [Title] Local prolactin is a target to prevent expansion of basal/stem cells in prostate tumors.
  • Androgen-independent recurrence is the major limit of androgen ablation therapy for prostate cancer.
  • Identification of alternative pathways promoting prostate tumor growth is thus needed.
  • Stat5 has been recently shown to promote human prostate cancer cell survival/proliferation and to be associated with early prostate cancer recurrence.
  • Stat5 is the main signaling pathway triggered by prolactin (PRL), a growth factor whose local production is also increased in high-grade prostate cancers.
  • The first aim of this study was to use prostate-specific PRL transgenic mice to address the mechanisms by which local PRL induces prostate tumorogenesis.
  • We report that (i) Stat5 is the major signaling cascade triggered by local PRL in the mouse dorsal prostate, (ii) this model recapitulates prostate tumorogenesis from precancer lesions to invasive carcinoma, and (iii) tumorogenesis involves dramatic accumulation and abnormal spreading of p63-positive basal cells, and of stem cell antigen-1-positive cells identified as a stem/progenitor-like subpopulation.
  • Because basal epithelial stem cells are proposed to serve as tumor-initiating cells, we challenged the relevance of local PRL as a previously unexplored therapeutic target.
  • Using a double-transgenic approach, we show that Delta1-9-G129R-hPRL, a competitive PRL-receptor antagonist, prevented early stages of prostate tumorogenesis by reducing or inhibiting Stat5 activation, cell proliferation, abnormal basal-cell pattern, and frequency or grade of intraepithelial neoplasia.
  • This study identifies PRL receptor/Stat5 as a unique pathway, initiating prostate tumorogenesis by altering basal-/stem-like cell subpopulations, and strongly supports the importance of further developing strategies to target locally overexpressed PRL in human prostate cancer.
  • [MeSH-minor] Animals. Base Sequence. Cell Proliferation. DNA Primers / genetics. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Inbred CBA. Mice, Transgenic. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Peptide Fragments / genetics. Peptide Fragments / metabolism. Prostate / metabolism. Prostate / pathology. Rats. Receptors, Prolactin / antagonists & inhibitors. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. STAT5 Transcription Factor / metabolism. Signal Transduction. Tissue Distribution

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  • (PMID = 20699217.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United Kingdom / Worldwide Cancer Research / / 05-0603
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Peptide Fragments; 0 / Receptors, Prolactin; 0 / Recombinant Proteins; 0 / STAT5 Transcription Factor; 9002-62-4 / Prolactin
  • [Other-IDs] NLM/ PMC2930529
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22. Roznovanu SL, Rădulescu D, Novac C, Stolnicu S: The morphologic changes induced by hormone and radiation therapy on prostate carcinoma. Rev Med Chir Soc Med Nat Iasi; 2005 Apr-Jun;109(2):337-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The morphologic changes induced by hormone and radiation therapy on prostate carcinoma.
  • The morphologic changes induced by hormone and radiation therapy were evaluated in prostate biopsy and prostatectomy specimens from patients with residual prostate carcinoma.
  • Following hormone therapy, the nonmalignant prostatic tissue showed atrophy of prostatic acini associated with fibrosis, basal cell hyperplasia, degenerative changes of the secretory epithelial cells, and a marked decrease of high-grade intraepithelial neoplasia (HGPIN).
  • In the fragments of residual carcinoma, squamous cell metaplasia, necrosis, and necrobiosis in the foci, vacuolization of the cell cytoplasm, smaller, rare nucleoli, intraluminal crystalloids, higher Gleason score associated with a lower capsular penetration, areas of necrosis and mitoses were found.
  • Following radiation therapy, the nontumoral prostatic tissue showed an increased number of atrophic acini, squamous cell metaplasia, and presence of atypical glands.
  • The morphologic changes induced by radiation therapy in the residual prostatic carcinoma were characterized by an abnormal architectural structure of the glands and presence of cell atypias correlated with the biochemical lowering of serum PSA.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma / pathology. Neoplasm, Residual / pathology. Prostate / drug effects. Prostate / radiation effects. Prostatic Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / blood. Biomarkers, Tumor / radiation effects. Biopsy. Chemotherapy, Adjuvant. Humans. Male. Prostate-Specific Antigen / blood. Prostate-Specific Antigen / radiation effects. Prostatectomy. Radiotherapy, Adjuvant

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  • (PMID = 16607796.001).
  • [ISSN] 0048-7848
  • [Journal-full-title] Revista medico-chirurgicală̆ a Societă̆ţ̜ii de Medici ş̧i Naturaliş̧ti din Iaş̧i
  • [ISO-abbreviation] Rev Med Chir Soc Med Nat Iasi
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 26
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23. Hudson E, Rashid M, Carter AC, Lester JF: Basaloid carcinoma of the prostate: a case report and review of the literature. Eur J Cancer Care (Engl); 2008 Sep;17(5):509-11
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  • [Title] Basaloid carcinoma of the prostate: a case report and review of the literature.
  • Malignant tumours arising from the basal cells of the prostate gland are extremely rare, and the majority of reports in the literature suggest a relatively indolent clinical course.
  • We report a case of infiltrative basaloid carcinoma of the prostate in a 68-year old man that did not respond to systemic chemotherapy.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 18616505.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 7
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24. Alberti C: Neuroendocrine differentiation in prostate carcinoma: focusing on its pathophysiologic mechanisms and pathological features. G Chir; 2010 Nov-Dec;31(11-12):568-74
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  • [Title] Neuroendocrine differentiation in prostate carcinoma: focusing on its pathophysiologic mechanisms and pathological features.
  • Neuroendocrine differentiation in prostate carcinoma: focusing on its pathophysiologic mechanisms and pathological features. C.
  • Alberti Prostate carcinoma, even at advanced stages, responds in most patients to androgen deprivation therapies, that are able to exploit the androgen-sensitivity of prostate cancer cells.
  • Intriguing links between the development of hormone-insensitivity and neuroendocrine (NE) differentiation in prostate carcinoma have been hypothesized.
  • While, some time ago, NE cells have been considered as derived from progenitor neural crest cells, currently are thought to arise, as well as both basal and secretory cells of prostate gland, from common pluripotent stem cells.
  • NE cell are nonproliferative, terminally differentiated, PSA/acid phosphatase and androgen receptor (AR)-negative cells, moreover exhibiting an antiapoptotic phenotype due to survivin expression.
  • The propensity of prostate cancer cells to undergo a transdifferentiation pathway towards NE phenotype is due to several microenvironmental conditions such as androgen depletion (induced by LH-RH analogs or antagonists, antiandrogens, 5-α-reductase inhibitors), ionizing-radiation therapy, adrenergic factors, increase in interleukin-6 signaling cascade.
  • NE differentiation in prostate malignancy arises in three different forms: carcinoid, oat cell carcinoma, focally NE-differentiated conventional tumor.
  • Selective expression of stem cell-associated markers, such as CD44/Oct4A gene, in NE cancerous cells explain their therapy escape together with tumor recurrence and metastasis.
  • Serum levels of CgA reflect NE differentiation in prostate carcinoma more suitably than those of NSE.
  • Although valuable insights into the nature of NE differentiation in prostate carcinoma have been achieved in the last decades, additional understanding is needed about its pathogenetic mechanisms in order to devise novel therapy strategies to target them.
  • [MeSH-major] Carcinoma / pathology. Carcinoma / physiopathology. Cell Transdifferentiation. Prostatic Neoplasms / pathology. Prostatic Neoplasms / physiopathology
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Androgens / metabolism. Antineoplastic Agents, Hormonal / therapeutic use. Apoptosis / drug effects. Biomarkers / metabolism. Cell Transformation, Neoplastic / drug effects. Chromogranins / metabolism. Humans. Male. Neoplasm Invasiveness. Phosphopyruvate Hydratase / metabolism. Pluripotent Stem Cells / metabolism. Prognosis. Prostate-Specific Antigen / metabolism. Receptors, Androgen / metabolism. Treatment Failure


25. Abdou AG, Aiad HA, Sultan SM: pS2 (TFF1) expression in prostate carcinoma: correlation with steroid receptor status. APMIS; 2008 Nov;116(11):961-71
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  • [Title] pS2 (TFF1) expression in prostate carcinoma: correlation with steroid receptor status.
  • It is also considered to be one of the major estrogen-regulated proteins and an indicator of estrogen receptor (ER) functionality. pS2 has previously been investigated in benign and malignant prostate lesions with little information about its relationship to steroid receptor status.
  • Our purpose was to correlate pS2 expression with steroid receptor status (ER alpha and progesterone receptor (PR)) and other pathologic variables in prostate carcinoma.
  • 15 benign prostate hyperplasia (BPH) and 47 prostate carcinoma cases were investigated by means of immunohistochemistry for pS2, ER and PR expression.
  • 80% of BPH showed pS2 cytoplasmic immunoreactivity in hyperplastic acini and about half of these cases also exhibited nuclear staining decorating basal or both basal and luminal nuclei. pS2 was highly expressed in prostate carcinoma (91.4%) with both cytoplasmic and nuclear patterns of staining.
  • The latter pattern was significantly associated with carcinoma having a low Gleason score (p=0.02).
  • The diagnostic value of pS2 expression in prostate carcinoma validated 74.19% accuracy, 91.48% sensitivity and 78.18% positive predictive value.
  • The high sensitivity of pS2 expression in prostate carcinoma could make it a suitable marker for diagnosis of prostate carcinoma, especially in metastatic cases of unknown origin.
  • The absence of correlation and dissimilarity in immunolocalization between pS2 and ER alpha leads to the assumption that ER alpha could not be the regulatory protein for pS2 and may raise questions about the functionality of ER alpha in prostate.
  • The nuclear pattern of pS2 immunoreactivity either in benign or malignant prostatic lesions is similar to the published data on ER beta distribution and could also identify a subset of carcinoma patients with a favorable prognosis.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Carcinoma / pathology. Estrogen Receptor alpha / metabolism. Presenilin-2 / biosynthesis. Prostate / pathology. Prostatic Neoplasms / pathology. Receptors, Progesterone / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Nucleus / metabolism. Cytoplasm / metabolism. Estrogens / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Predictive Value of Tests. Prognosis. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology

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  • (PMID = 19132993.001).
  • [ISSN] 1600-0463
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / PSEN2 protein, human; 0 / Presenilin-2; 0 / Receptors, Progesterone
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26. Shiran MS, Tan GC, Sabariah AR, Rampal L, Phang KS: p63 as a complimentary basal cell specific marker to high molecular weight-cytokeratin in distinguishing prostatic carcinoma from benign prostatic lesions. Med J Malaysia; 2007 Mar;62(1):36-9
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  • [Title] p63 as a complimentary basal cell specific marker to high molecular weight-cytokeratin in distinguishing prostatic carcinoma from benign prostatic lesions.
  • The diagnosis of prostatic carcinoma (Pca) on routine biopsies may be challenging, and to date the commonly used marker to distinguish prostate carcinoma from benign prostatic lesions has been High Molecular Weight-Cytokeratin (HMW-CK).
  • More recently, antibodies to p63 have been reported to be more sensitive than HMW-CK for the detection of prostatic basal cells. p63, a homologue of tumour suppressor gene p53, is essential for prostate development and is selectively expressed in the nuclei of basal cells of normal prostate glands.
  • The sensitivity of p63 and HMW-CK in identifying basal cells in benign glands was 88.37% and 90.70% respectively.
  • Thus, p63 is a useful complementary basal cell specific stain to HMW-CK, and would be very helpful to practicing pathologists in dealing with difficult cases.
  • [MeSH-major] Keratins. Membrane Proteins. Neoplasms / diagnosis. Neoplasms, Basal Cell / diagnosis

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  • (PMID = 17682568.001).
  • [ISSN] 0300-5283
  • [Journal-full-title] The Medical journal of Malaysia
  • [ISO-abbreviation] Med. J. Malaysia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Malaysia
  • [Chemical-registry-number] 0 / Biomarkers; 0 / CKAP4 protein, human; 0 / Membrane Proteins; 68238-35-7 / Keratins
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27. Liu YN, Jiang ZM, Wang XY, Zhang HZ, Chen JQ, Huang J, Yang QH: [The value of using an AMACR/34betaE12/p63 cocktail double staining for diagnosis of prostate carcinoma and precarcinomatous lesions]. Zhonghua Bing Li Xue Za Zhi; 2006 Jul;35(7):417-20
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  • [Title] [The value of using an AMACR/34betaE12/p63 cocktail double staining for diagnosis of prostate carcinoma and precarcinomatous lesions].
  • OBJECTIVE: To investigate the value of using an AMACR/34betaE12/p63 cocktail and double-staining for the diagnosis of small focal protatic carcinoma and precarcinomatous lesions.
  • METHODS: A total of 130 consecutive cases were examined over a 3-month period, including 105 prostate needle biopsy samples, 6 radical prostatectomy specimens and 19 benign prostatic hyperplasia specimens which were excised transurethra or above pubis.
  • RESULTS: In the sections stained by the 3-antibody cocktail, blue-black cytoplasmic staining was observed in the epithelial cells of prostatic carcinoma and high-grade prostatic intraepithelial neoplasia (HGPIN) the basal cells of benign glands were stained red.
  • There were no red basal cells around the blue-black glandular epithelium of carcinoma, but discontinuous or consecutive red basal cells were present around the blue-black glandular epithelium of HGPIN.
  • Prostatic carcinoma was found in 214 paraffin blocks (82%), including 31 small focal carcinoma.
  • No benign glands were simultaneously positive for AMACR and negative for basal cell markers.
  • CONCLUSION: Inmmunohistochemistry studies using a 3-antibody cocktail and double staining can improve the detection rate of small focal prostatic carcinoma and HGPIN.

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  • (PMID = 17069678.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CK-34 beta E12; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 68238-35-7 / Keratins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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28. Ali TZ, Epstein JI: False positive labeling of prostate cancer with high molecular weight cytokeratin: p63 a more specific immunomarker for basal cells. Am J Surg Pathol; 2008 Dec;32(12):1890-5
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  • [Title] False positive labeling of prostate cancer with high molecular weight cytokeratin: p63 a more specific immunomarker for basal cells.
  • Occasional nonspecific staining of prostate cancer cells with high molecular weight cytokeratin (HMWCK) can lead to false-negative diagnoses.
  • We compared p63 and HMWCK immunostaining to check their specificity for basal cell identification.
  • Out of 6887 prostate cancer cases sent in consultation to one of the authors over 1.5 years, we identified 22 (0.3%) cases with HMWCK labeling of cancer cells, including 20 needle biopsies and 2 transurethral resections of prostate (TURP).
  • Cases were sent in consultation because of the confusing immunostaining pattern, where prostate cancer cells labeled with HMWCK at the outside institutions.
  • To assess whether overstaining was a factor, we evaluated the intensity of HMWCK staining in the basal cells of the benign glands, which was moderate in 6 and strong in 16 cases.
  • HMWCK labeling of prostate cancer cells is uncommon and does not seem to be solely attributable to overstaining. p63 is a more specific marker for basal cells than HMWCK, with less labeling of tumor cells.
  • Recognition of this phenomenon and performing stains for p63 when it occurs can help prevent underdiagnosing prostatic carcinoma.
  • [MeSH-minor] False Positive Reactions. Humans. Immunohistochemistry. Male. Transurethral Resection of Prostate

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  • (PMID = 18813120.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins; 68238-35-7 / Keratins
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29. Paner GP, Luthringer DJ, Amin MB: Best practice in diagnostic immunohistochemistry: prostate carcinoma and its mimics in needle core biopsies. Arch Pathol Lab Med; 2008 Sep;132(9):1388-96
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  • [Title] Best practice in diagnostic immunohistochemistry: prostate carcinoma and its mimics in needle core biopsies.
  • CONTEXT: The unrelenting challenge encountered when differentiating limited-volume prostate carcinoma and sometimes subtle variants from its many morphologic mimics has increased the use of ancillary immunohistochemistry in routine prostate needle biopsies.
  • The availability of prostate cancer-associated and basal cell-associated markers has been an invaluable addition to diagnostic surgical pathology.
  • OBJECTIVE: To review commonly used immunohistochemical stains, including innovative combinations, for confirmation or differential diagnosis of prostate carcinoma, and to propose appropriately constructed panels using morphologic patterns in prostate needle biopsies.
  • CONCLUSIONS: Basal cell-associated markers p63, high-molecular-weight cytokeratin 34 beta E12, cytokeratin 5/6 or a cocktail containing p63 and high-molecular-weight cytokeratin 34 beta E12 or cytokeratin 5/6 and prostate carcinoma-specific marker alpha-methylacyl coenzyme A (coA) racemase alone or in combination are useful adjuncts in confirming prostatic carcinoma that either lacks diagnostic, qualitative or quantitative features or that has an unusual morphologic pattern (eg, atrophic, pseudohyperplastic) or is in the setting of prior treatment.
  • The combination of alpha-methylacyl coA racemase positivity with negative staining for basal cell-associated markers supports a malignant diagnosis in the appropriate morphologic context.
  • Dual chromogen basal cell- associated markers (p63 [nuclear] and high-molecular-weight cytokeratin 34 beta E12/cytokeratin 5/6 [cytoplasmic]) and alpha-methylacyl coA racemase in an antibody cocktail provide greater sensitivity for the basal cell layer, easing evaluation and minimizing loss of representation of the focal area interest because the staining is performed on one slide.
  • Prostate-specific antigen and prostatic acid phosphatase markers are helpful in excluding secondary malignancies involving the prostate, such as urothelial carcinoma, and occasionally in excluding nonprostatic benign mimickers, such as nephrogenic adenoma, mesonephric gland hyperplasia, and Cowper glands.

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  • (PMID = 18788849.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 47
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30. Ozawa MG, Yao VJ, Chanthery YH, Troncoso P, Uemura A, Varner AS, Kasman IM, Pasqualini R, Arap W, McDonald DM: Angiogenesis with pericyte abnormalities in a transgenic model of prostate carcinoma. Cancer; 2005 Nov 15;104(10):2104-15
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  • [Title] Angiogenesis with pericyte abnormalities in a transgenic model of prostate carcinoma.
  • BACKGROUND: Previous studies of the TRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model vasculature suggest that, as tumors develop, vessels invade the glandular epithelium.
  • METHODS: Eighty-micron cryostat sections of normal prostate and three histopathologic stages of TRAMP tumor sections, classified by epithelial cell E-cadherin immunoreactivity, were immunostained with vascular endothelial cell and pericyte receptor antibodies and evaluated by confocal microscopy.
  • RESULTS: In the normal mouse prostate, capillaries were most abundant in the fibromuscular tunica between the epithelium and smooth muscle of the ductules.
  • In the prostatic intraepithelial neoplasia (PIN) stage, vessels accompanied epithelial cell protrusions into the ductule lumen but remained in the connective tissue at the basal side of the epithelium.
  • Angiogenesis and loss of vascular hierarchy were also found in human prostate carcinoma.
  • CONCLUSIONS: Vascular abnormalities, which begin at the PIN stage and intensify in well differentiated and poorly differentiated tumors, may be useful readouts for early detection and treatment assessment in prostate carcinoma.

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  • [Copyright] Copyright 2005 American Cancer Society
  • (PMID = 16208706.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL-24136; United States / NHLBI NIH HHS / HL / P01 HL024136; United States / NHLBI NIH HHS / HL / R01 HL059157; United States / NCI NIH HHS / CA / P50 CA90270; United States / NHLBI NIH HHS / HL / HL-59157
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins
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31. Gu XJ, Lu JL, Lai RS, Zhang YD, Zhang P, Lu ZJ, Zhu QY: [Clinical value of CK34BE12 combining the expression of protein P53 gene and prostate specific antigen for the differential diagnosis of prostate carcinoma]. Zhonghua Nan Ke Xue; 2006 Apr;12(4):340-2
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  • [Title] [Clinical value of CK34BE12 combining the expression of protein P53 gene and prostate specific antigen for the differential diagnosis of prostate carcinoma].
  • OBJECTIVE: To improve the level of clinical diagnosis and differential diagnosis of benign and malignant prostate lesions.
  • METHODS: One hundred and nine cases of prostate cancer and prostate hyperplasia were evaluated by the expression of high molecular weight cytokeratin (CK34BE12), prostate specific antigen (PSA) and protein P53 gene using the immunohistochemical technique.
  • RESULTS: The basal-cells in all of the benign lesions were stained with the CK34BE12 and PSA, while it had not immunoreactivity with P53.
  • In contrast, the prostate carcinoma were not stained or partly stained with the CK34BE12 and PSA, but P53 show significant immunoreactivity with the tissue.
  • CONCLUSION: Based on the routine histological studies with the expression of CK34BE12 and PSA together, they can indicate the existence of basal-cell distinctly and show indirectly whether the basal-cell is integrated.
  • Combining the expression of P53 to determine the existence of cancer gene, it can help to distinguish benign and malignant prostate lesions.
  • [MeSH-major] Keratins / biosynthesis. Prostate-Specific Antigen / biosynthesis. Prostatic Neoplasms / diagnosis. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 16683569.001).
  • [ISSN] 1009-3591
  • [Journal-full-title] Zhonghua nan ke xue = National journal of andrology
  • [ISO-abbreviation] Zhonghua Nan Ke Xue
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CK-34 beta E12; 0 / Tumor Suppressor Protein p53; 68238-35-7 / Keratins; EC 3.4.21.77 / Prostate-Specific Antigen
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32. Molinié V, Baumert H: [New markers in prostate biopsies]. Actas Urol Esp; 2007 Oct;31(9):1009-24
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  • [Title] [New markers in prostate biopsies].
  • The use of serum prostate-specific antigen screening to facilitate early detection of prostate cancer has resulted in a dramatic increase in the number of prostate needle core biopsies which pathologists must examine.
  • When assessing small foci of atypical glands upon needle biopsy, the pathologist searches for differences between the benign glands and atypical glands in terms of usual morphological features and in such cases, immunohistochemical stains for basal cell markers such as 34betaE12 antibody or antibodies directed against cytokeratin 5 and 6 and more recently p63 may be a useful adjuvant to identify basal cells which are typically present in benign glands but absent in prostatic carcinoma.
  • However several benign mimickers of prostate carcinoma, including atrophy, atypical adenomatous hyperplasia, nephrogenic adenoma can stain negatively with these antibodies and thus a negative basal cell marker immunostain alone does not exclude a diagnosis of benignancy.
  • Alpha-methyl-coenzyme-A-racemase (AMACR) a new sensitive marker of prostate carcinoma, can be useful in confirming ambiguous lesion suspected for malignancy.
  • The aim of this review is to describe the histological features of prostatic carcinoma in case of small focus, and discuss the application of these new prostatic markers in the light of the current literature to highlight the best practice guidelines.

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  • (PMID = 18257370.001).
  • [ISSN] 0210-4806
  • [Journal-full-title] Actas urologicas españolas
  • [ISO-abbreviation] Actas Urol Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 68238-35-7 / Keratins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
  • [Number-of-references] 53
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33. Guo CC, Epstein JI: Intraductal carcinoma of the prostate on needle biopsy: Histologic features and clinical significance. Mod Pathol; 2006 Dec;19(12):1528-35
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  • [Title] Intraductal carcinoma of the prostate on needle biopsy: Histologic features and clinical significance.
  • Intraductal carcinoma of the prostate (IDC-P) has been described in radical prostatectomies.
  • However, there is limited information as to its histologic features and clinical significance when seen on prostate biopsy.
  • A total of 27 cases of prostate biopsies with only IDC-P (ie no infiltrating cancer anywhere on the biopsy) were studied from the consult files of one of the authors.
  • IDC-P was defined as malignant epithelial cells filling large acini and prostatic ducts, with preservation of basal cells forming either:.
  • Basal cells were observed on regular hematoxylin and eosin stained slides in 14 cases; in all the cases, basal cells were confirmed by immunohistochemical stains for high molecular weight cytokeratin (n=25) and/or p63 (n = 4).
  • After the diagnosis of IDC-P on prostate biopsies, patients were treated by radical prostatectomy (6), radiation (7), hormone (5), combined radiation and hormone (1), or watchful waiting (2).
  • In all six radical prostatectomy specimens, high-grade infiltrating carcinoma with Gleason score 8 or 9 was present with five cases also revealing prominent IDC-P.
  • Non-focal extraprostatic extension of carcinoma was observed in five of the six prostatectomy cases with two cases also demonstrating vascular invasion.
  • Our study indicates that IDC-P on prostate biopsies is frequently associated with high-grade cancer and poor prognostic parameters at radical prostatectomy as well as potentially advanced disease following other therapies.
  • [MeSH-major] Carcinoma, Ductal / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Biopsy, Needle. Cell Nucleus / pathology. Combined Modality Therapy. Diagnosis, Differential. Follow-Up Studies. Humans. Male. Middle Aged. Prognosis. Prostatectomy. Prostatic Intraepithelial Neoplasia / pathology. Treatment Outcome

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  • (PMID = 16980940.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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34. Calaluce R, Beck SK, Bair EL, Pandey R, Greer KA, Hoying AM, Hoying JB, Mount DW, Nagle RB: Human laminin-5 and laminin-10 mediated gene expression of prostate carcinoma cells. Prostate; 2006 Sep 15;66(13):1381-90
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  • [Title] Human laminin-5 and laminin-10 mediated gene expression of prostate carcinoma cells.
  • In prostate cancer progression, the basal lamina switches from predominantly laminin-5 to laminin-10.
  • DU-145 prostate cancer cells were treated with either soluble laminin-5 (20 ng/ml) or laminin-10 (1 microg/ml) for 6, 24, and 48 hr.
  • EGFR was validated by real-time PCR and laminin-10 mediated cell adhesion activated EGFR in DU-145 cells.
  • Both laminins appear to be important signal transducers in prostate cancer.

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  • (PMID = 16804886.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA056666; United States / NCI NIH HHS / CA / 2 P01 CA56666-08A1; United States / NCI NIH HHS / CA / K08 CA90662-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / DNA, Neoplasm; 0 / Laminin; 0 / RNA, Neoplasm; 0 / kalinin; 0 / laminin 10; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.4.22.- / Calpain
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35. Jiang Z, Li C, Fischer A, Dresser K, Woda BA: Using an AMACR (P504S)/34betaE12/p63 cocktail for the detection of small focal prostate carcinoma in needle biopsy specimens. Am J Clin Pathol; 2005 Feb;123(2):231-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Using an AMACR (P504S)/34betaE12/p63 cocktail for the detection of small focal prostate carcinoma in needle biopsy specimens.
  • We assessed the usefulness of immunohistochemical analysis with a 3-antibody cocktail (alpha-methylacyl coenzyme A racemase [AMACR, or P504S], 34betaE12, p63) and a double-chromogen reaction for detection of limited prostate cancer in 138 needle biopsy specimens, including 82 with small foci of prostatic adenocarcinoma and 56 benign prostates.
  • When carcinoma was present, red cytoplasmic granular staining (AMACR) in the malignant glands and cells and dark brown nuclear (p63) and cytoplasmic (34betaE12) staining in basal cells of adjacent nonmalignant glands were found.
  • Of 82 cases of small foci of prostatic adenocarcinoma, 78 (95%) expressed AMACR; all malignant glands were negative for basal cell staining.
  • All benign glands adjacent to malignant glands were recognized easily by basal cell marker positivity and little or no AMACR expression.
  • No benign glands were simultaneously positive for AMACR and negative for basal cell markers (specificity, 100%).
  • Our results indicate that immunohistochemistry with a 3-antibody cocktail and double chromogen is a simple and easy assay that can be used as a routine test, which overcomes the problems of studying small lesions in prostate needle biopsies with multiple immunohistochemical stains.
  • [MeSH-minor] Biomarkers, Tumor / analysis. Humans. Male. Prostate / anatomy & histology. Prostate / pathology. Sensitivity and Specificity

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  • (PMID = 15842047.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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36. Bianchi-Frias D, Vakar-Lopez F, Coleman IM, Plymate SR, Reed MJ, Nelson PS: The effects of aging on the molecular and cellular composition of the prostate microenvironment. PLoS One; 2010 Sep 01;5(9)
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  • [Title] The effects of aging on the molecular and cellular composition of the prostate microenvironment.
  • BACKGROUND: Advancing age is associated with substantial increases in the incidence rates of common diseases affecting the prostate gland including benign prostatic hyperplasia (BPH) and prostate carcinoma.
  • The prostate is comprised of a functional secretory epithelium, a basal epithelium, and a supporting stroma comprised of structural elements, and a spectrum of cell types that includes smooth muscle cells, fibroblasts, and inflammatory cells.
  • In this study we sought to identify aging-associated alterations in the mouse prostate microenvironment that could influence pathology.
  • By histology, immunofluorescence, and electron microscopy we determined that the collagen matrix is abundant and disorganized, smooth muscle cell orientation is disordered, and inflammatory infiltrates are significantly increased, and are comprised of macrophages, T cells and, to a lesser extent, B cells.
  • CONCLUSION/SIGNIFICANCE: These findings demonstrate that during normal aging the prostate stroma exhibits phenotypic and molecular characteristics plausibly contributing to the striking age associated pathologies affecting the prostate.

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  • (PMID = 20824135.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA103728; United States / NIDDK NIH HHS / DK / R01 DK069690; United States / NCI NIH HHS / CA / U54 CA126540; United States / NCI NIH HHS / CA / P50 CA103728
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2931699
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37. Ramos Soler D, Mayordomo Aranda E, Calatayud Blas A, Rubio Briones J, Solsona Narbón E, Llombart Bosch A: [Usefulness of bcl-2 expression as a new basal cell marker in prostatic pathology]. Actas Urol Esp; 2006 Apr;30(4):345-52
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  • [Title] [Usefulness of bcl-2 expression as a new basal cell marker in prostatic pathology].
  • INTRODUCTION AND OBJECTIVES: The diagnosis of invasive adenocarcinoma of the prostate is often difficult in needle prostatic cores, where, additionally, the assessment of the presence of basal cells has demonstrated to be of paramount importance.
  • In our study, we analyzed comparatively the expression of 34betaE12, p63, bcl-2 and alpha-methylacyl-CoA racemase in order to evaluate the usefulness of bcl-2 as a new marker of the basal cells in prostatic pathology.
  • METHODS AND RESULTS: This study comprises radical prostatectomy specimens from 48 patients which were studied in order to determine the lack of staining of basal cells in invasive tumor areas together with the expression of racemase.
  • Likewise, the presence of basal cells in areas of atrophy, hyperplasia, adenosis, and high-grade prostatic intraepithelial neoplasia (PIN) was also examined.
  • Within the areas of adenosis and PIN a discontinuous pattern of basal cell expression was found in some cases.
  • In 2 out of 48 cases (4,2%) of invasive carcinoma a weak bcl-2 expression without a basal cell distribution was found.
  • CONCLUSIONS: In addition to classical markers, we demonstrated the diagnostic value of bcl-2 as a new basal cell marker.

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  • (PMID = 16838605.001).
  • [ISSN] 0210-4806
  • [Journal-full-title] Actas urologicas españolas
  • [ISO-abbreviation] Actas Urol Esp
  • [Language] spa
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CK-34 beta E12; 0 / CKAP4 protein, human; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 68238-35-7 / Keratins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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38. White SJ, Lu P, Keller GM, Voelkel-Johnson C: Targeting the short form of cFLIP by RNA interference is sufficient to enhance TRAIL sensitivity in PC3 prostate carcinoma cells. Cancer Biol Ther; 2006 Dec;5(12):1618-23
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  • [Title] Targeting the short form of cFLIP by RNA interference is sufficient to enhance TRAIL sensitivity in PC3 prostate carcinoma cells.
  • Unfortunately, prostate cancer cells display little if any susceptibility to TRAIL-induced apoptosis.
  • Although proteasome inhibitors increased basal levels of short cFLIP isoforms, cFLIPS declined at a similar rate in the absence or presence of proteasome inhibition during doxorubicin treatment.
  • We conclude that doxorubicin-mediated downregulation of cFLIPS, which occurs at the post-transcriptional level independent of proteasome-mediated pathways, is sufficient to enhance TRAIL sensitivity in PC3 prostate carcinoma cells.
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. DNA Primers. Daunorubicin / pharmacology. Doxorubicin / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. TNF-Related Apoptosis-Inducing Ligand / physiology. Transfection

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  • (PMID = 17106251.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA102218
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / DNA Primers; 0 / RNA, Small Interfering; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 80168379AG / Doxorubicin; ZS7284E0ZP / Daunorubicin
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39. Klonisch T, Müller-Huesmann H, Riedel M, Kehlen A, Bialek J, Radestock Y, Holzhausen HJ, Steger K, Ludwig M, Weidner W, Hoang-Vu C, Hombach-Klonisch S: INSL3 in the benign hyperplastic and neoplastic human prostate gland. Int J Oncol; 2005 Aug;27(2):307-15
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  • [Title] INSL3 in the benign hyperplastic and neoplastic human prostate gland.
  • The human prostate gland is a well known source of H1 and H2 relaxin but information is lacking on the expression and potential role of the INSL3 peptide hormone within the prostate gland.
  • In the present study we have investigated the expression of human INSL3 in patients with benign prostate hyperplasia (BPH), prostate intraepithelial neoplasia (PIN) and prostate carcinoma tissues.
  • Of the prostate epithelial cells, strongest INSL3 expression was detected in the basal epithelial cell compartment.
  • Prostate epithelial cells were also a source for transcripts encoding the INSL3 receptor LGR8 suggesting the presence of an autocrine/paracrine INSL3-LGR8 ligand-receptor system within the human prostate.
  • Three human prostate carcinoma cell lines displayed differential gene activity for INSL3 and LGR8.
  • While LNCaP was devoid of INSL3, the androgen-insensitive PC-3 and the stromal prostate cell line hPCP co-expressed INSL3 and LGR8 transcripts.
  • In addition to expressing INSL3 mRNA, the LGR8-negative DU-145 also expressed an INSL3 splice form formerly demonstrated in thyroid carcinoma cells.
  • INSL3 did not alter the proliferative or metabolic activity of PC-3 carcinoma cells.
  • Instead, PC-3 responded to INSL3 with significantly enhanced tumor cell motility and a transcriptional down-regulation of ErbB receptors and EGF.
  • In conclusion, we have identified a functional INSL3-LGR8 ligand-receptor system in human prostate carcinoma cells.
  • [MeSH-minor] Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Cell Survival / drug effects. Cyclic AMP / metabolism. Dose-Response Relationship, Drug. Epidermal Growth Factor / pharmacology. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Gene Expression / drug effects. Humans. Immunohistochemistry. In Situ Hybridization. Male. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, G-Protein-Coupled / analysis. Receptors, G-Protein-Coupled / genetics. Recombinant Proteins / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tretinoin / pharmacology


40. Angelucci A, Muzi P, Cristiano L, Millimaggi D, Cimini A, Dolo V, Miano R, Vicentini C, Cerù MP, Bologna M: Neuroendocrine transdifferentiation induced by VPA is mediated by PPARgamma activation and confers resistance to antiblastic therapy in prostate carcinoma. Prostate; 2008 May 1;68(6):588-98
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  • [Title] Neuroendocrine transdifferentiation induced by VPA is mediated by PPARgamma activation and confers resistance to antiblastic therapy in prostate carcinoma.
  • BACKGROUND: Prostate cancer (PCa) is the most commonly diagnosed cancer in men in the Western Countries.
  • NET was an early event detectable through the expression of neuro-endocrine (NE) markers within 72 hr after VPA treatment and it was associated to a reduction in the overall cell proliferation.
  • When we interrupted VPA treatment we observed the recovery in residual cells of the basal proliferation rate both in vitro and in a xenograft model.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cell Transdifferentiation / drug effects. Enzyme Inhibitors / pharmacology. Neurosecretory Systems / drug effects. PPAR gamma / metabolism. Prostatic Neoplasms / drug therapy. Valproic Acid / pharmacology
  • [MeSH-minor] Anilides / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / pathology. Drug Combinations. Histone Deacetylase Inhibitors. Humans. Male. Mice. Mice, Nude. Proto-Oncogene Proteins c-bcl-2 / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 18288684.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Drug Combinations; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / PPAR gamma; 0 / Proto-Oncogene Proteins c-bcl-2; 614OI1Z5WI / Valproic Acid
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41. Yemelyanov A, Gasparian A, Lindholm P, Dang L, Pierce JW, Kisseljov F, Karseladze A, Budunova I: Effects of IKK inhibitor PS1145 on NF-kappaB function, proliferation, apoptosis and invasion activity in prostate carcinoma cells. Oncogene; 2006 Jan 19;25(3):387-98
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of IKK inhibitor PS1145 on NF-kappaB function, proliferation, apoptosis and invasion activity in prostate carcinoma cells.
  • A key antiapoptotic transcription factor, nuclear factor kappa-B (NF-kappaB), is known to be critically important for tumor cell growth, angiogenesis and development of metastatic lesions.
  • We and others showed previously that NF-kappaB transcription factor was constitutively activated in androgen-independent prostate carcinoma (PC) cell lines due to the upregulated activity of inhibitor of NF-kappaB kinases (IKK).
  • In this work, using luciferase assay, electrophoretic mobility shift assay and Northern blot analysis of expression of endogenous kappaB-responsive genes, we demonstrate that a novel highly specific small-molecule IKK inhibitor, PS1145, efficiently inhibited both basal and induced NF-kappaB activity in PC cells.
  • We also showed that PS1145 inhibited PC cell proliferation.
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Enzyme Inhibitors / pharmacology. Heterocyclic Compounds, 3-Ring / pharmacology. I-kappa B Kinase / antagonists & inhibitors. NF-kappa B / physiology. Neoplasm Invasiveness / prevention & control. Prostatic Neoplasms / pathology. Pyridines / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Male. Phosphorylation. Rats. Signal Transduction

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  • (PMID = 16170348.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Heterocyclic Compounds, 3-Ring; 0 / NF-kappa B; 0 / PS1145; 0 / Pyridines; EC 2.7.11.10 / I-kappa B Kinase
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42. Epstein JI, Herawi M: Prostate needle biopsies containing prostatic intraepithelial neoplasia or atypical foci suspicious for carcinoma: implications for patient care. J Urol; 2006 Mar;175(3 Pt 1):820-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prostate needle biopsies containing prostatic intraepithelial neoplasia or atypical foci suspicious for carcinoma: implications for patient care.
  • PURPOSE: We identified information critical for patient treatment on prostate needle biopsies diagnosed with prostatic intraepithelial neoplasia or atypical foci suspicious for carcinoma.
  • MATERIALS AND METHODS: A search was performed using the MEDLINE database and referenced lists of relevant studies to obtain articles addressing the significance of finding PIN or atypical foci suspicious for carcinoma on needle biopsy.
  • 3) Although the diagnosis of HGPIN is subjective, interobserver reproducibility for its diagnosis is fairly high among urological pathologists, and yet only moderate among pathologists without special expertise in prostate pathology.
  • There were certain results concerning atypical glands suspicious for carcinoma.
  • 1) An average of 5% of needle biopsy pathology reports are diagnosed as atypical glands suspicious for carcinoma.
  • 3) Ancillary techniques using basal cell markers and AMACR (alpha-methyl-acyl-coenzyme A racemase) can decrease the number of atypical diagnoses, and yet one must use these techniques with caution since there are numerous false-positive and false-negative results.
  • These 2 entities indicate different risks of carcinoma on re-biopsy and different recommendations for followup.

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  • (PMID = 16469560.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 102
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43. Hameed O, Humphrey PA: Pseudoneoplastic mimics of prostate and bladder carcinomas. Arch Pathol Lab Med; 2010 Mar;134(3):427-43
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  • [Title] Pseudoneoplastic mimics of prostate and bladder carcinomas.
  • CONTEXT: The differential diagnoses of prostatic carcinoma and bladder epithelial neoplasms include several histologic mimics that should be known to avoid misdiagnosis.
  • OBJECTIVE: To discuss pseudoneoplastic lesions of the prostate and bladder that could potentially be confused with prostatic carcinoma and bladder epithelial neoplasms, respectively, with specific focus on their distinguishing histopathologic features.
  • CONCLUSIONS: Pseudoneoplastic lesions in the prostate include those of prostatic epithelial origin, the most common being atrophy, adenosis (atypical adenomatous hyperplasia), basal cell hyperplasia, and crowded benign glands, as well as those of nonprostatic origin, such as seminal vesicle epithelium.
  • Such lesions often mimic lower-grade prostatic adenocarcinoma, whereas others, such as clear cell cribriform hyperplasia and granulomatous prostatitis, for example, are in the differential diagnosis of Gleason adenocarcinoma, Gleason grade 4 or 5.
  • Pseudoneoplastic lesions of the urinary bladder include lesions that could potentially be confused with urothelial carcinoma in situ, such as reactive urothelial atypia, and others, such as polypoid/papillary cystitis, where papillary urothelial neoplasms are the main differential diagnostic concern.
  • Several lesions can mimic invasive urothelial carcinoma, including pseudocarcinomatous hyperplasia, von Brunn nests, and nephrogenic adenoma.
  • [MeSH-major] Granuloma, Plasma Cell / diagnosis. Prostatic Diseases / diagnosis. Urinary Bladder Diseases / diagnosis

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  • (PMID = 20196670.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 83
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44. Bonkhoff H: [Differential diagnosis of prostate cancer: impact of pattern analysis and immunohistochemistry]. Pathologe; 2005 Nov;26(6):405-21
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  • [Title] [Differential diagnosis of prostate cancer: impact of pattern analysis and immunohistochemistry].
  • Prostate cancer offers a wide range of growth patterns depicted in the classical Gleason diagram.
  • In the present review, the use of immunohistochemical markers is discussed with emphasis to a pattern-based approach to differential diagnosis in prostate pathology.
  • Basal cell markers (34betaE12 and P63) are very useful to analyze histo-architectural features of small and large glandular lesions.
  • A number of lesions which may be confused with small acinar adenocarcinoma (Cowper's gland, nephrogenic metaplasia, mesonephric glands) and poorly differentiated prostate cancer (urothelial neoplasia, mucinous colon cancer and other metastatic lesions) lacks convincing PSA immunoreactivity.
  • Basal cell markers and the nuclear androgen receptors are important markers to differentiate Gleason grade 5 A und 5 B patterns from prostatic involvement by transitional cell carcinoma.
  • [MeSH-major] Biomarkers, Tumor / analysis. Prostate / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Carcinoma, Basal Cell / pathology. Cell Division / physiology. Diagnosis, Differential. Humans. Male. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial Neoplasia / pathology

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  • [Cites] Mod Pathol. 2004 Mar;17(3):328-48 [14976539.001]
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  • (PMID = 16205899.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 20
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45. Helpap B: [Small suggestive lesions of the prostate. Histological and immunohistochemical analyses -- report of the uropathology consultation service]. Pathologe; 2005 Nov;26(6):398-404
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Small suggestive lesions of the prostate. Histological and immunohistochemical analyses -- report of the uropathology consultation service].
  • Punch biopsies have been taken from the prostate with increasing frequency in recent years, with a resulting increase in the number of diagnoses made.
  • To check the diagnosis of "small two- or three-gland carcinoma" we prepared new H and E sections and, when the atypical glands were no longer available, also performed immunohistochemical analyses in 1,041 cases referred to our uropathology consultation service, comparing the diagnoses supplied by the referring doctors with the final diagnoses.
  • In 61.6 of these cases histology confirmed the diagnosis of adenocarcinoma of the prostate; the diagnosis recorded when the basal cell marker was absent and the tumour marker P504S was strongly expressed was atypical microglandular proliferation or suspected carcinoma.
  • Previous diagnoses of prostatic carcinoma were confirmed in 99% of cases.
  • In this way we also confirmed a further 27.9% of cases of prostate carcinoma in the grey area of diagnoses endorsed "suggestive" or "suspected".
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / analysis. Precancerous Conditions / pathology. Prostate / pathology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Biopsy. Cell Division / physiology. Cell Transformation, Neoplastic / pathology. Diagnosis, Differential. Humans. Immunoenzyme Techniques. Male. Prostatic Hyperplasia / pathology. Referral and Consultation

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  • (PMID = 16163479.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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46. Ma X, Ziel-van der Made AC, Autar B, van der Korput HA, Vermeij M, van Duijn P, Cleutjens KB, de Krijger R, Krimpenfort P, Berns A, van der Kwast TH, Trapman J: Targeted biallelic inactivation of Pten in the mouse prostate leads to prostate cancer accompanied by increased epithelial cell proliferation but not by reduced apoptosis. Cancer Res; 2005 Jul 1;65(13):5730-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted biallelic inactivation of Pten in the mouse prostate leads to prostate cancer accompanied by increased epithelial cell proliferation but not by reduced apoptosis.
  • The PTEN tumor suppressor gene is frequently inactivated in human tumors, including prostate cancer.
  • Based on the Cre/loxP system, we generated a novel mouse prostate cancer model by targeted inactivation of the Pten gene.
  • In this model, Cre recombinase was expressed under the control of the prostate-specific antigen (PSA) promoter.
  • Conditional biallelic and monoallelic Pten knock-out mice were viable and Pten recombination was prostate-specific.
  • A slightly increased proliferation rate of epithelial cells was observed in all prostate lobes of monoallelic Pten knock-out mice (PSA-Cre;Pten-loxP/+), but minimal pathologic changes were detected.
  • All homozygous knock-out mice (PSA-Cre;Pten-loxP/loxP) showed an increased size of the luminal epithelial cells, large areas of hyperplasia, focal prostate intraepithelial neoplasia lesions and an increased prostate weight at 4 to 5 months.
  • More extensive prostate intraepithelial neoplasia and focal microinvasion occurred at 7 to 9 months; invasive prostate carcinoma was detected in all male PSA-Cre;Pten-loxP/loxP mice at 10 to 14 months.
  • In hyperplastic and tumor cells, expression of luminal epithelial cell cytokeratins was up-regulated; tumor cells were negative for basal epithelial cell cytokeratins.
  • [MeSH-minor] Age Factors. Alleles. Animals. Cell Growth Processes / genetics. Epithelial Cells / pathology. Epithelial Cells / physiology. Gene Expression Regulation, Neoplastic. Gene Silencing. Male. Mice. Mice, Knockout. PTEN Phosphohydrolase. Phosphorylation. Prostatic Hyperplasia / genetics. Prostatic Hyperplasia / pathology. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt


47. Hameed O, Humphrey PA: Immunohistochemistry in diagnostic surgical pathology of the prostate. Semin Diagn Pathol; 2005 Feb;22(1):88-104
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemistry in diagnostic surgical pathology of the prostate.
  • Immunohistochemistry (IHC) can play an important role in diagnostic surgical pathology of the prostate.
  • Basal cell markers, such as the 34betaE12 antibody and antibodies directed against cytokeratin 5 and 6 or p63, are very useful for demonstration of basal cells as their presence argues against a diagnosis of invasive prostatic carcinoma (PC).
  • However, several benign mimickers of PC, including atrophy, atypical adenomatous hyperplasia (AAH), nephrogenic adenoma, and mesonephric hyperplasia, can stain negatively with these markers, and thus, a negative basal cell marker immunostain alone does not exclude a diagnosis of benignancy.
  • Although there are examples in the literature of high grade PC that stain focally with some of the basal cell markers, these cases are usually readily diagnosed based on H&E appearances and are unlikely to be confused with these benign mimickers.
  • The use of AMACR/basal cell antibody cocktails has been found to greatly facilitate the distinction between PC and its benign mimickers, especially when only limited tissue is available for staining.
  • Prostate specific antigen (PSA) and prostate specific acid phosphatase (PSAP) are both quite sensitive and fairly specific markers of PC (there are a few nonprostatic tumors that can express one or both), and are both very helpful in establishing or confirming the diagnosis of PC when the differential diagnosis includes other tumors that can involve the prostate such as urinary bladder urothelial carcinoma.
  • AMACR positivity and negative basal cell marker reactions are useful to confirm the presence of residual PC after hormonal or radiation therapy.
  • PSA and PSAP immunohistochemical stains are valuable in confirming metastatic carcinoma as being of prostatic origin and should always be utilized in the diagnostic evaluation of metastatic adenocarcinoma of unknown primary origin in males.
  • [MeSH-major] Carcinoma / diagnosis. Immunohistochemistry. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Biomarkers, Tumor / analysis. Carcinoma, Small Cell / diagnosis. Carcinoma, Small Cell / pathology. Diagnosis, Differential. Humans. Leukemia / diagnosis. Lymphoma / diagnosis. Male. Neoplasm Metastasis. Sarcoma / diagnosis. Sensitivity and Specificity. Urinary Bladder Neoplasms / diagnosis

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  • (PMID = 16512601.001).
  • [ISSN] 0740-2570
  • [Journal-full-title] Seminars in diagnostic pathology
  • [ISO-abbreviation] Semin Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 192
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48. Kuroda N, Katto K, Tamura M, Shiotsu T, Nakamura S, Ohtsuki Y, Hes O, Michal M, Inoue K, Ohara M, Mizuno K, Lee GH: Immunohistochemical application of D2-40 as basal cell marker in evaluating atypical small acinar proliferation of initial routine prostatic needle biopsy materials. Med Mol Morphol; 2010 Sep;43(3):165-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical application of D2-40 as basal cell marker in evaluating atypical small acinar proliferation of initial routine prostatic needle biopsy materials.
  • D2-40 has been recently discovered as a lymphatic endothelial cell marker, and some investigators have found that D2-40 is also expressed in myoepithelial cells of salivary gland or breast.
  • In this study, we evaluated D2-40 expression of basal cells and applied D2-40 immunohistochemistry in the combination of P504S, cytokeratin 5, and p63 for ten lesions with atypical small acinar proliferation (ASAP) in initial prostatic needle biopsy.
  • As a result, D2-40 was expressed in basal cells, lymphatic endothelial cells, and some stromal fibroblasts of normal prostatic tissue.
  • D2-40 was comparable to cytokeratin 5 and p63 as a basal cell marker, and there were no lesions that failed to provide an accurate final diagnosis using only D2-40 immunohistochemistry without cytokeratin 5 or p63.
  • Pathologists should pay attention to avoid recognizing these cells as basal cells.
  • [MeSH-major] Antibodies, Monoclonal / analysis. Biomarkers, Tumor / analysis. Carcinoma, Acinar Cell / diagnosis. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Aged, 80 and over. Antibodies, Monoclonal, Murine-Derived. Biopsy, Needle. Early Diagnosis. Humans. Immunohistochemistry. Keratin-5 / isolation & purification. Male. Membrane Proteins / isolation & purification. Middle Aged. Prostate / pathology. Racemases and Epimerases / isolation & purification. Sensitivity and Specificity

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  • (PMID = 20857265.001).
  • [ISSN] 1860-1499
  • [Journal-full-title] Medical molecular morphology
  • [ISO-abbreviation] Med Mol Morphol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Keratin-5; 0 / Membrane Proteins; 0 / monoclonal antibody D2-40; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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49. Yu T, Zhu SX, Zheng S, Chen SP: [Detection of AMACR (P504S), P63 and 34betaE12 cocktail in the early diagnosis of prostate cancer]. Zhonghua Nan Ke Xue; 2007 Mar;13(3):222-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Detection of AMACR (P504S), P63 and 34betaE12 cocktail in the early diagnosis of prostate cancer].
  • OBJECTIVE: To investigate the value of detection of AMACR (P504S), P63 and 34betaE12 cocktail in the early diagnosis of prostate cancer (PCa).
  • METHODS: The expressions of AMACR, P63 and 34betaE12 were examined in the biopsy specimens of 42 cases of prostate cancer, 12 cases of high-grade prostatic intraepithelial neoplasia (HGPIN) and 30 cases of benign prostatic hyperplasia (BPH) using the Maxvision single-step immunohistochemical method with triple-antibody cocktail (AMACR/P63/34betaE12) staining and double-color chromogens in single paraffin sections .
  • P63 and 34betaE12 cocktail staining can increase the sensitivity and specificity of the basal cell detection.
  • The immunohistochemical analysis with triple-antibody cocktail (AMACR/P63/34betaE12) staining and double-color chromogens can improve diagnostic accuracy and has an important applied value for the early diagnosis of prostate cancer.
  • [MeSH-minor] Aged. Carcinoma, Basal Cell / diagnosis. Carcinoma, Basal Cell / metabolism. Early Diagnosis. Humans. Immunohistochemistry. Male. Middle Aged. Prostatic Hyperplasia / diagnosis. Prostatic Hyperplasia / metabolism

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  • (PMID = 17393784.001).
  • [ISSN] 1009-3591
  • [Journal-full-title] Zhonghua nan ke xue = National journal of andrology
  • [ISO-abbreviation] Zhonghua Nan Ke Xue
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CK-34 beta E12; 0 / CKAP4 protein, human; 0 / Membrane Proteins; 68238-35-7 / Keratins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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50. Pearson HB, Phesse TJ, Clarke AR: K-ras and Wnt signaling synergize to accelerate prostate tumorigenesis in the mouse. Cancer Res; 2009 Jan 01;69(1):94-101
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  • [Title] K-ras and Wnt signaling synergize to accelerate prostate tumorigenesis in the mouse.
  • Aberrant Ras and Wnt signaling are emerging as key events in the multistep nature of prostate tumorigenesis and progression.
  • Here, we report the generation of a compound model of prostate cancer to define the synergism of activated K-ras (K-ras(+/V12)) and dominant stabilized beta-catenin (Catnb(+/lox(ex3))) in the murine prostate.
  • Concomitant with elevated mitogen-activated protein kinase (MAPK) signaling, PBCre(+)K-ras(+/V12) mice developed AH at 100 days (100% incidence) and low-grade prostate intraepithelial neoplasia and adenocarcinoma (60% and 7% incidence) by 500 days.
  • These lesions displayed elevated Wnt signaling and basal levels of MAPK signaling.
  • Synchronous activation of K-ras and beta-catenin significantly reduced survival (average 189 days), reflecting accelerated tumorigenesis and the development of invasive carcinoma that displayed activated Wnt and MAPK signaling.
  • Notably, expression of the basal cell marker p63 negatively correlated with tumor grade, resembling human prostate adenocarcinoma.
  • Taken together, our data show that combinatorial oncogenic mutations of K-ras and beta-catenin drive rapid progression of prostate tumorigenesis to invasive carcinoma, characterized by the synergistic elevation of androgen receptor, cyclooxygenase-2, and c-Myc.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Prostatic Neoplasms / metabolism. Wnt Proteins / metabolism. ras Proteins / metabolism

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  • (PMID = 19117991.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0301154
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / Myc protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptors, Androgen; 0 / Wnt Proteins; 0 / beta Catenin; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.6.5.2 / ras Proteins
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51. Samaratunga H, Delahunt B: Ductal adenocarcinoma of the prostate: current opinion and controversies. Anal Quant Cytol Histol; 2008 Aug;30(4):237-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ductal adenocarcinoma of the prostate: current opinion and controversies.
  • OBJECTIVE: To evaluate the morphologic spectrum and clinical significance of ductal adenocarcinoma of the prostate (DAP).
  • DAP is found in both the periurethral region and peripheral zone of the prostate and is considered high grade in the modified Gleason grading system.
  • Immunostaining for prostatic-specific antigen and prostate-specific acid phosphatase is present in these tumors, a high percentage of which overexpress alpha-methylacyl-coenzyme A racemase.
  • A basal cell layer can be seen in some of these tumors, which is probably due to tumor growth into preexisting ducts.
  • This usually represents an advanced stage of tumor progression and is not a precursor of invasive carcinoma.
  • The term ductal carcinoma is also inappropriate because this includes some urothelial carcinomas of ductal origin.

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  • (PMID = 18773743.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 36
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52. Nithipatikom K, Brody DM, Tang AT, Manthati VL, Falck JR, Williams CL, Campbell WB: Inhibition of carcinoma cell motility by epoxyeicosatrienoic acid (EET) antagonists. Cancer Sci; 2010 Dec;101(12):2629-36
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  • [Title] Inhibition of carcinoma cell motility by epoxyeicosatrienoic acid (EET) antagonists.
  • Cytochrome P450 (CYP) epoxygenases, CYP2C8, 2C9 and 2J2 mRNA and proteins, were expressed in prostate carcinoma (PC-3, DU-145 and LNCaP) cells.
  • Blocking EET synthesis by a selective CYP epoxygenase inhibitor (N-methylsulfonyl-6-(2-propargyloxyphenyl)hexanamide [MS-PPOH]) inhibited tonic (basal) invasion and migration (motility) while exogenously added EET induced cell motility in a concentration-dependent manner.
  • An epidermal growth factor receptor (EGFR) kinase inhibitor (AG494) or a PI3 kinase inhibitor (LY294002) inhibited cell migration and reduced 11,12-EET-induced cell migration.
  • Importantly, synthetic EET antagonists (14,15-epoxyeicosa-5(Z)-enoic acid [14,15-EEZE], 14,15-epoxyeicosa-5(Z)-enoic acid 2-[2-(3-hydroxy-propoxy)-ethoxy]-ethyl ester [14,15-EEZE-PEG] and 14,15-epoxyeicosa-5(Z)-enoic-methylsulfonylimide [14,15-EEZE-mSI]) inhibited EET-induced cell invasion and migration.
  • 11,12-EET induced cell stretching and myosin-actin microfilament formation as well as increased phosphorylation of EGFR and Akt (Ser473), while 14,15-EEZE inhibited these effects.
  • These results suggest that EET induce and EET antagonists inhibit cell motility, possibly by putative EET receptor-mediated EGFR and PI3K/Akt pathways, and suggest that EET antagonists are potential therapeutic agents for prostate cancer.

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  • [Copyright] © 2010 Japanese Cancer Association.
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  • (PMID = 20804500.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL051055; United States / NHLBI NIH HHS / HL / HL-51055; United States / NIGMS NIH HHS / GM / GM-31278; United States / NIDDK NIH HHS / DK / P01 DK038226; United States / NCI NIH HHS / CA / R01 CA136799; United States / NCI NIH HHS / CA / CA-136799; United States / NIGMS NIH HHS / GM / GM-069700; United States / NIGMS NIH HHS / GM / R01 GM031278; United States / NIGMS NIH HHS / GM / R01 GM069700
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 14,15-eicosa-5-enoic acid; 0 / RNA, Messenger; 7324-41-6 / 8,11,14-Eicosatrienoic Acid; 81276-02-0 / 11,12-epoxy-5,8,14-eicosatrienoic acid; 9035-51-2 / Cytochrome P-450 Enzyme System
  • [Other-IDs] NLM/ NIHMS383023; NLM/ PMC3398840
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53. Huang X, Zhu D, Lou Y: A novel anticancer agent, icaritin, induced cell growth inhibition, G1 arrest and mitochondrial transmembrane potential drop in human prostate carcinoma PC-3 cells. Eur J Pharmacol; 2007 Jun 14;564(1-3):26-36
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  • [Title] A novel anticancer agent, icaritin, induced cell growth inhibition, G1 arrest and mitochondrial transmembrane potential drop in human prostate carcinoma PC-3 cells.
  • We screened their effects on cell growth in human prostate carcinoma PC-3 cell line (estrogen receptor positive) in vitro.
  • PC-3 cell line was used for the measurement of anti-carcinoma activities of 0-100 micromol/l icaritin and 30 micromol/l icariin.
  • Primary cultured rat prostate basal cells used as cell growth selective control.
  • When treated with icaritin for 24 to 72 h, cell growth was strongly inhibited (at 48 h IC(50) was 10.74+/-1.59 micromol/l, P<0.001) companied with a mitochondrial transmembrane potential (_Psim) drop.
  • These findings suggested a novel anticancer efficacy of icaritin mediated selectively via induction of cell cycle arrest but not associated with estrogen receptors in PC-3 cells.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma / drug therapy. Flavonoids / pharmacology. G1 Phase / drug effects. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Cycle Proteins / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Estradiol / pharmacology. Flow Cytometry. G2 Phase / drug effects. Humans. Immunoblotting. Inhibitory Concentration 50. Male. Membrane Potential, Mitochondrial / drug effects

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  • (PMID = 17382317.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Cell Cycle Proteins; 0 / Flavonoids; 0 / icaritin; 489-32-7 / icariin; 4TI98Z838E / Estradiol
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54. Jarry H, Stromeier S, Wuttke W, Nahrstedt A: Petasiphenone, a phenol isolated from Cimicifuga racemosa, in vitro inhibits proliferation of the human prostate cancer cell line LNCaP. Planta Med; 2007 Feb;73(2):184-7
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  • [Title] Petasiphenone, a phenol isolated from Cimicifuga racemosa, in vitro inhibits proliferation of the human prostate cancer cell line LNCaP.
  • ) (CR) inhibit the proliferation of the human prostate cancer cell line LNCaP.
  • & Zucc. which inhibits the growth of various human leukemia cell lines.
  • Because of the structural similarity, we examined whether 1 affects the proliferation of LNCaP cells and the secretion of prostate-specific antigen (PSA).
  • Under basal conditions as well as under co-incubation with 10 nM estradiol [E2 or 1 nM dihydrotestosterone (DHT)], 1 dose-dependently inhibited proliferation of LNCaP cells while PSA release per cell was not altered.
  • We report for the first time that a defined compound isolated from CR inhibits the growth of the human prostate cancer cells LNCaP.
  • [MeSH-minor] Carcinoma / drug therapy. Carcinoma / pathology. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Male. Plant Extracts / chemistry

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  • (PMID = 17295185.001).
  • [ISSN] 0032-0943
  • [Journal-full-title] Planta medica
  • [ISO-abbreviation] Planta Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 3,4-dihydroxyphenacyl caffeate phenylpropanoid ester; 0 / Antineoplastic Agents, Phytogenic; 0 / Caffeic Acids; 0 / Phenols; 0 / Plant Extracts
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55. Lopez-Beltran A, Qian J, Montironi R, Luque RJ, Bostwick DG: Atypical adenomatous hyperplasia (adenosis) of the prostate: DNA ploidy analysis and immunophenotype. Int J Surg Pathol; 2005 Apr;13(2):167-73
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  • [Title] Atypical adenomatous hyperplasia (adenosis) of the prostate: DNA ploidy analysis and immunophenotype.
  • Atypical adenomatous hyperplasia (AAH) of the prostate is a microscopic proliferation of small acini that may be mistaken for adenocarcinoma.
  • There were rare scattered immunoreactive cells for chromogranin, bcl-2, and c-erbB-2 in nodular hyperplasia and AAH (mainly in the basal cell compartment) and in carcinoma.
  • The ki67-MIB1 labeling index was different between nodular hyperplasia and AAH (p<0.001) and carcinoma (p=0.003) but not between AAH and carcinoma (p=0.203).
  • Microvessel density was different between AAH and carcinoma (p=0.001) but not between nodular hyperplasia and AAH (p=0.105) or carcinoma (p=0.0820).
  • All foci of nodular hyperplasia, AAH, and carcinoma were diploid.

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  • (PMID = 15864380.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm
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56. D'Anello L, Sansone P, Storci G, Mitrugno V, D'Uva G, Chieco P, Bonafé M: Epigenetic control of the basal-like gene expression profile via Interleukin-6 in breast cancer cells. Mol Cancer; 2010;9:300
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  • [Title] Epigenetic control of the basal-like gene expression profile via Interleukin-6 in breast cancer cells.
  • BACKGROUND: Basal-like carcinoma are aggressive breast cancers that frequently carry p53 inactivating mutations, lack estrogen receptor-α (ERα) and express the cancer stem cell markers CD133 and CD44.
  • CONCLUSION: We conclude that IL-6, whose methylation-dependent autocrine loop is triggered by the inactivation of p53, induces an epigenetic reprogramming that drives breast carcinoma cells towards a basal-like/stem cell-like gene expression profile.
  • [MeSH-minor] Antigens, CD / genetics. Antigens, CD / metabolism. Antigens, CD44 / genetics. Antigens, CD44 / metabolism. Blotting, Western. Cell Line, Tumor. DNA Methylation / drug effects. DNA Methylation / genetics. DNA Methylation / physiology. Enzyme-Linked Immunosorbent Assay. Estrogen Receptor alpha / genetics. Estrogen Receptor alpha / metabolism. Female. Fluorescent Antibody Technique. Glycoproteins / genetics. Glycoproteins / metabolism. Humans. Peptides / genetics. Peptides / metabolism. RNA Interference. RNA, Messenger. Reverse Transcriptase Polymerase Chain Reaction. Tumor Suppressor Protein p53 / metabolism


57. Varma M, Jasani B: Diagnostic utility of immunohistochemistry in morphologically difficult prostate cancer: review of current literature. Histopathology; 2005 Jul;47(1):1-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic utility of immunohistochemistry in morphologically difficult prostate cancer: review of current literature.
  • Varma M & Jasani B (2005) Histopathology47, 1-16 Diagnostic utility of immunohistochemistry in morphologically difficult prostate cancer: review of current literatureImmunohistochemistry is widely used to distinguish prostate cancer from benign mimics and to establish the prostatic origin of poorly differentiated carcinoma.
  • We critically review the recent advances in prostate cancer immunohistochemistry, including the introduction of newer basal cell markers such as p63 and the discovery of the overexpression of alpha-methylacyl coenzyme A racemase (AMACR) in prostate cancer.
  • The description of newer urothelial markers to aid the distinction of prostate cancer from urothelial carcinoma is also presented together with refinements in the quality control of PSA and PSAP immunostaining.
  • Although AMACR is a useful immunohistochemical marker for prostate cancer, it has significant limitations.
  • These limitations are discussed and the need for interpreting AMACR immunoreactivity in the appropriate morphological context and in conjunction with basal call markers is emphasized.
  • We also describe the utility of an immunohistochemical panel composed of PSA, PSAP and high molecular weight cytokeratin for distinguishing poorly differentiated prostate cancer from high-grade urothelial carcinoma.
  • A morphological differential diagnosis based selection of immunohistochemical markers is highlighted as a novel approach in the diagnosis of prostate cancer in routine surgical pathology practice.
  • [MeSH-minor] Biomarkers, Tumor. Diagnosis, Differential. Humans. Male. Prostate / chemistry. Prostate / pathology. Sensitivity and Specificity


58. Wang Y, Revelo MP, Sudilovsky D, Cao M, Chen WG, Goetz L, Xue H, Sadar M, Shappell SB, Cunha GR, Hayward SW: Development and characterization of efficient xenograft models for benign and malignant human prostate tissue. Prostate; 2005 Jul 1;64(2):149-59
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  • [Title] Development and characterization of efficient xenograft models for benign and malignant human prostate tissue.
  • BACKGROUND: Various research groups have attempted to grow fresh, histologically intact human prostate cancer tissues in immunodeficient mice.
  • Furthermore, xenografts could only be established using high-grade, advanced stage, but not low- or moderate-grade prostate cancer tissues.
  • METHODS: This paper describes methods for xenografting both benign and malignant human prostate tissue to severe combined immunodeficient (SCID) mice.
  • Grafted benign tissues in all sites appropriately expressed AR, PSA, cytokeratins 8, 18, and 14 as well as p63; carcinoma tissues did not express the basal cell markers.
  • CONCLUSIONS: These data suggest that sub-renal capsule and orthotopic grafting of human prostate tissue can be used for many basic scientific and translational studies.
  • [MeSH-major] Neoplasm Transplantation. Prostate / pathology. Prostatic Hyperplasia / pathology. Prostatic Neoplasms / pathology. Transplantation, Heterologous

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • [CommentIn] Asian J Androl. 2014 May-Jun;16(3):407-12 [24589467.001]
  • (PMID = 15678503.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA89520; United States / NCI NIH HHS / CA / CA96403; United States / NIDDK NIH HHS / DK / DK063587; United States / NCI NIH HHS / CA / P30 CA68485
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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59. Yaskiv O, Cao D, Humphrey PA: Microcystic adenocarcinoma of the prostate: a variant of pseudohyperplastic and atrophic patterns. Am J Surg Pathol; 2010 Apr;34(4):556-61
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  • [Title] Microcystic adenocarcinoma of the prostate: a variant of pseudohyperplastic and atrophic patterns.
  • Cystic change in adenocarcinoma of the prostate is unusual and may be confused with benign cystic atrophy.
  • The aim of this study was to assess histologic and immunohistologic characteristics of microcystic adenocarcinoma of the prostate.
  • This alteration was defined as cystic dilatation and rounded expansion of the malignant gland profile, with a flat luminal cell lining layer.
  • Ninety-six percent of the microcystic cases showed alpha-methylacyl CoA racemase overexpression and all cases showed complete basal cell loss (using 34betaE12 and p63 antibodies) in immunohistochemistry.
  • Microcystic adenocarcinoma of the prostate is a distinctive histomorphologic presentation of prostatic adenocarcinoma that is deceptively benign-looking at low magnifications.
  • Detection of intraluminal crystalloids or wispy blue mucin at low magnification, immunostains for alpha-methylacyl CoA racemase, and basal cells, and a search for adjacent usual small acinar adenocarcinoma are helpful diagnostic aids.
  • Diagnostic awareness of this growth pattern of prostatic carcinoma is important to avoid underdiagnosis of adenocarcinoma of the prostate.
  • [MeSH-major] Adenocarcinoma / pathology. Prostate / pathology. Prostatic Hyperplasia / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 20216381.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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60. Pascal LE, True LD, Campbell DS, Deutsch EW, Risk M, Coleman IM, Eichner LJ, Nelson PS, Liu AY: Correlation of mRNA and protein levels: cell type-specific gene expression of cluster designation antigens in the prostate. BMC Genomics; 2008 May 23;9:246
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  • [Title] Correlation of mRNA and protein levels: cell type-specific gene expression of cluster designation antigens in the prostate.
  • BACKGROUND: : Expression levels of mRNA and protein by cell types exhibit a range of correlations for different genes.
  • In this study, we compared levels of mRNA abundance for several cluster designation (CD) genes determined by gene arrays using magnetic sorted and laser-capture microdissected human prostate cells with levels of expression of the respective CD proteins determined by immunohistochemical staining in the major cell types of the prostate - basal epithelial, luminal epithelial, stromal fibromuscular, and endothelial - and for prostate precursor/stem cells and prostate carcinoma cells.
  • Immunohistochemical stains of prostate tissues from more than 50 patients were scored for informative CD antigen expression and compared with cell-type specific transcriptomes.

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  • (PMID = 18501003.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK63630; United States / NCI NIH HHS / CA / CA98699; United States / PHS HHS / / PM50 GMO76547; United States / NIDDK NIH HHS / DK / U01 DK063630; United States / NCI NIH HHS / CA / P01 CA085859; United States / NCI NIH HHS / CA / R21 CA098699; United States / NIGMS NIH HHS / GM / P50 GM076547; United States / NIDDK NIH HHS / DK / R01 DK069690; United States / NIDDK NIH HHS / DK / DK069690; United States / NCI NIH HHS / CA / CA111244; United States / NCI NIH HHS / CA / CA85859; United States / NCI NIH HHS / CA / U01 CA111244
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / RNA, Messenger; 0 / RNA, Neoplasm
  • [Other-IDs] NLM/ PMC2413246
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61. Cavalcanti Fde B, Alves VA, Pereira J, Kanamura CT, Wakamatsu A, Saldanha LB: Proliferative lesions of prostate: a multivariate approach to differential diagnosis. Pathol Oncol Res; 2005;11(2):103-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proliferative lesions of prostate: a multivariate approach to differential diagnosis.
  • Of these parameters, seven (glandular fusion, crystalloids, nucleolomegaly, papillary architecture, visibility of basal cell layer, areas of normal luminal cell nucleus/cytoplasm ratio and areas of high luminal cell nucleus/cytoplasm ratio) remained significant in discriminating the groups.
  • Multivariate analysis selected a small panel of histological features as those most helpful in the differential diagnosis of proliferative lesions in prostate biopsies.
  • [MeSH-major] Adenocarcinoma / diagnosis. Carcinoma, Acinar Cell / diagnosis. Prostatic Intraepithelial Neoplasia / diagnosis. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Biopsy, Needle. Cell Proliferation. Diagnosis, Differential. Humans. Male

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  • (PMID = 15999155.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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62. Kido T, Hatakeyama S, Ohyama C, Lau YF: Expression of the Y-Encoded TSPY is Associated with Progression of Prostate Cancer. Genes (Basel); 2010;1(2):283-93

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of the Y-Encoded TSPY is Associated with Progression of Prostate Cancer.
  • TSPY is a Y-encoded gene that is expressed in normal testicular germ cells and various cancer types including germ cell tumor, melanoma, hepatocellular carcinoma, and prostate cancer.
  • To establish such correlation, we analyzed the expression of TSPY, in reference to its interactive oncoprotein, EEF1A, tumor biomarker, AMACR, and normal basal cell biomarker, p63, in 41 cases of clinical prostate cancers (CPCa), 17 cases of latent prostate cancers (LPCa), and 19 cases of non-cancerous prostate (control) by immunohistochemistry.
  • Our results show that TSPY was detected more frequently (78%) in the clinical prostate cancer specimens than those of latent prostate cancer (47%) and control (50%).
  • The expression of the TSPY binding partner EEF1A was detectable in all prostate specimens, but the levels were higher in cancer cells in clinical and latent prostate cancer specimens than normal prostatic cells.
  • These observations suggest that expressions of TSPY and its binding partner EEF1A are associated with the development and progression of prostate cancer.

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  • (PMID = 24710046.001).
  • [ISSN] 2073-4425
  • [Journal-full-title] Genes
  • [ISO-abbreviation] Genes (Basel)
  • [Language] eng
  • [Grant] United States / BLRD VA / BX / I01 BX000865
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC3954091
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63. Uphoff J, Woziwodzki J, Schattka SO, Kollias A: [Loss of differentiation of a prostate adenocarcinoma after hormone therapy: the example of a metastasis in the spongy body of the penis]. Aktuelle Urol; 2008 Sep;39(5):373-7
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  • [Title] [Loss of differentiation of a prostate adenocarcinoma after hormone therapy: the example of a metastasis in the spongy body of the penis].
  • Prostate cancer as the most frequent malignoma of the male is the main primary lesion.
  • Changes in the morphology of the prostate carcinoma are specially known for the occurrence of small-cell neuroendocrine and undifferentiated carcinomas.
  • [MeSH-major] Adenocarcinoma / secondary. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma, Basal Cell / secondary. Carcinoma, Transitional Cell / secondary. Cell Transformation, Neoplastic / pathology. Diphosphonates / therapeutic use. Gonadotropin-Releasing Hormone / antagonists & inhibitors. Neoplasms, Multiple Primary / drug therapy. Penile Neoplasms / secondary. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biopsy. Bone Neoplasms / drug therapy. Bone Neoplasms / pathology. Bone Neoplasms / secondary. Bone Neoplasms / surgery. Combined Modality Therapy. Cystectomy. Diagnosis, Differential. Disease Progression. Humans. Lymphatic Metastasis. Male. Neoplasm Staging. Penis / pathology. Penis / surgery. Prostate / pathology. Prostate / surgery. Prostatectomy

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  • (PMID = 18798127.001).
  • [ISSN] 0001-7868
  • [Journal-full-title] Aktuelle Urologie
  • [ISO-abbreviation] Aktuelle Urol
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Diphosphonates; 33515-09-2 / Gonadotropin-Releasing Hormone
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64. Nanni S, Priolo C, Grasselli A, D'Eletto M, Merola R, Moretti F, Gallucci M, De Carli P, Sentinelli S, Cianciulli AM, Mottolese M, Carlini P, Arcelli D, Helmer-Citterich M, Gaetano C, Loda M, Pontecorvi A, Bacchetti S, Sacchi A, Farsetti A: Epithelial-restricted gene profile of primary cultures from human prostate tumors: a molecular approach to predict clinical behavior of prostate cancer. Mol Cancer Res; 2006 Feb;4(2):79-92
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  • [Title] Epithelial-restricted gene profile of primary cultures from human prostate tumors: a molecular approach to predict clinical behavior of prostate cancer.
  • The histopathologic and molecular heterogeneity of prostate cancer and the limited availability of human tumor tissue make unraveling the mechanisms of prostate carcinogenesis a challenging task.
  • Our goal was to develop an ex vivo model that could be reliably used to define a prognostic signature based on gene expression profiling of cell cultures that maintained the tumor phenotype.
  • To this end, we derived epithelial cultures from tissue explanted from 59 patients undergoing radical prostatectomy or cistoprostatectomy because of prostate benign hyperplasia/prostate cancer or bladder carcinoma.
  • Cultures from normal/hyperplastic tissues with a prevalent luminal phenotype and from normal prostate epithelial tissue with basal phenotype (PrEC) served as controls.
  • We have established a large number of prostate primary cultures highly enriched in the secretory phenotype.
  • Our findings provide (a) a method to expand human primary prostate carcinoma cells with a luminal phenotype, (b) a powerful experimental model to study primary prostate cancer biology, and (c) a novel means to characterize these tumors from a molecular genetic standpoint for prognostic and/or predictive purposes.
  • [MeSH-minor] Aged. Cell Differentiation. Cells, Cultured. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Oligonucleotide Array Sequence Analysis. Phenotype. Prognosis. Prostate / metabolism. Prostatectomy. Prostatic Hyperplasia / genetics. Prostatic Hyperplasia / pathology. Tumor Cells, Cultured

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  • (PMID = 16513839.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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65. Levi F, Randimbison L, Te VC, Conconi MM, La Vecchia C: Risk of prostate, breast and colorectal cancer after skin cancer diagnosis. Int J Cancer; 2008 Dec 15;123(12):2899-901
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  • [Title] Risk of prostate, breast and colorectal cancer after skin cancer diagnosis.
  • Ultraviolet radiation is the major cause of skin cancer, but promotes vitamin D synthesis, and vitamin D has been inversely related to the risk of several common cancers including prostate, breast and colorectum.
  • We therefore computed the incidence of prostate, breast and colorectal cancer following skin cancer using the datasets of the Swiss cancer Registries of Vaud and Neuchâtel.
  • Between 1974 and 2005, 6,985 histologically confirmed squamous cell skin cancers, 21,046 basal cell carcinomas and 3,346 cutaneous malignant melanomas were registered, and followed up to the end of 2005 for the occurrence of second primary cancer of the prostate, breast and colorectum.
  • Overall, 680 prostate cancers were observed versus 568.3 expected (standardized incidence ratio (SIR) = 1.20; 95% confidence interval (CI): 1.11-1.29), 440 breast cancers were observed versus 371.5 expected (SIR = 1.18; 95% CI: 1.08-1.30) and 535 colorectal cancers were observed versus 464.6 expected (SIR = 1.15; 95% CI: 1.06-1.25).
  • When basal cell, squamous cell and skin melanoma were considered separately, all the SIRs for prostate, breast and colorectal cancers were around or slightly above unity.
  • These findings, based on a population with a long tradition of systematic histologic examination of all surgically treated skin lesions, do not support the hypothesis that prostate, breast and colorectal cancer risk is decreased following skin cancer.
  • [MeSH-minor] Adult. Aged. Carcinoma, Basal Cell / epidemiology. Carcinoma, Squamous Cell / epidemiology. Female. Humans. Incidence. Male. Melanoma / epidemiology. Middle Aged. Odds Ratio. Registries. Risk Assessment. Risk Factors. Switzerland / epidemiology


66. Harvey AM, Grice B, Hamilton C, Truong LD, Ro JY, Ayala AG, Zhai QJ: Diagnostic utility of P504S/p63 cocktail, prostate-specific antigen, and prostatic acid phosphatase in verifying prostatic carcinoma involvement in seminal vesicles: a study of 57 cases of radical prostatectomy specimens of pathologic stage pT3b. Arch Pathol Lab Med; 2010 Jul;134(7):983-8
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  • [Title] Diagnostic utility of P504S/p63 cocktail, prostate-specific antigen, and prostatic acid phosphatase in verifying prostatic carcinoma involvement in seminal vesicles: a study of 57 cases of radical prostatectomy specimens of pathologic stage pT3b.
  • CONTEXT: Seminal vesicle invasion by prostatic carcinoma is directly associated with tumor staging; verification is challenging when the tumor demonstrates cribriform or papillary growth patterns or there are back-to-back small-gland proliferations.
  • P504S is overexpressed in prostatic carcinoma and high-grade prostatic intraepithelial neoplasia with cytoplasmic immunoreactivity. p63 has positive immunoreactivity in basal cell nuclei of benign prostatic glands.
  • OBJECTIVE: To evaluate the usefulness of a single-color P504S/p63 cocktail immunostain in verifying prostatic carcinoma within the seminal vesicle.
  • DESIGN: Sections from 57 radical prostatectomy specimens of pathologic stage pT3b that contain seminal vesicle with prostatic carcinoma involvement were immunostained with primary antibodies against prostate-specific antigen (PSA) and prostatic acid phosphatase (PAP) and a cocktail of antibodies against P504S and p63.
  • RESULTS: Prostatic carcinoma cells from all 57 cases were diffusely positive for P504S, PSA, and PAP with cytoplasmic staining and no p63 nuclear staining.
  • Seminal vesicle epithelium from all 57 cases was negative for all 3 markers with distinct p63 nuclear staining of the basal cells.
  • CONCLUSIONS: The P504S/p63 one-color cocktail is a practical and cost-effective stain to differentiate prostatic carcinoma that involves the seminal vesicle from seminal vesicle epithelium.
  • [MeSH-major] Carcinoma / diagnosis. Membrane Proteins / analysis. Prostate-Specific Antigen / analysis. Prostatic Neoplasms / diagnosis. Protein Tyrosine Phosphatases / analysis. Racemases and Epimerases / analysis. Seminal Vesicles / chemistry
  • [MeSH-minor] Acid Phosphatase. Cost-Benefit Analysis. Humans. Immunohistochemistry / economics. Immunohistochemistry / standards. Male. Neoplasm Invasiveness. Neoplasm Staging. Prostate / chemistry. Prostatectomy. Staining and Labeling / economics. Staining and Labeling / standards

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  • (PMID = 20586625.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CKAP4 protein, human; 0 / Membrane Proteins; EC 3.1.3.2 / Acid Phosphatase; EC 3.1.3.2 / prostatic acid phosphatase; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.4.21.77 / Prostate-Specific Antigen; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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67. Bühler P, Wolf P, Katzenwadel A, Schultze-Seemann W, Wetterauer U, Freudenberg N, Elsässer-Beile U: Primary prostate cancer cultures are models for androgen-independent transit amplifying cells. Oncol Rep; 2010 Feb;23(2):465-70
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  • [Title] Primary prostate cancer cultures are models for androgen-independent transit amplifying cells.
  • Numerous efforts exist for developing primary prostate cancer cultures for studying the biology of this tumor entity and for evaluation of the effectiveness of novel therapies.
  • The aim of the present study was to characterize primary outgrowing prostate epithelial cells due to their basal or luminal characteristics and their potential for serving as androgen-responsible model.
  • From fresh prostate cancer radical prostatectomy specimens, pieces of approximately 2-4 mm diameter were placed on top of transwell culture chambers, which were coated with matrigel and cultured in prostate epithelial selection medium with 10% fetal calf serum.
  • From the monolayer of the outgrowing cells, RNA was isolated and the expression of androgen receptor (AR), prostate-specific antigen (PSA), Kallikrein 2 (KlK2), prostate-specific membrane antigen (PSMA), and prostate stem cell antigen (PSCA), cytokeratin (CK)5, and CK18 was determined by realtime quantitative PCR.
  • The outgrowing cells from the prostate cancer tissue pieces could be characterized as epithelial cells with basal and transit amplifying characteristics as shown by co-expression of CK5 and CK18.
  • In all cultures, a very low expression of the luminal cell marker genes AR, PSA and KLK2 was measured.
  • Due to the co-expression of basal and luminal marker genes, primary prostate cancer cultures can be charaterized as models of transit amplifying cells of the prostatic epithelium.
  • They do not represent the differentiated secretory androgen-responsive cell phenotype.
  • [MeSH-major] Androgens / pharmacology. Carcinoma / pathology. Cell Proliferation / drug effects. Prostatic Neoplasms / pathology
  • [MeSH-minor] Androgen Antagonists / pharmacology. Antigens, Neoplasm. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Cell Culture Techniques. Cell Differentiation / drug effects. Cell Differentiation / genetics. Epithelial Cells / pathology. GPI-Linked Proteins. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Membrane Glycoproteins / genetics. Membrane Glycoproteins / metabolism. Models, Biological. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Phenotype. Receptors, Androgen / genetics. Receptors, Androgen / metabolism. Tumor Cells, Cultured


68. Suraneni MV, Schneider-Broussard R, Moore JR, Davis TC, Maldonado CJ, Li H, Newman RA, Kusewitt D, Hu J, Yang P, Tang DG: Transgenic expression of 15-lipoxygenase 2 (15-LOX2) in mouse prostate leads to hyperplasia and cell senescence. Oncogene; 2010 Jul 29;29(30):4261-75
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  • [Title] Transgenic expression of 15-lipoxygenase 2 (15-LOX2) in mouse prostate leads to hyperplasia and cell senescence.
  • 15-Lipoxygenase 2 (15-LOX2), a lipid-peroxidizing enzyme, is mainly expressed in the luminal compartment of the normal human prostate, and is often decreased or lost in prostate cancer.
  • To better understand the biological role of 15-LOX2 in vivo, we generated prostate-specific 15-LOX2 transgenic mice using the ARR2PB promoter.
  • Unexpectedly, transgenic expression of 15-LOX2 or 15-LOX2sv-b, a splice variant that lacks arachidonic acid-metabolizing activity, resulted in age-dependent prostatic hyperplasia and enlargement of the prostate.
  • Prostatic hyperplasia induced by both 15-LOX2 and 15-LOX2sv-b was associated with an increase in luminal and Ki-67(+) cells; however, 15-LOX2-transgenic prostates also showed a prominent increase in basal cells.
  • Microarray analysis revealed distinct gene expression profiles that could help explain the prostate phenotypes.
  • Strikingly, 15-LOX2, but not 15-LOX2sv-b, transgenic prostate showed upregulation of several well-known stem or progenitor cell molecules including Sca-1, Trop2, p63, Nkx3.1 and Psca.
  • Prostatic hyperplasia caused by both 15-LOX2 and 15-LOX2sv-b did not progress to prostatic intraprostate neoplasia or carcinoma and, mechanistically, prostate lobes (especially those of 15-LOX2 mice) showed a dramatic increase in senescent cells as revealed by increased SA-betagal, p27(Kip1) and heterochromatin protein 1gamma staining.
  • Collectively, our results suggest that 15-LOX2 expression in mouse prostate leads to hyperplasia and also induces cell senescence, which may, in turn, function as a barrier to tumor development.

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  • (PMID = 20514017.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01-AG023374; United States / NIA NIH HHS / AG / R01 AG023374-01A1; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIEHS NIH HHS / ES / ES015888-03; United States / NIEHS NIH HHS / ES / R01 ES015888-03; United States / NIA NIH HHS / AG / AG023374-04; United States / NIA NIH HHS / AG / R01 AG023374-03; United States / NIA NIH HHS / AG / R01 AG023374; United States / NIA NIH HHS / AG / AG023374-02; United States / NIA NIH HHS / AG / R01 AG023374-02; United States / NIEHS NIH HHS / ES / R21 ES015893-01A1; United States / NIEHS NIH HHS / ES / ES015888-01; United States / NIEHS NIH HHS / ES / R21-ES015893-01A1; United States / NIEHS NIH HHS / ES / R01-ES01588; United States / NIEHS NIH HHS / ES / R21 ES015893-02; United States / NIEHS NIH HHS / ES / P30 ES007784; United States / NIEHS NIH HHS / ES / ES015893-02; United States / NIEHS NIH HHS / ES / R01 ES015888-04; United States / NIA NIH HHS / AG / AG023374-03; United States / NIEHS NIH HHS / ES / ES07784; United States / NIEHS NIH HHS / ES / R01 ES015888-01; United States / NIEHS NIH HHS / ES / ES015888-02; United States / NIA NIH HHS / AG / R01 AG023374-05; United States / NIEHS NIH HHS / ES / R01 ES015888; United States / NIEHS NIH HHS / ES / ES015893-01A1; United States / NIEHS NIH HHS / ES / R21 ES015893; United States / NIA NIH HHS / AG / AG023374-01A1; United States / NIA NIH HHS / AG / R01 AG023374-04; United States / NIEHS NIH HHS / ES / R01 ES015888-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Ki-67 Antigen; 0 / Mki67 protein, mouse; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 1.13.11.33 / Arachidonate 15-Lipoxygenase
  • [Other-IDs] NLM/ NIHMS199837; NLM/ PMC3042242
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69. de Vries E, Soerjomataram I, Houterman S, Louwman MW, Coebergh JW: Decreased risk of prostate cancer after skin cancer diagnosis: a protective role of ultraviolet radiation? Am J Epidemiol; 2007 Apr 15;165(8):966-72
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  • [Title] Decreased risk of prostate cancer after skin cancer diagnosis: a protective role of ultraviolet radiation?
  • Ultraviolet radiation causes skin cancer but may protect against prostate cancer.
  • The authors hypothesized that skin cancer patients had a lower prostate cancer incidence than the general population.
  • In the southeastern part of the Netherlands, a population-based cohort of male skin cancer patients diagnosed since 1970 (2,620 squamous cell carcinomas, 9,501 basal cell carcinomas, and 1,420 cutaneous malignant melanomas) was followed up for incidence of invasive prostate cancer until January 1, 2005, within the framework of the Eindhoven Cancer Registry.
  • The incidence rates of prostate cancer among skin cancer patients were compared with those in the reference population, resulting in standardized incidence ratios.
  • Skin cancer patients were at decreased risk of developing prostate cancer compared with the general population (standardized incidence ratio (SIR) = 0.89, 95% confidence interval (CI): 0.78, 0.99), especially shortly after diagnosis.
  • The risk of advanced prostate cancer was significantly decreased (SIR = 0.73, 95% CI: 0.56, 0.94), indicating a possible antiprogression effect of ultraviolet radiation.
  • Patients with a skin cancer in the chronically ultraviolet radiation-exposed head and neck area (SIR = 0.84, 95% CI: 0.73, 0.97) and those diagnosed after the age of 60 years (SIR = 0.86, 95% CI: 0.75, 0.97) had decreased prostate cancer incidence rates.
  • These results support the hypothesis that ultraviolet radiation protects against prostate cancer.
  • [MeSH-minor] Age Factors. Aged. Carcinoma, Basal Cell / epidemiology. Carcinoma, Squamous Cell / epidemiology. Humans. Incidence. Male. Melanoma / epidemiology. Middle Aged. Prostate / pathology. Risk Factors. Time Factors


70. Algaba F, Trias I, Arce Y: Natural history of prostatic carcinoma: the pathologist's perspective. Recent Results Cancer Res; 2007;175:9-24
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  • [Title] Natural history of prostatic carcinoma: the pathologist's perspective.
  • The stem (basal) cells of prostate acini are considered the origin of prostate cancer.
  • The progressive knowledge of the stromal invasion in prostate cancer (loss of some cell-cell adhesion molecules and expression of others) can be correlated with the Gleason grading system, and the molecular changes in the progression to androgen-independent carcinoma can be used as a prognostic marker in conjunction with the classical pathological markers.
  • [MeSH-major] Precancerous Conditions / pathology. Prostate / pathology. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 17432551.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 65
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76. Humphrey PA: Diagnosis of adenocarcinoma in prostate needle biopsy tissue. J Clin Pathol; 2007 Jan;60(1):35-42
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  • [Title] Diagnosis of adenocarcinoma in prostate needle biopsy tissue.
  • Prostate cancer is a major public health problem throughout the developed world.
  • For patients with clinically localised prostate cancer, the diagnosis is typically established by histopathological examination of prostate needle biopsy samples.
  • Major criteria include an infiltrative glandular growth pattern, an absence of basal cells and nuclear atypia in the form of nucleomegaly and nucleolomegaly.
  • In difficult cases, basal cell absence may be confirmed by immunohistochemical stains for high-molecular-weight cytokeratins (marked with antibody 34betaE12) or p63, which are basal cell markers.
  • Cocktails of antibodies directed against basal cell markers and AMACR are particularly useful in evaluating small foci of atypical glands, and in substantiating a diagnosis of a minimal adenocarcinoma.
  • Measures of tumour extent are (1) number of cores positive for cancer in the number of cores examined, (2) percentage of needle core tissue affected by carcinoma and (3) linear millimetres of carcinoma present.
  • [MeSH-major] Adenocarcinoma / pathology. Prostate / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 17213347.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 74
  • [Other-IDs] NLM/ PMC1860598
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77. Escaff S, Fernández JM, González LO, Suárez A, González-Reyes S, González JM, Vizoso FJ: Study of matrix metalloproteinases and their inhibitors in prostate cancer. Br J Cancer; 2010 Mar 2;102(5):922-9
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Study of matrix metalloproteinases and their inhibitors in prostate cancer.
  • BACKGROUND: Extracellular matrix metalloproteases (MMPs) have raised an extraordinary interest in cancer research because of their potential role in basal membrane and extracellular matrix degradation, consequently facilitating tumour invasion and metastases development.
  • More than 2600 determinations on cancer specimens from 133 patients with clinically localised prostate carcinoma, 20 patients with prostatic intraepithelial neoplasia and 50 patients with benign prostate hyperplasia and controls, were performed.
  • RESULTS: When compared with benign pathologies, prostate carcinomas had higher expression of all MMPs and TIMPs.
  • CONCLUSION: The expression of MMPs and TIMPs seems to have an important role in the molecular biology of prostate carcinomas, and their expression by tumours may be of clinical interest to used as indicators of tumour aggressiveness.

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  • (PMID = 20160732.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tissue Inhibitor of Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases
  • [Other-IDs] NLM/ PMC2833257
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78. Mazzucchelli R, Lopez-Beltran A, Cheng L, Scarpelli M, Kirkali Z, Montironi R: Rare and unusual histological variants of prostatic carcinoma: clinical significance. BJU Int; 2008 Nov;102(10):1369-74
MedlinePlus Health Information. consumer health - Prostate Cancer.

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  • [Title] Rare and unusual histological variants of prostatic carcinoma: clinical significance.
  • We review the clinicopathological features of the following unusual histological variants of prostatic carcinoma: small cell carcinoma, ductal adenocarcinoma, sarcomatoid (carcinosarcoma), basal cell, squamous cell and adenosquamous, and urothelial carcinoma.
  • These variants are rare and account for 5-10% of carcinomas that originate in the prostate.
  • Only basal cell carcinoma is seen as a low-grade carcinoma.
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Carcinoma, Acinar Cell / pathology. Carcinoma, Small Cell / pathology. Carcinoma, Squamous Cell / pathology. Carcinoma, Transitional Cell / pathology. Carcinosarcoma / pathology. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 18793296.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 56
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79. Adley BP, Yang XJ: Application of alpha-methylacyl coenzyme A racemase immunohistochemistry in the diagnosis of prostate cancer: a review. Anal Quant Cytol Histol; 2006 Feb;28(1):1-13
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Application of alpha-methylacyl coenzyme A racemase immunohistochemistry in the diagnosis of prostate cancer: a review.
  • Since its discovery, AMACR has gained wide acceptance for use in the diagnosis of prostatic adenocarcinoma in conjunction with morphology and immunohistochemical staining for basal cell markers.
  • Numerous studies have consistently shown high sensitivity and specificity of AMACR for prostate cancer.
  • This review focuses on AMACR expression in prostate cancer and its morphologic variants, high grade prostatic intraepithelial neoplasia, adenosis and benign conditions of the prostate.
  • Finally, we emphasize diagnostic pitfalls in the application of AMACR to small, atypical foci of glands seen on prostate needle core biopsy and project future diagnostic as well as clinical applications for the protein.

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  • (PMID = 16566275.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
  • [Number-of-references] 63
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80. Chakraborty S, Swanson BJ, Bonthu N, Batra SK: Aberrant upregulation of MUC4 mucin expression in cutaneous condyloma acuminatum and squamous cell carcinoma suggests a potential role in the diagnosis and therapy of skin diseases. J Clin Pathol; 2010 Jul;63(7):579-84
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  • [Title] Aberrant upregulation of MUC4 mucin expression in cutaneous condyloma acuminatum and squamous cell carcinoma suggests a potential role in the diagnosis and therapy of skin diseases.
  • RESULTS: While the normal epidermis showed a negative to weak-positive expression of MUC4, its expression was significantly upregulated in squamous cell carcinomas (SCCs) where the intensity of staining correlated negatively with tumour grade and positively with age.
  • Malignant melanoma, basal cell carcinoma and cutaneous cysts were negative.

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  • (PMID = 20591909.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA078590-13; United States / NCI NIH HHS / CA / U01 CA111294; United States / NCI NIH HHS / CA / R01 CA78590; United States / NCI NIH HHS / CA / P50 CA127297; United States / NCI NIH HHS / CA / R01 CA078590; United States / NCI NIH HHS / CA / R01 CA131944; United States / NCI NIH HHS / CA / R01 CA 133774; United States / NCI NIH HHS / CA / R01 CA133774
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MUC4 protein, human; 0 / Mucin-4; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ NIHMS224552; NLM/ PMC2920126
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81. Yang J, Wahdan-Alaswad R, Danielpour D: Critical role of Smad2 in tumor suppression and transforming growth factor-beta-induced apoptosis of prostate epithelial cells. Cancer Res; 2009 Mar 15;69(6):2185-90
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  • [Title] Critical role of Smad2 in tumor suppression and transforming growth factor-beta-induced apoptosis of prostate epithelial cells.
  • Transforming growth factor-beta (TGF-beta) functions as a tumor suppressor of the prostate through mechanisms that remain unresolved.
  • Although TGF-beta receptors directly activate both Smads 2 and 3, to date, Smad3 has been shown to be the essential mediator of most Smad-dependent TGF-beta responses, including control of gene expression, cell growth, apoptosis, and tumor suppression.
  • Using a robust lentiviral short hairpin RNA system to silence Smads 2 and/or 3 in the NRP-152 nontumorigenic rat prostate basal epithelial cell line, we provide the first evidence for Smad2 as a critical mediator of TGF-beta-induced apoptosis and gene expression.
  • Parallel analyses revealed that Smad3 is the major mediator of TGF-beta-induced transcriptional and apoptotic responses in the NRP-154 rat prostate carcinoma cell line.
  • Given previous reports that NRP-152 cells have a stem cell phenotype, we speculate a critical role for Smad2 as a tumor suppressor in the basal epithelial or stem cell compartment of the prostate.

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  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102074; United States / NCI NIH HHS / CA / R01CA102074; United States / NCI NIH HHS / CA / P30 CA043703; United States / NCI NIH HHS / CA / T32 CA059366; United States / NCI NIH HHS / CA / R01 CA092102; United States / NCI NIH HHS / CA / R01CA092102; United States / NCI NIH HHS / CA / P30 CA43703
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Madh2 protein, rat; 0 / Madh3 protein, rat; 0 / RNA, Small Interfering; 0 / Smad2 Protein; 0 / Smad3 Protein; 0 / Transforming Growth Factor beta
  • [Other-IDs] NLM/ NIHMS373062; NLM/ PMC3345028
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82. Lovrić E, Gatalica Z, Eyzaguirre E, Kruslin B: Expression of maspin and glutathionine-S-transferase-pi in normal human prostate and prostatic carcinomas. Appl Immunohistochem Mol Morphol; 2010 Oct;18(5):429-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of maspin and glutathionine-S-transferase-pi in normal human prostate and prostatic carcinomas.
  • Maspin expression functions as an inhibitor of tumor progression preventing the local invasion and etastatic spread of prostate cancer cells.
  • DESIGN: Maspin and GST-pi expression were assessed in needle core and transurethral resection prostatic biopsies from 42 patients (34 with carcinoma, and 8 with normal prostate gland) using immunohistochemical methods.
  • RESULTS: Maspin and GST-pi were strongly and consistently coexpressed in the cytoplasm of basal cells of normal prostatic glands, whereas normal luminal cells were inconsistently weakly positive.
  • In contrast, only 1 case of prostatic carcinoma expressed GST-pi.
  • CONCLUSION: Consistent coexpression of maspin and GST-pi was observed in basal cells of the prostatic glands, which could be used as an additional immunohistochemical test in the evaluation of prostatic malignancy.

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  • (PMID = 20453817.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SERPIN-B5; 0 / Serpins; EC 2.5.1.18 / Glutathione S-Transferase pi
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83. Hu DG, Mackenzie PI: Forkhead box protein A1 regulates UDP-glucuronosyltransferase 2B15 gene transcription in LNCaP prostate cancer cells. Drug Metab Dispos; 2010 Dec;38(12):2105-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Forkhead box protein A1 regulates UDP-glucuronosyltransferase 2B15 gene transcription in LNCaP prostate cancer cells.
  • Although regulation of these UGT genes by various endogenous and exogenous ligands, including steroid hormones and bile acids, is well documented, the mechanisms controlling their basal gene expression are poorly understood.
  • We recently reported that Forkhead box protein A1 (FOXA1) regulates the basal expression of the UGT2B17 gene in prostate cancer cells.
  • In this study, we show that FOXA1 also regulates basal expression of the UGT2B15 gene in the prostate cell line LNCaP (lymph node carcinoma of the prostate).
  • Mutation of this site prevents binding and substantially decreases basal UGT2B15 promoter activity.
  • Because local inactivation of active androgens by UGT2B15 and UGT2B17 has been shown to be a major determinant of androgen response and signaling activity, regulation of the UGT2B15 and UGT2B17 genes by FOXA1 may have an important role in the maintenance of androgen homeostasis within prostate cancer cells.

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  • (PMID = 20736324.001).
  • [ISSN] 1521-009X
  • [Journal-full-title] Drug metabolism and disposition: the biological fate of chemicals
  • [ISO-abbreviation] Drug Metab. Dispos.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FOXA1 protein, human; 0 / Hepatocyte Nuclear Factor 3-alpha; EC 2.4.1.17 / Glucuronosyltransferase; EC 2.4.1.17 / UDP-glucuronosyltransferase 2B15, human; EC 2.4.1.17 / UGT2B17 protein, human
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84. Veeramani S, Yuan TC, Lin FF, Lin MF: Mitochondrial redox signaling by p66Shc is involved in regulating androgenic growth stimulation of human prostate cancer cells. Oncogene; 2008 Aug 28;27(37):5057-68
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  • [Title] Mitochondrial redox signaling by p66Shc is involved in regulating androgenic growth stimulation of human prostate cancer cells.
  • Recent reports, however, revealed that p66Shc protein level is significantly elevated in several human cancer tissues and growth-stimulated carcinoma cells, suggesting a mitogenic and carcinogenic role for p66Shc.
  • In this communication, we demonstrate for the first time that p66Shc mediates androgenic growth signals in androgen-sensitive human prostate cancer cells through mitochondrial ROS production.
  • Growth stimulation of prostate cancer cells with 5alpha-dihydrotestosterone (DHT) is accompanied by increased p66Shc level and ROS production, which is abolished by antioxidant treatments.
  • However, antioxidant treatments do not affect the transcriptional activity of androgen receptor (AR) as observed by its inability to block DHT-induced prostate-specific antigen expression, an AR-dependent correlate of prostate cancer progression.
  • Elevated expression of p66Shc by cDNA transfection increases the basal cell proliferation and, thus, reduces additional DHT-induced cell proliferation.
  • Conversely, both redox-negative p66Shc mutant (W134F), which is deficient in cytochrome c interaction, and p66Shc small interfering RNA decrease DHT-induced cell proliferation.
  • These results collectively reveal a novel role for p66Shc-ROS pathway in androgen-induced prostate cancer cell proliferation and, thus, may play a role in early prostate carcinogenesis.

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  • (PMID = 18504439.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA088184; United States / NCI NIH HHS / CA / R01 CA088184-09; United States / NCI NIH HHS / CA / P30 CA036727; United States / NCI NIH HHS / CA / CA088184-09; United States / NCI NIH HHS / CA / R01 CA88184; United States / NCI NIH HHS / CA / P30CA036727
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Androgens; 0 / Reactive Oxygen Species; 0 / SHC1 protein, human; 0 / Shc Signaling Adaptor Proteins; 0 / Shc1 protein, mouse; 3XMK78S47O / Testosterone; 5H7I2IP58X / boldenone; 9007-43-6 / Cytochromes c
  • [Other-IDs] NLM/ NIHMS156177; NLM/ PMC2776635
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85. Pascal LE, Vêncio RZ, Page LS, Liebeskind ES, Shadle CP, Troisch P, Marzolf B, True LD, Hood LE, Liu AY: Gene expression relationship between prostate cancer cells of Gleason 3, 4 and normal epithelial cells as revealed by cell type-specific transcriptomes. BMC Cancer; 2009 Dec 18;9:452
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression relationship between prostate cancer cells of Gleason 3, 4 and normal epithelial cells as revealed by cell type-specific transcriptomes.
  • BACKGROUND: Prostate cancer cells in primary tumors have been typed CD10-/CD13-/CD24hi/CD26+/CD38lo/CD44-/CD104-.
  • METHODS: CD26+ cancer cells were isolated from Gleason 3+3 (G3) and Gleason 4+4 (G4) tumors by cell sorting, and their gene expression or transcriptome was determined by Affymetrix DNA array analysis.
  • Dataset analysis was used to determine gene expression similarities and differences between G3 and G4 as well as to prostate cancer cell lines and histologically normal prostate luminal cells.
  • RESULTS: The G3 and G4 transcriptomes were compared to those of prostatic cell types of non-cancer, which included luminal, basal, stromal fibromuscular, and endothelial.
  • Dataset comparison also showed that the cancer transcriptomes differed substantially from those of prostate cancer cell lines.
  • Differentially expressed genes likely contribute to the prostate cancer phenotype and constitute the signatures of these particular cancer cell types.

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  • (PMID = 20021671.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / FDA HHS / BP / BP50-GMO-76547; United States / NIDDK NIH HHS / DK / DK63630; United States / NCI NIH HHS / CA / CA98699; United States / NCI NIH HHS / CA / CA111244; United States / NCI NIH HHS / CA / CA85859
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC2809079
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86. Chung AC, Zhou S, Liao L, Tien JC, Greenberg NM, Xu J: Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice. Cancer Res; 2007 Jun 15;67(12):5965-75
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  • [Title] Genetic ablation of the amplified-in-breast cancer 1 inhibits spontaneous prostate cancer progression in mice.
  • Although the amplified-in-breast cancer 1 (AIB1; SRC-3, ACTR, or NCoA3) was defined as a coactivator for androgen receptor (AR) by in vitro studies, its role in AR-mediated prostate development and prostate cancer remained unexplored.
  • We report here that AIB1 is expressed in the basal and stromal cells but not in the epithelial cells of the normal mouse prostates.
  • AIB1 deficiency only slightly delayed prostate growth and had no effect on androgen-dependent prostate regeneration, suggesting an unessential role of AIB1 in AR function in the prostate.
  • Surprisingly, when prostate tumorigenesis was induced by the SV40 transgene in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice, AIB1 expression was observed in certain epithelial cells of the prostate intraepithelial neoplasia (PIN) and well-differentiated carcinoma and in almost all cells of the poorly differentiated carcinoma.
  • After AIB1 was genetically inactivated in AIB1-/-/TRAMP mice, the progression of prostate tumorigenesis in most AIB1-/-/TRAMP mice was arrested at the well-differentiated carcinoma stage.
  • Wild-type (WT)/TRAMP mice developed progressive, multifocal, and metastatic prostate tumors and died between 25 and 34 weeks.
  • In contrast, AIB1-/-/TRAMP mice only exhibited PIN and early-stage well-differentiated carcinoma by 39 weeks.
  • AIB1-/-/TRAMP prostates showed much lower cell proliferation than WT/TRAMP prostates.
  • Our results indicate that induction of AIB1 expression in partially transformed epithelial cells is essential for progression of prostate tumorigenesis into poorly differentiated carcinoma.
  • Inhibition of AIB1 expression or function in the prostate epithelium may be a potential strategy to suppress prostate cancer initiation and progression.

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  • (PMID = 17575167.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK58242; United States / NIDDK NIH HHS / DK / DK058242-05; United States / NCI NIH HHS / CA / CA119689-03; United States / NCI NIH HHS / CA / CA112403; United States / NCI NIH HHS / CA / R01 CA112403-02; United States / NCI NIH HHS / CA / CA112403-02; United States / NIDDK NIH HHS / DK / R01 DK058242-05; United States / NCI NIH HHS / CA / R01 CA119689-03; United States / NCI NIH HHS / CA / CA119689; United States / NCI NIH HHS / CA / R01 CA112403; United States / NIDDK NIH HHS / DK / R01 DK058242; United States / NCI NIH HHS / CA / R01 CA119689
  • [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 / Receptors, Androgen; 0 / Trans-Activators; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / Ncoa3 protein, mouse; EC 2.3.1.48 / Nuclear Receptor Coactivator 3
  • [Other-IDs] NLM/ NIHMS50339; NLM/ PMC2898573
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87. Montironi R, Mazzucchelli R, Lopez-Beltran A, Cheng L, Scarpelli M: Mechanisms of disease: high-grade prostatic intraepithelial neoplasia and other proposed preneoplastic lesions in the prostate. Nat Clin Pract Urol; 2007 Jun;4(6):321-32
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  • [Title] Mechanisms of disease: high-grade prostatic intraepithelial neoplasia and other proposed preneoplastic lesions in the prostate.
  • This lesion is characterized by cellular proliferations within pre-existing ducts and acini, with nuclear and nucleolar enlargements similar to those seen in prostate cancer, although unlike cancer HGPIN retains a basal-cell layer.
  • The recognition of HGPIN is clinically important because of the strong association between this disease and prostatic carcinoma.
  • Other possible findings in the prostate might indicate premalignant disease (low-grade prostatic intraepithelial neoplasia, atrophy, malignancy-associated changes, and atypical adenomatous hyperplasia or adenosis), but the data for these premalignant diseases are much less convincing than those for HGPIN.

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  • (PMID = 17551536.001).
  • [ISSN] 1743-4289
  • [Journal-full-title] Nature clinical practice. Urology
  • [ISO-abbreviation] Nat Clin Pract Urol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 78
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88. Biermann K, Montironi R, Lopez-Beltran A, Zhang S, Cheng L: Histopathological findings after treatment of prostate cancer using high-intensity focused ultrasound (HIFU). Prostate; 2010 Aug;70(11):1196-200
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  • [Title] Histopathological findings after treatment of prostate cancer using high-intensity focused ultrasound (HIFU).
  • BACKGROUND: High-intensity focused ultrasound (HIFU) treatment is a novel minimally invasive therapeutic option for patients with localized prostate cancer.
  • Little is known about the histological findings in prostate biopsies upon HIFU treatment.
  • METHOD: We examined the spectrum of histological changes in prostate biopsies of 25 prostate cancer patients who were previously treated with HIFU.
  • In benign glands, histological examination revealed a heterogeneous cellular damage and cellular response including cytologic atypia and basal cell hyperplasia.
  • Eleven patients (44%) had residual prostatic carcinoma after treatment.

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  • [Copyright] 2010. (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20564422.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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89. Barron DA, Strand DW, Ressler SJ, Dang TD, Hayward SW, Yang F, Ayala GE, Ittmann M, Rowley DR: TGF-β1 induces an age-dependent inflammation of nerve ganglia and fibroplasia in the prostate gland stroma of a novel transgenic mouse. PLoS One; 2010 Oct 29;5(10):e13751
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  • [Title] TGF-β1 induces an age-dependent inflammation of nerve ganglia and fibroplasia in the prostate gland stroma of a novel transgenic mouse.
  • TGF-β1 is overexpressed in wound repair and in most proliferative disorders including benign prostatic hyperplasia and prostate cancer.
  • To address the actions of TGF-β1 in prostate disorders, we targeted expression of an epitope tagged and constitutively active TGF-β1 via the enhanced probasin promoter to the murine prostate gland epithelium.
  • Transgenic mice developed age-dependent lesions leading to severe, yet focal attenuation of epithelium, and a discontinuous basal lamina.
  • Similar phenotypic changes were observed using a human prostate epithelium tissue recombination xenograft model, where epithelial cells engineered to overexpress TGF-β1 induced fibrosis and altered matrix deposition concurrent with inflammation in the stromal compartment.
  • The novel findings of ganglia and vessel inflammation associated with formation of collagenous micronodules in collapsed acini is important as each of these are observed in human prostate carcinoma and may play a role in disease progression.

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  • (PMID = 21060787.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA058093; United States / NIDDK NIH HHS / DK / R01 DK083293; United States / NCI NIH HHS / CA / U54 CA126568; United States / NCI NIH HHS / CA / R01 CA58093
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Transforming Growth Factor beta1
  • [Other-IDs] NLM/ PMC2966419
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90. Schulz WA, Ingenwerth M, Djuidje CE, Hader C, Rahnenführer J, Engers R: Changes in cortical cytoskeletal and extracellular matrix gene expression in prostate cancer are related to oncogenic ERG deregulation. BMC Cancer; 2010;10:505
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  • [Title] Changes in cortical cytoskeletal and extracellular matrix gene expression in prostate cancer are related to oncogenic ERG deregulation.
  • BACKGROUND: The cortical cytoskeleton network connects the actin cytoskeleton to various membrane proteins, influencing cell adhesion, polarity, migration and response to extracellular signals.
  • Previous studies have suggested changes in the expression of specific components in prostate cancer, especially of 4.1 proteins (encoded by EPB41 genes) which form nodes in this network.
  • METHODS: Expression of EPB41L1, EPB41L2, EPB41L3 (protein: 4.1B), EPB41L4B (EHM2), EPB41L5, EPB49 (dematin), VIL2 (ezrin), and DLG1 (summarized as "cortical cytoskeleton" genes) as well as ERG was measured by quantitative RT-PCR in a well-characterized set of 45 M0 prostate adenocarcinoma and 13 benign tissues.
  • Protein 4.1B was detected most strongly in the basal cells of normal prostate epithelia.
  • Its expression in carcinoma cells was similar to the weaker one in normal luminal cells.
  • CONCLUSIONS: Specific changes in the cortical cytoskeleton were observed during prostate cancer progression.
  • We hypothesize that these alterations may contribute to the increased invasivity conferred to prostate cancer cells by ERG deregulation.

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  • (PMID = 20860828.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Cytoskeletal Proteins; 0 / ERG protein, human; 0 / Membrane Proteins; 0 / Neuropeptides; 0 / Trans-Activators; 0 / erythrocyte membrane protein band 4.1-like 1; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi
  • [Other-IDs] NLM/ PMC2955608
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91. Perk J, Gil-Bazo I, Chin Y, de Candia P, Chen JJ, Zhao Y, Chao S, Cheong W, Ke Y, Al-Ahmadie H, Gerald WL, Brogi E, Benezra R: Reassessment of id1 protein expression in human mammary, prostate, and bladder cancers using a monospecific rabbit monoclonal anti-id1 antibody. Cancer Res; 2006 Nov 15;66(22):10870-7
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  • [Title] Reassessment of id1 protein expression in human mammary, prostate, and bladder cancers using a monospecific rabbit monoclonal anti-id1 antibody.
  • Id proteins are a class of dominant-negative antagonists of helix-loop-helix transcription factors and have been shown to control differentiation of a variety of cell types in diverse organisms.
  • To explore this issue, we developed and characterized a highly specific rabbit monoclonal antibody against Id1 to assess its expression in human breast, prostate, and bladder malignancies.
  • Interestingly, we detected nuclear expression of the Id1 protein in the tumor cells in 10 of 45 cases of poorly differentiated and highly aggressive carcinoma with metaplastic morphology.
  • Similarly, only 1 of 30 prostate cancer samples showed Id1-positive tumor cells, whereas in almost all, endothelial cells showed high Id1 expression.
  • Intriguingly, whereas normal prostate glands do not show any Id1 protein expression, basal layer cells of benign prostate glands in proximity to tumors expressed high levels of the Id1 protein.
  • In contrast to the lack of Id1 expression in the usual types of mammary and prostate cancers, the majority of transitional cell bladder tumors showed Id1 protein expression in both tumor and endothelial cells.

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  • (PMID = 17108123.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / ID1 protein, human; 0 / Inhibitor of Differentiation Protein 1
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92. Wang Z, Prins GS, Coschigano KT, Kopchick JJ, Green JE, Ray VH, Hedayat S, Christov KT, Unterman TG, Swanson SM: Disruption of growth hormone signaling retards early stages of prostate carcinogenesis in the C3(1)/T antigen mouse. Endocrinology; 2005 Dec;146(12):5188-96
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  • [Title] Disruption of growth hormone signaling retards early stages of prostate carcinogenesis in the C3(1)/T antigen mouse.
  • Recent epidemiological studies suggest that elevated serum titers of IGF-I, which are, to a large degree, regulated by GH, are associated with an increase in prostate cancer risk.
  • The purpose of the current study was to develop the first animal models to directly test the hypothesis that a normal, functional GH/IGF-I axis is required for prostate cancer progression.
  • The GH receptor (GHR) gene-disrupted mouse (Ghr(-/-)), which has less than 10% of the plasma IGF-I found in GHR wild-type mice, was crossed with the C3(1)/T antigen (Tag) mouse, which develops prostatic intraepithelial neoplasia driven by the large Tag that progress to invasive prostate carcinoma in a manner similar to the process observed in humans.
  • Disruption of the GHR gene altered neither prostate androgen receptor expression nor serum testosterone titers.
  • Immunohistochemistry revealed a significant decrease in prostate epithelial cell proliferation and an increase in basal apoptotic indices.
  • These results indicate that disruption of GH signaling significantly inhibits prostate carcinogenesis.
  • [MeSH-minor] Animals. Antigens, Differentiation / metabolism. Apoptosis. Cell Differentiation. Cell Proliferation. Epithelial Cells / metabolism. Epithelial Cells / pathology. Male. Mice. Mice, Knockout. Mice, Transgenic. Prostate / pathology. Prostate / physiopathology. Receptors, Androgen / metabolism. Testosterone / blood

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  • (PMID = 16141391.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R03 AG020820
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Antigens, Polyomavirus Transforming; 0 / Receptors, Androgen; 0 / Receptors, Somatotropin; 3XMK78S47O / Testosterone; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
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93. Bozdogan O, Atasoy P, Bozdogan N, Erekul S, Batislam E, Yilmaz E, Başar MM: BAG-1 expression in hyperplastic and neoplastic prostate tissue: is there any relationship with BCL-related proteins and androgen receptor status? Tumori; 2005 Nov-Dec;91(6):539-45
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  • [Title] BAG-1 expression in hyperplastic and neoplastic prostate tissue: is there any relationship with BCL-related proteins and androgen receptor status?
  • AIMS AND BACKGROUND: To evaluate the function and distribution of BAG-1 protein in hyperplastic and neoplastic prostate tissue and establish the relationship between this protein and BCL-related proteins (BCL-2 and BAX), androgen receptor (AR) expression and chromogranin A.
  • METHODS: Twenty-eight prostatic adenocarcinomas and 16 prostate hyperplasias were included in this retrospective study.
  • RESULTS: Statistical analysis showed a significant difference in HSCOREs of BAX, M30 and AR between the carcinoma and hyperplasia groups.
  • In the carcinoma group there was a positive correlation (Pearson) between BCL-2 and cytoplasmic/nuclear BAG-1.
  • BAG-1 showed the same specific basal cell localization as BCL-2 in hyperplastic and normal glands.
  • CONCLUSIONS: The BAG-1 protein showed a distinct distribution pattern in hyperplastic and neoplastic prostate.

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  • (PMID = 16457154.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / BCL2-associated athanogene 1 protein; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Receptors, Androgen; 0 / Transcription Factors
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94. Rana S, Sen R, Kalra R, Arora B, Sharma P, Gahlawat S: Immunohistochemical study of the expression of epidermal growth factor receptor in benign prostatic hypertrophy, prostatic intraepithelial neoplasia and prostatic carcinoma. Indian J Pathol Microbiol; 2006 Oct;49(4):495-9
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  • [Title] Immunohistochemical study of the expression of epidermal growth factor receptor in benign prostatic hypertrophy, prostatic intraepithelial neoplasia and prostatic carcinoma.
  • The present study provides an analysis of immunohistochemical expression and localization of epidermal growth factor receptor (EGFR) in formalin fixed paraffin embedded specimens of prostate.
  • Thirty-five cases each of benign prostatic hypertrophy (BPH) and prostatic carcinoma and 30 cases of prostatic intraepithelial neoplasia (PIN) were taken up for study.
  • EGFR positivity was observed in all the cases (100%) of BPH and PIN and in only 10 cases (28.5%) of prostatic carcinoma.
  • In both BPH and PIN the basal cells revealed significantly higher intensity and percentage cell positivity than the luminal cells.
  • Intensity and percentage of positively stained basal cells in BPH was higher than PIN basal cells but the difference was not statistically significant.
  • The intensity and percentage cell positivity of BPH basal cells and PIN basal and luminal cells were significantly greater than the epithelial cells of prostatic carcinoma.

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  • (PMID = 17183836.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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95. Wei W, Barron PD, Rheinwald JG: Modulation of TGF-β-inducible hypermotility by EGF and other factors in human prostate epithelial cells and keratinocytes. In Vitro Cell Dev Biol Anim; 2010 Dec;46(10):841-55
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  • [Title] Modulation of TGF-β-inducible hypermotility by EGF and other factors in human prostate epithelial cells and keratinocytes.
  • The development and tissue architecture of stratified squamous and prostate epithelia are very different, yet the basal cells of both express p63, α6β4 integrin, and Lam332.
  • Keratinocytes and prostate epithelial cells grow well in nutritionally optimized culture media with pituitary extract and certain mitogens.
  • We report that prostate epithelial cells display hypermotility responses indistinguishable from those of keratinocytes.
  • Prostate epithelial cells have a short replicative lifespan, restricted both by p16(INK4A) and telomere-related mechanisms.
  • We immortalized the normal prostate epithelial cell line HPrE-1 by transduction to express bmi1 and TERT.
  • Prostate epithelial cells lose expression of p63, β4 integrin, and Lam332 when they transform to invasive carcinoma.
  • Thus, keratinocytes and prostate epithelial cells possess common hypermotility and senescence mechanisms and immortalized prostate cell lines can be engineered using defined methods to yield cells retaining normal properties.

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  • (PMID = 21042878.001).
  • [ISSN] 1543-706X
  • [Journal-full-title] In vitro cellular & developmental biology. Animal
  • [ISO-abbreviation] In Vitro Cell. Dev. Biol. Anim.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / P30 AR042689; United States / NIDCR NIH HHS / DE / R01 DE013178; United States / NIAMS NIH HHS / AR / P30-AR42689; United States / NIDCR NIH HHS / DE / R01 DE 13178
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Transforming Growth Factor beta; 0 / kalinin; 62229-50-9 / Epidermal Growth Factor
  • [Other-IDs] NLM/ NIHMS438604; NLM/ PMC3568941
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96. Hameed O, Sublett J, Humphrey PA: Immunohistochemical stains for p63 and alpha-methylacyl-CoA racemase, versus a cocktail comprising both, in the diagnosis of prostatic carcinoma: a comparison of the immunohistochemical staining of 430 foci in radical prostatectomy and needle biopsy tissues. Am J Surg Pathol; 2005 May;29(5):579-87
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical stains for p63 and alpha-methylacyl-CoA racemase, versus a cocktail comprising both, in the diagnosis of prostatic carcinoma: a comparison of the immunohistochemical staining of 430 foci in radical prostatectomy and needle biopsy tissues.
  • The diagnosis of prostatic carcinoma and especially minimal prostatic carcinoma can sometimes be challenging on needle core biopsy and occasionally immunohistochemistry is an aid in the diagnosis.
  • Immunostains, such as those directed against the basal cell marker p63 and, more recently, employing antibodies reactive with alpha-methylacyl-CoA racemase (AMACR), can be useful in this situation.
  • A retrospective review of 31 consecutive radical prostatectomy specimens and 150 prostate needle biopsy samples was performed to select histologic sections showing foci of prostatic carcinoma and/or minimal prostatic carcinoma, high-grade prostatic intraepithelial neoplasia (HGPIN), as well as common benign mimickers of prostatic carcinoma, to include atrophy and basal cell hyperplasia, especially with prominent nucleoli.
  • The cocktail was very useful in highlighting prostatic carcinoma associated with HGPIN, flat and cribriform HGPIN, and distorted foci of minimal prostatic carcinoma.
  • These data indicate that use of a p63/AMACR cocktail is essentially equivalent to use of each antibody separately for immunohistochemical confirmation of a diagnosis of prostatic carcinoma in needle biopsy.
  • This cocktail would be of diagnostic utility when only limited tissue is available for immunohistochemical evaluation of small, diagnostically difficult foci in prostate needle biopsy tissue.
  • [MeSH-minor] Biomarkers, Tumor / analysis. Biopsy, Needle. Cell Nucleus / chemistry. Cell Nucleus / pathology. Humans. Male. Retrospective Studies

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  • (PMID = 15832080.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Clinical Conference; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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97. Puebla-Mora AG, Heras A, Cano-Valdez AM, Domínguez-Malagón H: Human telomerase and alpha-methylacyl-coenzyme A racemase in prostatic carcinoma. A comparative immunohistochemical study. Ann Diagn Pathol; 2006 Aug;10(4):205-8
MedlinePlus Health Information. consumer health - Prostate Cancer.

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  • [Title] Human telomerase and alpha-methylacyl-coenzyme A racemase in prostatic carcinoma. A comparative immunohistochemical study.
  • Human telomerase detected by in situ hybridization has been demonstrated to be a useful tool for the diagnosis of malignancy and has also been tested by reverse transcriptase-polymerase chain reaction in several tumors such as hepatic cell carcinoma, melanoma, colonic carcinoma, gastric carcinoma, biliary carcinoma, breast carcinoma, mesothelioma, lung carcinoma, female tract carcinoma, and prostatic carcinoma.
  • Carcinomas of cervix, endometrium, and breast have been studied by this method, but its value in prostatic carcinoma has not been explored; for that reason, we studied benign and malignant prostatic lesions by immunohistochemistry using paraffin embedded tissue.
  • The aim of the study was to define the sensitivity and specificity of hTERT in prostate cancer, in comparison with alpha-methylacyl-coenzyme A racemase (AMACR) (P504-S).
  • Fifty-five specimens of diverse prostatic lesions were selected for study (43 needle biopsies and 12 transurethral resections); there were 61 malignancies (47 infiltrating carcinomas and 14 high-grade prostatic intraepithelial neoplasias [PIN]) and 29 benign lesions (10 basal cell hyperplasias, 12 nodular hyperplasias, 4 chronic prostatitis, and 3 atrophic glands).

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  • (PMID = 16844561.001).
  • [ISSN] 1092-9134
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; EC 2.7.7.49 / Telomerase; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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98. Amann T, Bataille F, Spruss T, Dettmer K, Wild P, Liedtke C, Mühlbauer M, Kiefer P, Oefner PJ, Trautwein C, Bosserhoff AK, Hellerbrand C: Reduced expression of fibroblast growth factor receptor 2IIIb in hepatocellular carcinoma induces a more aggressive growth. Am J Pathol; 2010 Mar;176(3):1433-42
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • [Title] Reduced expression of fibroblast growth factor receptor 2IIIb in hepatocellular carcinoma induces a more aggressive growth.
  • Here, we analyzed the expression and function of FGFR2-IIIb in hepatocellular carcinoma (HCC).
  • FGFR2-IIIb expression in HCC tissues and cell lines was lower than in primary human hepatocytes and nontumorous tissue.
  • A decrease in FGFR-2IIIb expression in HCC cell lines was not related to promoter hypermethylation.
  • FGFR2-IIIb re-expression in stable transfected HCC cell lines induced a higher basal apoptosis rate and a significantly reduced proliferation and migratory potential in vitro.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / pathology. Liver Neoplasms / genetics. Liver Neoplasms / pathology. Receptor, Fibroblast Growth Factor, Type 2 / genetics
  • [MeSH-minor] Aged. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. DNA Methylation / drug effects. DNA Methylation / genetics. Down-Regulation / drug effects. Down-Regulation / genetics. Female. Fibroblast Growth Factor 7 / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Mice. Middle Aged. Promoter Regions, Genetic / genetics. Protein Kinase Inhibitors / pharmacology. Pyrroles / pharmacology

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  • (PMID = 20093481.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrroles; 0 / SU 5402; 126469-10-1 / Fibroblast Growth Factor 7; EC 2.7.1.- / keratinocyte growth factor receptor; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2
  • [Other-IDs] NLM/ PMC2832162
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99. Leinonen T, Pirinen R, Böhm J, Johansson R, Rinne A, Weber E, Kosma VM: Biological and prognostic role of acid cysteine proteinase inhibitor (ACPI, cystatin A) in non-small-cell lung cancer. J Clin Pathol; 2007 May;60(5):515-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Biological and prognostic role of acid cysteine proteinase inhibitor (ACPI, cystatin A) in non-small-cell lung cancer.
  • AIM: To analyse the expression and prognostic role of ACPI in non-small-cell lung cancer (NSCLC).
  • RESULTS: A normal bronchial epithelium showed positive staining for ACPI in the basal cells, whereas the upper two-thirds of the dysplastic epithelium was ACPI positive.
  • High staining for ACPI was found in 74% (91/123) of squamous-cell carcinomas, whereas 16% (8/49) of adenocarcinomas and 30% of (8/27) large-cell carcinomas showed the high expression of ACPI (p<0.001).
  • Among squamous-cell carcinomas, low expression of ACPI was correlated with poor tumour differentiation (p=0.032).
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Cystatins / metabolism. Cysteine Proteinase Inhibitors / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Follow-Up Studies. Humans. Immunoenzyme Techniques. Middle Aged. Neoplasm Staging. Precancerous Conditions / metabolism. Prognosis. Survival Analysis

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  • (PMID = 16790691.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cystatins; 0 / Cysteine Proteinase Inhibitors
  • [Other-IDs] NLM/ PMC1994551
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100. Epstein JI: Prostatic ductal adenocarcinoma: a mini review. Med Princ Pract; 2010;19(1):82-5
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • Other than the prostatic intraepithelial neoplasia (PIN)-like ductal pattern, which behaves like Gleason pattern 3, ductal adenocarcinoma is comparable to Gleason pattern 4 prostate cancer.
  • Ductal adenocarcinoma can have a patchy basal cell layer and typically expresses prostate-specific antigen (PSA) immunohistochemically.
  • Mimickers of ductal adenocarcinoma include prostatic urethral polyps, hyperplastic benign prostate glands, high-grade PIN, colorectal adenocarcinoma, and papillary urothelial carcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Ductal / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Humans. Male. Transurethral Resection of Prostate

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19996627.001).
  • [ISSN] 1423-0151
  • [Journal-full-title] Medical principles and practice : international journal of the Kuwait University, Health Science Centre
  • [ISO-abbreviation] Med Princ Pract
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 19
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