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Titolo:
E-cadherin expression in prostate cancer: A broad survey using high-density tissue microarray technology
Autore:
Rubin, MA; Mucci, NR; Figurski, J; Fecko, A; Pienta, KJ; Day, ML;
Indirizzi:
Univ Michigan, Dept Pathol, Surg Urol Sect, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 g Urol Sect, Ann Arbor, MI 48109 USA Univ Michigan, Dept Internal Med, Hematol Oncol Sect, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 Oncol Sect, Ann Arbor, MI 48109 USA Univ Michigan, Comprehens Canc & Geriatr Ctr, Ann Arbor, MI 48109 USA UnivMichigan Ann Arbor MI USA 48109 Geriatr Ctr, Ann Arbor, MI 48109 USA
Titolo Testata:
HUMAN PATHOLOGY
fascicolo: 7, volume: 32, anno: 2001,
pagine: 690 - 697
SICI:
0046-8177(200107)32:7<690:EEIPCA>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-ADHESION MOLECULES; ALPHA-CATENIN EXPRESSION; P-CADHERIN; DECREASED EXPRESSION; BREAST-CARCINOMA; N-CADHERIN; LINES; PROGRESSION; SURVIVAL; BLADDER;
Keywords:
adenocarcinoma; prostate; E-cadherin; immunohistochemistry; tissue microarray;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Rubin, MA Univ Michigan, Dept Pathol, Surg Urol Sect, 1500 E Med Ctr Dr,Room 2G332,Box 0054, Ann Arbor, MI 48109 USA Univ Michigan 1500 E Med Ctr Dr,Room 2G332,Box 0054 Ann Arbor MI USA 48109
Citazione:
M.A. Rubin et al., "E-cadherin expression in prostate cancer: A broad survey using high-density tissue microarray technology", HUMAN PATH, 32(7), 2001, pp. 690-697

Abstract

E-cadherin is a calcium 2+-dependent cell-adhesion molecule that determines epithelial development in the embryo and maintains adult differentiated epithelium and homeostasis. Aberrant or decreased expression has been reported to be associated with prostate carcinoma progression. The degree of E-cadherin expression in prostate cancer remains controversial. Some studies have reported decreased expression of E-cadherin as tumors advance and metastasize. Other studies have not demonstrated this relationship. To address these variations, we undertook a study to systematically evaluate E-cadherin expression in a broad range of prostate tissue. Benign prostate, clinicallylocalized prostate cancer, and hormone-refractory metastatic prostate cancer were analyzed under uniform conditions using high-density tissue microarrays (TMA). Formalin-fixed, paraffin-embedded prostate carcinoma from men with clinically localized prostate carcinoma and autopsy material from men who died of widely metastatic, hormone-refractory prostate carcinoma were arrayed into 6 high-density TMA blocks. Benign and atrophic prostate tissue and high-grade prostatic intraepithelial neoplasia (PIN) were also included from the clinically localized cases. Immunohistochemistry was performed using the immunoglobulin GI mouse monoclonal antibody (HECD-1; Zymed, San Francisco, CA). Membranous staining was recorded as low (aberrant) or high (normal). E-cadherin expression was considered aberrant if less than 70% of thecells had strong membranous staining. A total of 1,220 prostate TMA samples were analyzed. High (normal) E-cadherin expression was seen in 87% of 757benign, 80% of 41 high-grade PIN, 82% of 325 prostate carcinoma and 90% of97 hormone-refractory prostate carcinoma TMA samples. Mean E-cadherin expression was determined for each of the 128 clinically localized prostate cancer cases. Aberrant E-cadherin expression showed a statistical trend towardan association with positive surgical margins (P = .012), higher Gleason score (P = .18), and prostate-specific antigen (PSA) failure (Kaplan-Meier analysis, log-rank P = .09). There was a statistically significant association between aberrant E-cadherin expression and larger tumor size (P = .01). No significant associations were seen with extraprostatic extension and seminal vesicle invasion. The current study shows a broad-spectrum approach toevaluating E-cadherin protein expression in prostate carcinoma. Clinicallylocalized prostate tumors, treated with surgery alone, show a high level of E-cadherin expression. Aberrant expression was identified in tumors with positive surgical margins, higher Gleason score, and a higher rate of PSA failure. However, these trends were not statistically significant. A statically significant association between aberrant E-cadherin expression and larger tumor size was identified. In the metastatic hormone-refractory prostatetumors, E-cadherin expression was vastly expressed, and only rare cases had aberrant expression. Therefore, the findings of this study are most consistent with a transient down-regulation of E-cadherin in localized pro. ratecancer. Metastatic prostate cancer shows strong E-cadherin expression as determined by anti-E-cadherin antibody HECD-1. HUM PATHOL 32:690-697. Copyright (C) 2001 by W.B. Saunders Company.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 13:20:14