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Titolo:
E-cadherin expression as a marker of tumor aggressiveness in routinely processed radical prostatectomy specimens
Autore:
De Marzo, AM; Knudsen, B; Chan-Tack, K; Epstein, JI;
Indirizzi:
Johns Hopkins Univ, Dept Pathol, Inst Med, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 st Med, Baltimore, MD 21205 USA Cornell Univ, Med Ctr, New York Hosp, Dept Pathol, New York, NY 10021 USA Cornell Univ New York NY USA 10021 p, Dept Pathol, New York, NY 10021 USA Univ Penn, Sch Med, Dept Med, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Dept Med, Philadelphia, PA 19104 USA
Titolo Testata:
UROLOGY
fascicolo: 4, volume: 53, anno: 1999,
pagine: 707 - 713
SICI:
0090-4295(199904)53:4<707:EEAAMO>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALPHA-CATENIN EXPRESSION; MOLECULE E-CADHERIN; CLINICAL IMPLICATIONS; CELL-ADHESION; DECREASED EXPRESSION; PROSTATIC-CARCINOMA; DISEASE RECURRENCE; PATHOLOGICAL STAGE; CANCER-CELLS; HIGH-RISK;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: De Marzo, AM Johnsmore,ins Univ, Dept Pathol, Inst Med, Ross 512B,720 Rutland Ave, Balti Johns Hopkins Univ Ross 512B,720 Rutland Ave Baltimore MD USA 21205
Citazione:
A.M. De Marzo et al., "E-cadherin expression as a marker of tumor aggressiveness in routinely processed radical prostatectomy specimens", UROLOGY, 53(4), 1999, pp. 707-713

Abstract

Objectives. Approximately 30% of clinically localized prostate adenocarcinomas treated by radical prostatectomy (RP) will recur within 10 years. To prevent recurrence, new adjuvant therapies are in development that seek to treat high-risk patients after surgery. To identify patients as candidates for these treatments, improved biomarkers for predicting prognosis are needed. Reduced expression of E-cadherin has been proposed as a new marker for predicting prognosis in prostate adenocarcinoma. Since few studies have examined the relation between risk factors for disease progression and E-cadherin expression using routinely processed RP specimens, we used RP specimens to correlate downregulation of E-cadherin and pathologic stage at RP. Methods. Primary adenocarcinomas (n = 76) from formalin-fixed and paraffin-embedded RP specimens were evaluated by immunohistochemistry against E-cadherin (HECD-1) using heat-induced epitope retrieval and automated staining (BioTek Solutions). Normal appearing prostate epithelium was used as an internal control for each specimen. Staining was scored as an estimate of the percentage of tumor cells in each specimen that showed strong plasma membrane staining. Results. Specimens were divided into three categories with respect to Gleason score: intermediate (score 5 to 6, n = 31), intermediate to high (score7, n = 25), and high (score 8 to 9, n = 20). For pathologic stage, specimens were divided into three categories: low stage/organ confined (pT2, n = 30), intermediate stage/ limited extraprostatic extension (pT3a, n = 25), and high stage/seminal vesicle-pelvic lymph node metastases (pT3b-any pTN1, n= 21). In univariate analysis, reduced levels of E-cadherin correlated with advanced Gleason score (P = 0.003) and advanced pathologic stage (P = 0.008). In multivariate analysis, E-cadherin, preoperative prostate-specific antigen, and Gleason score all contributed independently to the prediction of high-stage disease (P <0.0001). Ten pelvic lymph node metastases from this same patient cohort were stained for E-cadherin. All were positive and 9 of 10 were moderately to strongly positive. Conclusions, Since essentially all patients in the high-stage category have a very high likelihood of disease recurrence, we conclude that the study of E-cadherin in a prospective manner as a potential biomarker of disease progression in patients with clinically organ-confined prostate cancer who undergo RP is warranted. Additionally, our finding that most metastatic tumor cells in pelvic lymph nodes express E-cadherin supports the notion that the establishment of the distant colonization and growth of metastatic tumorcells may be facilitated by expression or re-expression of previously downregulated E-cadherin. This would strongly suggest that irreversible geneticinactivation through mutation or allelic loss at 16q2.3 is probably not the mechanism of E-cadherin downregulation in most abnormally expressing primary prostate carcinomas. (C) 1999, Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 13:50:57