CEBP Frontiers in Cancer Prevention Research - 2008 Cancer Health Disparities Conference 2009
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Cancer Epidemiology Biomarkers & Prevention 17, 1505-1509, June 1, 2008. doi: 10.1158/1055-9965.EPI-07-2778
© 2008 American Association for Cancer Research

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Differential Expression of Genes Related to Androgen and Estrogen Metabolism in Hereditary versus Sporadic Prostate Cancer

Gaelle Fromont1,4, Mokrane Yacoub4, Antoine Valeri1,5, Philippe Mangin1,6, Guy Vallancien1,2, Geraldine Cancel-Tassin1 and Olivier Cussenot1,3

1 Centre de Recherche sur les Pathologies Prostatiques; 2 Department of Urology, Institut Mutualiste Montsouris; 3 Department of Urology, Tenon Hospital, Assistance Publique Hopitaux de Paris, Paris, France; 4 Department of Pathology, CHU/Universite de Poitiers, Poitiers, France; 5 Department of Urology, CHU/Universite de Brest, Brest, France; and 6 Department of Urology, CHU/Universite de Nancy, Nancy, France

Requests for reprints: Gaelle Fromont, Service d'Anatomie Pathologique, CHU Jean Bernard, Rue de la Miletrie, 86000 Poitiers, France. Phone: 33-5-49-44-40-23; Fax: 33-5-49-44-39-47. E-mail: g.fromont{at}chu-poitiers.fr

The hereditary predisposition to prostate cancer is rare and accounts for <5% of cases. Except for younger age at diagnosis, no phenotypic features have been clearly associated with hereditary prostate cancer. The aim of the study was to analyze the expression of genes related to androgen and estrogen metabolism in both hereditary and sporadic prostate cancers in patients matched for clinicopathologic features. Tissues were obtained from patients included in a national familial prostate cancer registry. From the 120 cases of hereditary forms suggesting autosomal dominant Mendelian inheritance, 21 patients were treated by radical prostatectomy for whom formalin-fixed tissue was available. Twenty-one sporadic cases were then matched according to age, Gleason score, and pathologic stage. Immunohistochemistry was done on tissue microarray using antibodies directed against androgen receptor (AR), estrogen receptor {alpha} (ERA), estrogen receptor β, 5{alpha}-reductase I and II, aromatase, and the proliferation marker Ki67. The percentage of AR-positive cancer cells was higher in hereditary cancer compared with sporadic cases (P < 0.004). In contrast, the mean number of ERA-positive stromal cells was lower in hereditary versus sporadic cancer (P < 0.03). This differential expression of AR and ERA suggests that a specific pattern of hormone receptors is associated with hereditary predisposition to prostate cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1505–9)







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Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2008 by the American Association for Cancer Research.