HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: ERC-08-0135v1 16/3/1005    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Ludwig, A. H. Articles by Kupryjanczyk, J. PubMed PubMed Citation Articles by Ludwig, A. H. Articles by Kupryjanczyk, J.

Departments of
¹ Molecular Pathology,
² Biostatistics
³ Gynecologic Oncology, The Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Roentgena 5, 02-781 Warsaw, Poland
⁴ Chair and Department of Obstetrics, Gynecology and Oncology, IInd Faculty of Medicine, Warsaw Medical University and Brodnowski Hospital, Kondratowicza 8, 03-242 Warsaw, Poland

(Correspondence should be addressed to J Kupryjanczyk; Email: jkupry{at}coi.waw.pl)

Genes encoding hormone receptors are among candidate genes modulating the risk of ovarian cancer. We aimed to assess a frequency of PGRG+331A, FSHRAla307Thr, and FSHRSer680Asn polymorphic variants, and the length of (CAG)n and (GGN)n repeat tracts in the androgen receptor gene (AR) with respect to ovarian cancer risk and outcome. We genotyped 215 ovarian cancer patients and 352 unaffected control subjects. Statistical analysis was performed with the logistic regression model with adjustment for age. Clinical importance of the polymorphic variants was evaluated in multivariate models on 69 patients treated with taxane–platinum chemotherapy, with respect to TP53 status. Longer AR (GGN)n and (CAG)n repeat tracts decreased the risk of ovarian cancer. For (GGN)n, each additional repeat decreased the risk by 17% (P=0.011) or 27% (P=0.002), while the presence of at least 23 repeats decreased the risk by 41% (P=0.032) or 68% (P=0.008), for the shorter or longer allele respectively. The risk of disease was also decreased by 11% with each additional (CAG)n repeat (P=0.006 for the longer allele). FSHRAla307Ala or FSHRSer680Ser polymorphisms increased ovarian cancer risk by 1.8 times (P=0.042). In all 69 patients, longer AR (CAG)n repeats decreased the risk of recurrence (P=0.031). In the group with TP53 accumulation, longer AR (CAG)n repeats decreased the risk of recurrence (P=0.003) and death (P=0.03), while the FSHRSer680Ser polymorphism increased the risk of recurrence (P=0.037). Progesterone receptor polymorphisms analyzed did not show any associations. Our results support both the androgen and gonadotropin hypotheses of ovarian cancer development.