Genetic Epidemiology, Translational Neurogenomics, Psychiatric Genetics and Statistical Genetics Laboratories investigate the pattern of disease in families, particularly identical and non-identical twins, to assess the relative importance of genes and environment in a variety of important health problems.
QIMR Home Page
GenEpi Home Page
About GenEpi
Publications
Contacts
Research
Staff Index
Collaborators
Software Tools
Computing Resources
Studies
Search
GenEpi Intranet
PMID
10925355
TITLE
Androgen receptor exon 1 CAG repeat length and risk of ovarian cancer.
ABSTRACT
Epidemiological studies indicate that ovarian cancer is an endocrine-related tumour. We conducted a case-control comparison to assess the androgen receptor (AR) exon 1 polymorphic CAG repeat length (CAG(n)) as a risk factor for epithelial ovarian cancer. AR CAG(n) was determined for 319 case subjects with ovarian adenocarcinoma and 853 unaffected control subjects (comprising 300 unrelated adult female monozygotic twins, and 553 adult females sampled randomly from the population using the electoral rolls). The CAG(n) distributions of case subjects and control subjects were compared as a continuum, and by dichotomising alleles according to different CAG(n) cut-points. Logistic regression was used to calculate age-adjusted odds ratio (OR) estimates. Analyzed as a continuous variable, there was no difference between case subjects and control subjects for the smaller, larger or average allele sizes of the CAG(n) genotype, before or after adjusting for age. The mean (95% CI) for the average CAG(n) was 22.0 (21.8-22.2) for case subjects and 22.0 (21.9-22.1) for control subjects (p>.9). Analysis of CAG(n) as a dichotomous variable showed no difference between case subjects and control subjects for the median cutpoint (>/= 22), or for another cut-point previously reported to act as a modifier of breast cancer risk (>/= 29). Our data provide no evidence for an association between ovarian cancer risk and the genotype defined by the AR exon 1 CAG(n) polymorphism, although we cannot exclude small effects, or threshold effects in a small subgroup.
Copyright 2000 Wiley-Liss, Inc.
DATE PUBLISHED
2000 Sep 01
HISTORY
PUBSTATUS PUBSTATUSDATE
pubmed 2000/08/05 11:00
medline 2000/08/19 11:00
entrez 2000/08/05 11:00
AUTHORS
NAME COLLECTIVENAME LASTNAME FORENAME INITIALS AFFILIATION AFFILIATIONINFO
Spurdle AB Spurdle A B AB Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research and The University of Queensland, Brisbane, Queensland, Australia. mandyS@qimr.edu.au
Webb PM Webb P M PM
Chen X Chen X X
Martin NG Martin N G NG
Giles GG Giles G G GG
Hopper JL Hopper J L JL
Chenevix-Trench G Chenevix-Trench G G
INVESTIGATORS
JOURNAL
VOLUME: 87
ISSUE: 5
TITLE: International journal of cancer
ISOABBREVIATION: Int J Cancer
YEAR: 2000
MONTH: Sep
DAY: 01
MEDLINEDATE:
SEASON:
CITEDMEDIUM: Print
ISSN: 0020-7136
ISSNTYPE: Print
MEDLINE JOURNAL
MEDLINETA: Int J Cancer
COUNTRY: United States
ISSNLINKING: 0020-7136
NLMUNIQUEID: 0042124
PUBLICATION TYPE
PUBLICATIONTYPE TEXT
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
COMMENTS AND CORRECTIONS
GRANTS
GENERAL NOTE
KEYWORDS
MESH HEADINGS
DESCRIPTORNAME QUALIFIERNAME
Adenocarcinoma genetics
Adult genetics
Age Factors genetics
Aged genetics
Aged, 80 and over genetics
Alleles genetics
Case-Control Studies genetics
Exons genetics
Female genetics
Genotype genetics
Humans genetics
Middle Aged genetics
Ovarian Neoplasms genetics
Polymorphism, Genetic genetics
Receptors, Androgen genetics
Risk Factors genetics
Trinucleotide Repeats genetics
Twins, Monozygotic genetics
SUPPLEMENTARY MESH
GENE SYMBOLS
CHEMICALS
REGISTRYNUMBER NAMEOFSUBSTANCE
0 Receptors, Androgen
OTHER ID's