A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Androgen receptor CAG polymorphism and prostate cancer risk
Tekijät: Mononen N, Ikonen T, Autio V, Rokman A, Matikainen MP, Tammela TLJ, Kallioniemi OP, Koivisto PA, Schleutker J
Kustantaja: SPRINGER-VERLAG
Julkaisuvuosi: 2002
Journal: Human Genetics
Tietokannassa oleva lehden nimi: HUMAN GENETICS
Lehden akronyymi: HUM GENET
Vuosikerta: 111
Numero: 2
Aloitussivu: 166
Lopetussivu: 171
Sivujen määrä: 6
ISSN: 0340-6717
DOI: https://doi.org/10.1007/s00439-002-0776-5
Tiivistelmä
Recent studies have suggested that polymorphisms of the androgen receptor gene (AR) may influence the risk of prostate cancer (PC) development and progression. Here, we analyzed the length of the CAG repeat of the AR gene in 1363 individuals, including patients with PC, benign prostate hyperplasia (BPH), and population controls. There was a tendency for short CAG repeats to be associated with PC. The Odds Ratio (OR) for PC was 1.47 (P=0.05) when individuals with short CAG repeats (less than or equal to18) were compared with those having long repeats (>18). CAG repeat length was not significantly associated with family history, disease stage, grade, age at diagnosis, prostate-specific antigen (PSA) level at diagnosis, or prognosis of the patients. Unexpectedly, short CAG repeats were significantly less common in patients with BPH compared with controls (OR=0.47, P=0.03). Our results suggest that the CAG polymorphism of the AR gene is unlikely to have a major role in the development or progression of PC in the Finnish population. The association of CAG repeats with the risk of BPH warrants further study.
Recent studies have suggested that polymorphisms of the androgen receptor gene (AR) may influence the risk of prostate cancer (PC) development and progression. Here, we analyzed the length of the CAG repeat of the AR gene in 1363 individuals, including patients with PC, benign prostate hyperplasia (BPH), and population controls. There was a tendency for short CAG repeats to be associated with PC. The Odds Ratio (OR) for PC was 1.47 (P=0.05) when individuals with short CAG repeats (less than or equal to18) were compared with those having long repeats (>18). CAG repeat length was not significantly associated with family history, disease stage, grade, age at diagnosis, prostate-specific antigen (PSA) level at diagnosis, or prognosis of the patients. Unexpectedly, short CAG repeats were significantly less common in patients with BPH compared with controls (OR=0.47, P=0.03). Our results suggest that the CAG polymorphism of the AR gene is unlikely to have a major role in the development or progression of PC in the Finnish population. The association of CAG repeats with the risk of BPH warrants further study.
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