Format

Send to

Choose Destination
See comment in PubMed Commons below
Anticancer Res. 2008 Nov-Dec;28(6A):3711-6.

Lack of involvement of the GNAS1 T393C polymorphism in prostate cancer risk in a Japanese population.

Author information

1
Department of Pathologic Oncology, Institute of Molecular and Experimental Medicine, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Japan.

Abstract

BACKGROUND:

GNAS1 encodes the a-subunit of the Gs protein (Gsa), which binds GTP and stimulates adenylyl cyclase. Activating mutations lead to somatotroph, thyroid, adrenal and gonadal adenomas or the McCune-Albright syndrome and recently the T399C polymorphism in GNAS1 has been reported to be associated with malignancies. The purpose of the present case-control study with 349 Japanese prostate cancer patients and 203 urological controls was to determine whether the GNAS1 T393C polymorphism is associated with prostate cancer risk.

MATERIALS AND METHODS:

The GNAS1 T393C polymorphism was examined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. Odds ratios (OR) were adjusted for age using multiple logistic regression analysis with SPSS Medical Pack.

RESULTS:

The allele frequencies were compatible with the control population in Hardy-Weinberg equilibrium with 80, 169 and 100 for GNAS1 C/C, C/T and T/T, respectively in the patients with prostate cancer, compared with 42, 94 and 67 in the controls. No association between the GNAS1 polymorphism and prostate cancer risk was apparent. The C/C genotype was more frequent among the prostate cancer patients (22.9%) than the controls (20.7%), although without significance (OR, 1.30; 95% CI, 0.80-2.12; p=0.29).

CONCLUSION:

This pilot study does not support involvement of the GNAS1 polymorphism in prostate cancer risk.

PMID:
19189654
[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Support Center