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Lack of involvement of the GNAS1 T393C polymorphism in prostate cancer risk in a Japanese population.
- Source :
-
Anticancer research [Anticancer Res] 2008 Nov-Dec; Vol. 28 (6A), pp. 3711-6. - Publication Year :
- 2008
-
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.<br />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.<br />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).<br />Conclusion: This pilot study does not support involvement of the GNAS1 polymorphism in prostate cancer risk.
- Subjects :
- Adenocarcinoma pathology
Aged
Case-Control Studies
Chromogranins
Genetic Predisposition to Disease
Humans
Male
Polymorphism, Single Nucleotide
Prostatic Hyperplasia genetics
Prostatic Neoplasms pathology
Adenocarcinoma genetics
GTP-Binding Protein alpha Subunits, Gs genetics
Prostatic Neoplasms genetics
Subjects
Details
- Language :
- English
- ISSN :
- 0250-7005
- Volume :
- 28
- Issue :
- 6A
- Database :
- MEDLINE
- Journal :
- Anticancer research
- Publication Type :
- Academic Journal
- Accession number :
- 19189654