No association between a polymorphic variant of the IRS-1 gene and prostate cancer risk

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Fall, Katja,1971-Karolinska Institutet (author)

No association between a polymorphic variant of the IRS-1 gene and prostate cancer risk

Article/chapterEnglish2008

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Hoboken, USA :John Wiley & Sons,2008
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LIBRIS-ID:oai:DiVA.org:oru-41463
https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-41463URI
https://doi.org/10.1002/pros.20797DOI
http://kipublications.ki.se/Default.aspx?queryparsed=id:117549840URI

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Language:English
Summary in:English

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Objective: Insulin receptor substrate-1 (IRS-1) acts as a docking protein between the insulin-like growth factor-1 (IGF-1) receptor and intracellular signaling molecules in the IGF-1 signaling pathway. Accumulating data support a role of IGF-1 in prostate carcinogenesis. We assessed the influence of the most common IRS-1 gene polymorphism (Gly972Arg) on prostate cancer risk, alone and in combination with IGF-1 and other components in the IGF-1 signaling pathway.Materials and methods: In a nested case-control study within the Physicians' Health Study, the IRS-1 polymorphism was assayed from prospectively collected samples from 564 incident prostate cancer cases and 758 controls matched on age and smoking. We calculated relative risks (RR) and 95% confidence intervals (CI) using conditional logistic regression.Results: Among the controls, 0.8% were homozygous (AA) and 12% were heterozygous (GA) for the polymorphic allele. There was no association between carriage of the A allele and total prostate cancer risk (RR = 1.1 95% CI = 0.8-1.5), advanced disease (stage C or D or lethal prostate cancer, RR = 1.3 95% CI = 0.8-2.3), or plasma IGF-1 levels. We explored possible interactions with body mass index and components in the IGF-1 pathway including IGFBP3, PI3k, and PTEN but none of these factors influenced the relation between IRS-1 genotype and prostate cancer risk.Conclusions: Our data do not support an association between carriage of the variant IRS-1 gene and prostate cancer risk.

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Stark, J. R.Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham Women’s Hospital and Harvard Medical School, Boston, USA (author)
Mucci, L. A.Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA (author)
Chan, J.Departments of Epidemiology & Biostatistics and Urology, University of California, San Francisco, USA (author)
Stampfer, M. J.Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA (author)
Kurth, T.Department of Epidemiology, Harvard School of Public Health, Boston, USA; Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA (author)
Febbo, P. G.Duke University School of Medicine, Durham, USA (author)
Kantoff, P.Division of Solid Tumor Oncology, Dana-Farber Cancer Institute, Boston, USA (author)
Ma, J.Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA (author)
Karolinska InstitutetDepartment of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham Women’s Hospital and Harvard Medical School, Boston, USA (creator_code:org_t)

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In:The ProstateHoboken, USA : John Wiley & Sons68:13, s. 1416-200270-41371097-0045

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