CYP17 and breast cancer: no overall effect, but what about interactions?

doi:10.1186/bcr1320

Breast Cancer Research

Volume 7
Issue 6

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Commentary

CYP17 and breast cancer: no overall effect, but what about interactions?

Julian Little¹ and Jacques Simard²

¹Canada Research Chair in Human Genome Epidemiology, Department of Epidemiology and Community Medicine, University of Ottawa, Ontario, Canada

²Canada Research Chair in Oncogenetics, Cancer Genomics Laboratory, Oncology and Molecular Endocrinology Research Center, CHUQ Research Center and Laval University, Quebec, Canada

author email corresponding author email

Breast Cancer Research 2005, 7:238-242doi:10.1186/bcr1320


Published:	20 September 2005

See related research articles by Verla-Tebit et al (http://breast-cancer-research.com/content/7/4/R455), Chang et al (http://breast-cancer-research.com/content/7/4/R513) and Einarsdottir et al (http://breast-cancer-research.com/content/7/4/R890).

Abstract

Three large studies published in recent issues of Breast Cancer Research reported no overall evidence of an association between the CYP17 5'-untranslated region MspA1 polymorphism and breast cancer. The present commentary briefly highlights a few important observations and discusses some additional approaches to further assessment of associations between CYP17 common variants and breast cancer risk. In particular, the evolution of evidence on breast cancer and the CYP17 MspA1 variant suggests that determination of possible interactions between gene variants postulated to influence risk and nongenetic risk factors would be more efficiently accomplished by pooled analyses, ideally involving all studies of breast cancer, than by attempting to synthesize published information. Furthermore, such analyses would also be relevant to investigation of potential gene–gene interactions between CYP17 and other common variants in genes encoding enzymes that are involved in the synthesis and inactivation of sex steroid hormones, preferably using optimal sets of single nucleotide polymorphisms.