Powerful Set-Based Gene-Environment Interaction Testing Framework for Complex Diseases

Genet Epidemiol. 2015 Dec;39(8):609-18. doi: 10.1002/gepi.21908. Epub 2015 Jun 10.

Abstract

Identification of gene-environment interaction (G × E) is important in understanding the etiology of complex diseases. Based on our previously developed Set Based gene EnviRonment InterAction test (SBERIA), in this paper we propose a powerful framework for enhanced set-based G × E testing (eSBERIA). The major challenge of signal aggregation within a set is how to tell signals from noise. eSBERIA tackles this challenge by adaptively aggregating the interaction signals within a set weighted by the strength of the marginal and correlation screening signals. eSBERIA then combines the screening-informed aggregate test with a variance component test to account for the residual signals. Additionally, we develop a case-only extension for eSBERIA (coSBERIA) and an existing set-based method, which boosts the power not only by exploiting the G-E independence assumption but also by avoiding the need to specify main effects for a large number of variants in the set. Through extensive simulation, we show that coSBERIA and eSBERIA are considerably more powerful than existing methods within the case-only and the case-control method categories across a wide range of scenarios. We conduct a genome-wide G × E search by applying our methods to Illumina HumanExome Beadchip data of 10,446 colorectal cancer cases and 10,191 controls and identify two novel interactions between nonsteroidal anti-inflammatory drugs (NSAIDs) and MINK1 and PTCHD3.

Keywords: G × E screening statistics; GWAS; eSBERUA; rare variants.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / metabolism*
  • Colorectal Neoplasms / drug therapy
  • Colorectal Neoplasms / genetics*
  • Gene-Environment Interaction*
  • Genome-Wide Association Study
  • Humans
  • Models, Genetic
  • Polymorphism, Single Nucleotide / genetics
  • Protein Serine-Threonine Kinases / drug effects
  • Protein Serine-Threonine Kinases / genetics*
  • Receptors, Cell Surface / drug effects
  • Receptors, Cell Surface / genetics*

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • PTCHD3 protein, human
  • Receptors, Cell Surface
  • MINK1 protein, human
  • Protein Serine-Threonine Kinases