Abstract

Genetic studies of cancer susceptibility have shown that most heritable risk cannot be explained by the main effects of common alleles. This may be due to unknown gene–gene or gene–environment interactions and the complex roles of many genes at different stages of cancer. Studies using mouse models of cancer suggest that methods that integrate genetic analysis and genomic networks with knowledge of cancer biology can help to extend our understanding of heritable cancer susceptibility.

Author affiliations

1. David Quigley and Allan Balmain are at the Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94115, USA.

Correspondence to: Allan Balmain¹ Email: abalmain@cc.ucsf.edu

Published online 28 July 2009

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