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Aberrant activation of the phosphatidylinositol 3-kinase (PI3K) pathway by genetic alterations in the PI3K downstream effector AKT may promote cancer development and progression. We examined the association between germline mutations in PI3K pathway genes (PIK3CA, PTEN, AKT1, AKT2, PIK3R1) and familial breast cancer risk in two independent hospital-based series of breast cancer patients. In the first series (N = 2,098), a high-risk PIK3CA mutation was detected in one case and an association between the mutation and risk of breast cancer was observed (OR 8.4; 95% CI 1.3-52.3; p = 0.02). In the second series (N = 1,939), an association was also found for the low-risk PTEN mutation, but the association was not statistically significant (OR 1.5; 95% CI 0.7-3.5; p = 0.31). We also examined the relation of a germline mutation in the AKT1 gene with breast cancer risk and found an association between the K40N mutation and increased risk of breast cancer. The high-risk mutation was detected in 7.1% (95% CI 5.3-9.5) of breast cancer patients and in 0.07% (95% CI 0.04-0.13) of controls (OR 15.6; 95% CI 4.5-53.1; p < 0.0001). The mutation was more frequent in postmenopausal than in premenopausal cases (OR 2.8; 95% CI 1.5-5.3; p = 0.0005) and in ER-negative than in ER-positive cases (OR 6.9; 95% CI 3.8-12.6; p < 0.0001). In addition, there was a significant interaction between the K40N mutation and a high-risk PIK3CA mutation (OR 5.4; 95% CI 2.6-11.4; p = 0.0001). In summary, our results suggest that the K40N mutation may contribute to breast cancer risk especially when combined with a high-risk PIK3CA mutation, and that the AKT1 gene should be further investigated as a candidate breast cancer susceptibility gene.
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One of the drawbacks to this approach was that we needed to recompile every time we made even a small change to the code. This slowed everything else we were doing down and because we couldn't always have someone waiting for the application to finish building. 827ec27edc