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PIK3CA Exon 20 Mutation is Independently Associated with a Poor Prognosis in Breast Cancer Patients
Background Prognostic factors that could select breast cancer patients with poor survival, and influence clinical trials of targeted therapy, are needed. However, the reported observations regarding the impact of PI3KCA mutation on breast cancers are controversial. Methods We analyzed exons 4, 7, 9,...
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Published in: | Annals of surgical oncology 2008-04, Vol.15 (4), p.1064-1069 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Background
Prognostic factors that could select breast cancer patients with poor survival, and influence clinical trials of targeted therapy, are needed. However, the reported observations regarding the impact of
PI3KCA
mutation on breast cancers are controversial.
Methods
We analyzed exons 4, 7, 9, and 20 of
PI3KCA
on a series of 158 patients. Clinicopathological characteristics were correlated with the mutation data.
Results
Among 152 patients who were available for follow-up (median follow-up time, 6.57 years), 26% had
PIK3CA
mutations, more than half of which occurred in exon 20. The five-year survival rate of patients with exon 20 mutations (46%) was significantly lower than that of patients without (75%) (
p
= 0.0054). Multivariate analysis showed that
PIK3CA
exon 20 mutations and nodal involvement were independent risk factors for overall survival. The relative risk of death in patients with
PIK3CA
exon 20 mutations was 2.881 (95% CI, 1.406–5.900;
p
= 0.0038).
Conclusions
PIK3CA
mutations are common in invasive ductal carcinomas of the breast. Our result suggests that
PIK3CA
exon 20 mutation is an independent risk factor for poor prognosis in breast cancer patients, indicating that differences in patient numbers with
PIK3CA
exon 20 mutations in study and control arms should be avoided in clinical trials of PI3K inhibitors. |
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ISSN: | 1068-9265 1534-4681 |
DOI: | 10.1245/s10434-007-9751-7 |