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Title
Dichotomy effects of Akt signaling in breast cancer
Authors
Keywords
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Journal
Molecular Cancer
Volume 11, Issue 1, Pages 61
Publisher
Springer Nature
Online
2012-08-24
DOI
10.1186/1476-4598-11-61
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- (2009) S. Sharma et al. CARCINOGENESIS
- Epithelial-Mesenchymal Transitions in Development and Disease
- (2009) Jean Paul Thiery et al. CELL
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