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. 2012 Jul 4;4(7):56. doi: 10.1186/gm357

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Copyright ©2012 Demeure et al.; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Simplified map and interactions of the phosphoinositide 3-kinase (PI3K) and RAS pathways highlighting the genomic aberrations (-, loss of function mutation, *gain of function mutation) identified in a cancer of the ampulla of Vater and the putative therapeutic site of vulnerability. ERK, extracellular-signal-regulated kinase; grb2, growth factor receptor bound protein 2; mTOR, mammalian target of rapamycin; RTK, receptor tyrosine kinase; SHC, SHC (Src homology 2 domain containing) transforming protein 1; SOS, son of sevenless.