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. 2015 Feb 2;1(2):76–82. doi: 10.1002/cjp2.8

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© 2014 John Wiley and Sons Ltd and The Pathological Society of Great Britain and Ireland

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Proposed progression model from multiple PanINs. Early precursor lesions (PanINs) with wild‐type KRAS emerged to create field of cancer, and some of them acquired oncogenic KRAS, p.T58I and p.Q61H (Founder lesion). Additional somatic mutation in p53 p.T175H occurred in part of the PanINs with the unique KRAS haplotype, which may in turn spread into other area of the pancreas (‘early dissemination' indicated by arrows). One of them progressed into invasive PDA (PDA‐A), which was resected by the Whipple's procedure with negative surgical margin. However, other disseminated precursors independently progressed to form other PDAs in the tail (PDA‐B) and body (PDA‐C) of the pancreas, finally connecting each other through main pancreatic duct (dotted line). In addition to the typical mutations in KRAS and p53, PDA‐B has other somatic mutations in Smad4 and VHL.