Intra-pancreatic Distal Bile Duct Carcinoma is Morphologically, Genetically, and Clinically Distinct from Pancreatic Duc.Intra-pancreatic远端胆管癌形态,从胰腺导管腺.pdf

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Intra-pancreatic Distal Bile Duct Carcinoma is Morphologically, Genetically, and Clinically Distinct from Pancreatic Duc.Intra-pancreatic远端胆管癌形态,从胰腺导管腺.pdf

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Intra-pancreatic Distal Bile Duct Carcinoma is Morphologically, Genetically, and Clinically Distinct from Pancreatic Duc.Intra-pancreatic远端胆管癌形态,从胰腺导管腺

J Gastrointest Surg (2016) 20:953–959 DOI 10.1007/s11605-016-3108-0 ORIGINAL ARTICLE Intra-pancreatic Distal Bile Duct Carcinoma is Morphologically, Genetically, and Clinically Distinct from Pancreatic Ductal Adenocarcinoma Vikram Deshpande 1 & Ioannis T. Konstantinidis2 & Carlos Fernandez-del Castillo2 & Aram F. Hezel 3 & Kevin M. Haigis 1 & David T. Ting 3 & Nabeel Bardeesy3 & Lipika Goyal3 & Andrew X. Zhu 3 & Andrew L. Warshaw 2 & Keith D. Lillemoe2 & Cristina R. Ferrone2 Received: 2 November 2015 /Accepted: 15 February 2016 /Published online: 8 March 2016 # 2016 The Society for Surgery of the Alimentary Tract Abstract Purpose Differentiating intra-pancreatic distal bile duct carcinoma invading the pancreas from pancreatic ductal adenocarci- nomas (PDAC) surrounding the distal common bile duct (CBD) can be challenging. Our aim is to identify clinical, morpholog- ical, and genetic features characteristic of intra-pancreatic distal bile duct carcinoma. Methods Clinicopathologic data of 550 patients undergoing a pancreaticoduodenectomy between September 1990 and May 2008 were reviewed. KRAS status was assessed with mass-spectrometric genotyping. Results Ninety-seven patients with intra-pancreatic adenocarcinomas surrounding the CBD were identified; slides were available for 80. Two relationships with the CBD were recognized as follows: type I (n = 42): cancer grew concentrically around the CBD and type II (n = 38): cancer grew asymmetrically around the CBD. Type I adenocarcinomas were associated with high-grade biliary dysplasia (45 vs. 13 %; p = 0.003); type II were associated with high-grade pancreatic intra-epithelial neoplasia (PanIN-2 or -3) (39 vs. 9 %; p = 0.003). Type I tumors had a better median survival (46 months) compared to type II (23 months) or other PDAC (20 months) (p < 0.001). Mutated KRAS was identified in 3/26 (11 %) type I and 20/21 (95 %) type II cancers (p < 0.001). There may be poorer survival in the presence of a