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Background/aims: Radical distal pancreatectomy with en-bloc resection of the common hepatic, celiac, and left gastric arteries for pancreatic body cancer that involves these arteries does not routinely require arterial reconstruction because the collateral pathways via the pancreatoduodenal arcades from the superior mesenteric artery are recruited immediately. However, accidental injury to the pancreatoduodenal artery compromises collateral blood flow and may lead to fatal complications. This article describes the middle colic artery-gastroepiploic artery bypass as an emergent salvage procedure for restoring collateral flow., Methodology: The inferior pancreatoduodenal artery was accidentally injured in 2 of 9 patients who underwent the radical procedure between 1997 and 2001. Microvascular anastomosis between the left branch of the middle colic artery and the gastroepiploic artery in an end-to-side fashion was employed., Results: The pulsation of the gastroepiploic artery and the color of the stomach recovered immediately after completion of the middle colic artery-gastroepiploic artery bypass. No ischemia-related complication developed postoperatively. Postoperative angiography showed the middle colic artery-gastroepiploic artery bypass supplying arterial flow to the liver, stomach, duodenum, and pancreas., Conclusions: The middle colic artery-gastroepiploic artery bypass is an excellent alternative restoring compromised collateral flow via the pancreatoduodenal arcades when microsurgical technique is available.

Almost all reported cases of intraductal papillary-mucinous tumors of the pancreas (IPMTs) originate from Wirsung’s duct (WD), the main pancreatic duct, or their branches. IPMTs arising from Santorini’s duct (SD) and its branches have rarely been reported. This article presents the clinicopathologic features of IPMTs originating in SD and its branches. Of 36 IPMTs resected in our institution, 5 originated in the region of SD: 3 in SD and 2 from its branches. Both SD and WD were dilated in all cases on radiographic and ultrasonographic studies. The maximum diameter of SD, determined by computed tomography or ultrasonography, was larger than that of WD in all cases. Seven reports of IPMT arising from SD have been published. Four lesions originated from SD and the others from its branches. Overall, 9 of 12 lesions (75%) were considered malignant. In conclusion, the coexistence of an IPMT and a dilated SD suggests an origin in the SD. These tumors have a high malignant potential and should be excised. [ABSTRACT FROM AUTHOR]

Background & Aims Intraductal papillary mucinous neoplasms (IPMNs) are regarded as precursors of pancreatic ductal adenocarcinomas (PDAs), but little is known about the mechanism of progression. This makes it challenging to assess cancer risk in patients with IPMNs. We investigated associations of IPMNs with concurrent PDAs by genetic and histologic analyses. Methods We obtained 30 pancreatic tissues with concurrent PDAs and IPMNs, and 168 lesions, including incipient foci, were mapped, microdissected, and analyzed for mutations in 18 pancreatic cancer-associated genes and expression of tumor suppressors. Results We determined the clonal relatedness of lesions, based on driver mutations shared by PDAs and concurrent IPMNs, and classified the lesions into 3 subtypes. Twelve PDAs contained driver mutations shared by all concurrent IPMNs, which we called the sequential subtype. This subset was characterized by less diversity in incipient foci with frequent GNAS mutations. Eleven PDAs contained some driver mutations that were shared with concurrent IPMNs, which we called the branch-off subtype. In this subtype, PDAs and IPMNs had identical KRAS mutations but different GNAS mutations, although the lesions were adjacent. Whole-exome sequencing and methylation analysis of these lesions indicated clonal origin with later divergence. Ten PDAs had driver mutations not found in concurrent IPMNs, called the de novo subtype. Expression profiles of TP53 and SMAD4 increased our ability to differentiate these subtypes compared with sequencing data alone. The branch-off and de novo subtypes had substantial heterogeneity among early clones, such as differences in KRAS mutations. Patients with PDAs of the branch-off subtype had a longer times of disease-free survival than patients with PDAs of the de novo or the sequential subtypes. Conclusions Detailed histologic and genetic analysis of PDAs and concurrent IPMNs identified 3 different pathways by which IPMNs progress to PDAs—we call these the sequential, branch-off, and de novo subtypes. Subtypes might be associated with clinical and pathologic features and be used to select surveillance programs for patients with IPMNs. Graphical abstract [ABSTRACT FROM AUTHOR]