Unresectable pancreatic ductal adenocarcinoma in the remnant pancreas diagnosed during every-6-month surveillance after resection of branch duct intraductal papillary mucinous neoplasm: a case report.

CONTEXT: There are few studies regarding the surveillance period and interval of resected or observed branch duct intraductal papillary mucinous neoplasms (IPMNs) of the pancreas in terms of early detection of concomitant pancreatic ductal adenocarcinoma. Despite a strict surveillance protocol, some patients are diagnosed with metastatic distinct ductal adenocarcinoma after resection of IPMN. CASE REPORT: We herein report a patient with unresectable pancreatic ductal adenocarcinoma that developed in the remnant pancreas 18 months after resection of branch duct IPMN. Although the patient was surveyed every 6 months after the operation and imaging studies at 6 and 12 months postoperatively demonstrated no evidence of recurrence, invasive ductal adenocarcinoma with liver metastasis appeared 18 months after the operation. The patient subsequently underwent chemotherapy; however, he died 9 months after the diagnosis of metachronous pancreatic ductal adenocarcinoma. CONCLUSIONS: In some patients with branch duct IPMNs, 6-month surveillance seems to be insufficient to detect resectable concomitant pancreatic ductal adenocarcinoma. Therefore, identification of high-risk patients who require surveillance at shorter intervals is urgently needed.

Targeting the hedgehog signaling pathway with interacting peptides to Patched-1.

BACKGROUND: The hedgehog (Hh) signaling pathway is aberrantly activated in many cancers. Overproduction of sonic hedgehog (Shh), a ligand in the Hh pathway, increases Hh signaling activity by inhibiting Patched-1 (Ptch1), a suppressive receptor in the Hh pathway. The purpose of this study was to establish a novel strategy for treating pancreatic cancer and other Hh-dependent cancers through control of the tumor-suppressive function of Ptch1. METHODS: We synthesized seven interacting peptides to the amino-acid sequence of the Ptch1 docking site for Shh. Human pancreatic cancer cell lines (AsPC-1, SUIT2) were cultured in the presence or absence of the peptides. Cell proliferation was assessed by cell counting and by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The activity of the Hh pathway was estimated by real-time polymerase chain reaction of the target gene product Gli1. To confirm their anti-tumor activity in vivo, the effect of the peptides in a mouse model of pancreatic cancer was determined. Finally, the Hh signaling activity of the xenograft was examined. RESULTS: Three of the interacting peptides to Ptch1 suppressed the proliferation of the two pancreatic cancer cell lines and decreased the expression of Gli1, both in vitro and in vivo. CONCLUSIONS: This study suggests that interacting peptides to Ptch1 may be a new tool for controlling the Hh-dependent growth of pancreatic cancer.