Naoki Yazawa

Background: Pancreatic cancer has a very high mortality rate worldwide, and about 30-40% of all patients have extensive vascular involvement at initial diagnosis that precludes surgical intervention. Here, we describe our experience in a patient with locally advanced pancreatic cancer (LAPC) who underwent R0 conversion surgery after undergoing a combination of chemotherapy and carbon-ion radiotherapy (CIRT), which led to long-term relapse-free survival (23 months). Case presentation: A 41-year-old woman presented a month ago with epigastralgia referred to our facility and was subsequently diagnosed with pancreatic cancer cStage III (Ph, TS2 (35 mm), cT4, cCH1, cDU1, cS1, cRP1, cPL1, cVsm0, cAsm1, cN0, cM0) that was also categorized as an unresectable LAPC. She immediately underwent 3 cycles of induction chemotherapy (gemcitabine + nanoparticle albumin-bound (nab-) paclitaxel) followed by CIRT with concurrent gemcitabine. Although significant shrinkage of the primary tumor occurred, frequent cholangitis due to duodenal stenosis of unknown etiology prevented continued chemotherapy, and 9 months after the first visit, she underwent a radical, subtotal, stomach-preserving, pancreaticoduodenectomy (SSPPD). Histopathologic examination of the resected tissue revealed a R0 resection with a histological response of Evans grade IIB. She was administered an almost full dose of S-1 as adjuvant chemotherapy for 6 months and has shown no signs of recurrence in 23 months. Conclusions: We report a first case of successful conversion surgery for an initially unresectable LAPC after rapid induction GEM + nab-PTX chemotherapy followed by CIRT. Rapid induction GEM + nab-PTX chemotherapy followed by CIRT for LAPC might be a safe and effective treatment option.

We encountered a very rare case of bile duct carcinoma associated with congenital biliary dilatation (CBD) in a 16-year-old female who was admitted to our hospital because of right upper abdominal pain and vomiting. Abdominal computed tomography demonstrated a cystic dilatation of the common bile duct measuring 7 cm in diameter and two enhanced tumors 4 cm in diameter located in the inferior bile duct and middle bile duct. Magnetic resonance cholangiopancreatography clearly demonstrated a cystic dilatation of the extrahepatic bile duct (Todani’s CBD classification: type 4-A). Endoscopic retrograde cholangiopancreatography also revealed two tumors. Biopsy results of one of the tumors confirmed adenocarcinoma. Excision of the perihilar bile duct and subtotal stomach-preserving pancreaticoduodenectomy with dissection of the major lymph nodes were performed. A postoperative histopathologic examination revealed a well-differentiated tubular adenocarcinoma, which remained within the mucosal layer, and no lymph node metastasis was found. The postoperative course was uneventful, and the patient was discharged 10 days after surgery and has remained disease-free for 21 months.

Various immunological strategies for tolerance induction against allogeneic tissue grafts (allografts) have been tested in islet transplant recipients; for example, T cell activating co-stimulatory pathway blockade has been shown to prolong islet allograft survival. However, little is known about whether infiltrating inflammatory cells (e.g., basophils) affect islet allograft fates before antigen-specific immune cell development. Herein, we treated mice with a basophil-specific monoclonal antibody (mAb) and examined whether early acute-phase islet allograft rejection could be prevented in recipients. Pancreatic islets isolated from C57BL/6 (H-2b) or DBA/2 (H-2d) mice were transplanted under the renal capsules of C57BL/6 recipient mice. Recipients receiving allografts were administered the anti-basophil mAb MAR-1 to examine the antibody-mediated effect on graft survival. At days 4 and 7 post-transplantation, graft-bearing recipient kidneys were harvested for immunohistological analysis and stained with anti-insulin antibody to compare the sizes of grafted islets. On day 7 post-transplantation, the transplanted pancreatic islet clusters in allograft-recipient kidneys had rapidly decreased in size, whereas those in syngeneic recipients remained larger in both size and number. However, MAR-1-treated recipients had increased the numbers of larger insulin-positive allograft islet cell clusters. Basophil-specific mAb treatment contributes to enhance and prolong transplanted islet survival in allogeneic recipient mice.