Pancreatic Acinar Cell Carcinoma Presenting with Diffuse Pancreatic Enlargement.

Pancreatic acinar cell carcinoma (PACC) is a rare tumor of the exocrine pancreas. It accounts for only 1% of all pancreatic malignancies. A 39-year woman sought treatment for repeated abdominal pain and jaundice. The computed tomography (CT) and magnetic resonance imaging (MRI) suggested diffuse enlargement of the pancreas. 18 F-fluorodeoxyglucose (FDG) positron emission tomography (PET)/CT showed diffuse enlargement of the pancreas and increased glucose uptake. The endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) biopsy of the pancreas was performed, and the case was finally diagnosed as PACC. After the sixth course of chemotherapy with gemcitabine and albumin paclitaxel, a CT scan showed significant shrinkage of the pancreas. PACC very rarely presents with diffuse enlargement of the pancreas. This case illustrates a rare presentation of PACC with diffuse pancreatic enlargement, which was effectively treated with gemcitabine and albumin paclitaxel chemotherapy. Key Words: Pancreatic acinar cell carcinoma, Positron emission tomography/computed tomography, Chemotherapy.

Plasmacytoid Dendritic Cell-Derived Type I Interferon Is Involved in Helicobacter pylori Infection-Induced Differentiation of Schlafen 4-Expressing Myeloid-Derived Suppressor Cells.

During chronic infection with Helicobacter pylori, Schlafen 4-expressing myeloid-derived suppressor cells (SLFN4+ MDSCs) create a microenvironment favoring intestinal metaplasia and neoplastic transformation. SLFN4 can be induced by alpha interferon (IFN-α), which is mainly secreted from plasmacytoid dendritic cells (pDCs). This study tested the hypothesis that Helicobacter pylori infection promotes SLFN4+ MDSC differentiation by inducing pDCs to secrete IFN-α. C57BL/6 mice were gavaged with H. pylori, and infection lasted 2, 4, or 6 months. Mouse pDCs were isolated from bone marrow of wild-type C57BL/6J mice. The results showed that H. pylori infection increased the number of SLFN4+ MDSCs by inducing IFN-α expression in mice. Further mechanistic experiments unraveled that IFN-α induced SLFN4 transcription by binding to the Slfn4 promoter. Furthermore, H. pylori infection stimulated pDCs to secrete IFN-α by activating the TLR9-MyD88-IRF7 pathway. Collectively, Helicobacter pylori infection promotes SLFN4+ MDSC differentiation by inducing secretion of IFN-α from pDCs.