Congratulations on the Golden Anniversaries of the American Pancreatic Association and Japan Pancreas Society No abstract available

2019 American Pancreatic Association Presidential Address: On Our Golden Jubilee No abstract available

2019 Japan Pancreas Society Presidential Address: The American Pancreatic Association/Japan Pancreas Society Joint Meeting on Maui Island — The Third American Pancreatic Association/Japan Pancreas Society Joint Meeting No abstract available

The 50th Anniversary of the American Pancreatic Association and Japan Pancreas Society: The Vay Liang and Frisca Go Award for Lifetime Achievement and the Distinguished Service Award No abstract available

Barriers and Research Priorities for Implementing Precision Medicine No abstract available

Precision Medicine in Pancreatic Disease—Knowledge Gaps and Research Opportunities: Summary of a National Institute of Diabetes and Digestive and Kidney Diseases Workshop A workshop on research gaps and opportunities for Precision Medicine in Pancreatic Disease was sponsored by the National Institute of Diabetes and Digestive Kidney Diseases on July 24, 2019, in Pittsburgh. The workshop included an overview lecture on precision medicine in cancer and 4 sessions: (1) general considerations for the application of bioinformatics and artificial intelligence; (2) omics, the combination of risk factors and biomarkers; (3) precision imaging; and (4) gaps, barriers, and needs to move from precision to personalized medicine for pancreatic disease. Current precision medicine approaches and tools were reviewed, and participants identified knowledge gaps and research needs that hinder bringing precision medicine to pancreatic diseases. Most critical were (a) multicenter efforts to collect large-scale patient data sets from multiple data streams in the context of environmental and social factors; (b) new information systems that can collect, annotate, and quantify data to inform disease mechanisms; (c) novel prospective clinical trial designs to test and improve therapies; and (d) a framework for measuring and assessing the value of proposed approaches to the health care system. With these advances, precision medicine can identify patients early in the course of their pancreatic disease and prevent progression to chronic or fatal illness.

Reducing Pancreatic Fibrosis Using Antioxidant Therapy Targeting Nrf2 Antioxidant Pathway: A Possible Treatment for Chronic Pancreatitis Chronic pancreatitis is the progressive inflammation of the pancreas resulting in the irreversible damage of pancreatic structure and function by means of fibrosis. Chronic pancreatitis is most commonly caused by alcohol consumption, although the direct molecular etiology is unknown. Recent studies suggest oxidative stress as a catalyst for pancreatic stellate cell activation leading to the deposition of collagenous extracellular matrix causing pancreatic fibrosis. We review the effect of oxidative stress on pancreatic fibrogenesis and indicate the molecular pathways involved in preventing oxidant-related cell damage. Likewise, we summarize existing antioxidative therapies for chronic pancreatitis and discuss a novel nuclear factor erythroid 2–related factor 2 activator, dimethyl fumarate, and its potential to reduce fibrogenesis by downregulating pancreatic stellate cell activation.

Drug-Induced Acute Pancreatitis in Adults: An Update Drug-induced acute pancreatitis (DIAP) is a rare entity that is often challenging for clinicians. The aim of our study was to provide updated DIAP classes considering the updated definition of acute pancreatitis (AP) and in light of new medications and new case reports. A MEDLINE search (1950–2018) of the English language literature was performed looking for all adult (≥17 years old) human case reports with medication/drug induced as the cause of AP. The included case reports were required to provide the name of the drug, and diagnosis of AP must have been strictly established based on the revised Atlanta Classification criteria. A total of 183 medications were found to be implicated in 577 DIAP cases. A total of 78 cases were excluded because of minimal details or lack of definite diagnosis of AP. Drug-induced AP is rare, and most drugs cause mild DIAP. Only 2 drugs are well described in the literature to explain causation rather than association (azathioprine and didanosine). Larger case-control studies and a formal standardized DIAP reporting system are essential to study the true potential of the DIAP-implicated drugs described in this review.

Evaluation of Phase II Trial Design in Advanced Pancreatic Cancer Objectives We evaluated how well phase II trials in locally advanced and metastatic pancreatic cancer (LAMPC) meet current recommendations for trial design. Methods We conducted a systematic review of phase II first-line treatment trial for LAMPC. We assessed baseline characteristics, type of comparison, and primary end point to examine adherence to the National Cancer Institute recommendations for trial design. Results We identified 148 studies (180 treatment arms, 7505 participants). Forty-seven (32%) studies adhered to none of the 5 evaluated National Cancer Institute recommendations, 62 (42%) followed 1, 31 (21%) followed 2, and 8 (5%) followed 3 recommendations. Studies varied with respect to the proportion of patients with good performance status (range, 0%–80%) and locally advanced disease (range, 14%–100%). Eighty-two (55%) studies concluded that investigational agents should progress to phase III testing; of these, 24 (16%) had documented phase III trials. Three (8%) phase III trials demonstrated clinically meaningful improvements for investigational agents. One of 38 phase II trials that investigated biological investigational agents was enriched for a biomarker. Conclusions Phase II trials do not conform well to current recommendations for trial design in LAMPC.

Establishment and Characterization of 10 Human Pancreatic Cancer Cell Lines Including a HER2 Overexpressed Cell Line Objective The incidence of pancreatic adenocarcinoma (PA) approximates its prevalence, as the malignancy is almost consistently fatal within a year. Although the currently available adjuvant therapy seems to provide survival benefit, it is only moderate, and the standard regimen has not yet been established. Therefore, more biological resources to investigate the PA are needed. Methods Here, we established and characterized 10 human pancreatic cancer cell lines derived from primary tumor mass. Whole exome sequencing technique was used to identify driver mutations and aberrant pathways in each cell line. Results Five anticancer drugs were treated to find half maximal effective concentration (EC50), and the response was analyzed in reference to mutational status. Frame shift mutations in ARID1A gene and HER2 amplification were mutually related to better response to the anticancer drugs. In contrast, frame shift mutation in MSH6 gene was associated with resistance to anticancer drugs. Conclusions In summary, we established 10 pancreatic cancer cell lines and integrated various molecular aberrations and features of pancreatic cancer cells. Our biological resources are expected to contribute to facilitating research on PA.