Associated Papers
Tumor microenvironment-preserving gliosarcoma organoids as an in vitro preclinical platform: a comparative analysis with glioblastoma models.
Park J et al.
Journal of Translational Medicine, 2025
40813987 (PubMed )
Supplement: 12967_2025_6952_MOESM2_ESM.xlsx › GS21-01
Surveillance Outcome and Genetic Findings in Individuals at High Risk of Pancreatic Cancer.
Rosner G et al.
Clinical and Translational Gastroenterology, 2024
Circulating tumor DNA as a marker of treatment response in BRAF V600E mutated non-melanoma solid tumors.
Ahlborn LB et al.
Oncotarget, 2018
30220966 (PubMed )
Supplement: oncotarget-09-32570-s003.xlsx › Sheet1
Human cationic trypsinogen (PRSS1) variants and chronic pancreatitis.
Németh BC et al.
American Journal of Physiology. Gastrointestinal and Liver Physiology, 2014
Functional effects of 13 rare PRSS1 variants presumed to cause chronic pancreatitis.
Schnúr A et al.
Gut, 2014
Genetics and pathogenesis of chronic pancreatitis: the 2012 update.
Chen JM et al.
Clinics and Research in Hepatology and Gastroenterology, 2012
Pancreas divisum is not a cause of pancreatitis by itself but acts as a partner of genetic mutations.
Bertin C et al.
The American Journal of Gastroenterology, 2012
Uncertainties in the classification of human cationic trypsinogen (PRSS1) variants as hereditary pancreatitis-associated mutations.
Szmola R et al.
Journal of Medical Genetics, 2010
Pathology analysis reveals that dysplastic pancreatic ductal lesions are frequent in patients with hereditary pancreatitis.
Rebours V et al.
Clinical Gastroenterology and Hepatology : the Official Clinical Practice Journal of the American Gastroenterological Association, 2010
The natural history of hereditary pancreatitis: a national series.
Rebours V et al.
Gut, 2009
Risk of pancreatic adenocarcinoma in patients with hereditary pancreatitis: a national exhaustive series.
Rebours V et al.
The American Journal of Gastroenterology, 2008
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