ReviewCurrent opinion in gastroenterology2017
Genetic risk in chronic pancreatitis: the misfolding-dependent pathway.
Review in Current opinion in gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 3 syntheses or guidelines pooled it, 105 citations in OpenAlex.
- Endoplasmic stress-inducing variants in CPB1 and CPA1 and risk of pancreatic cancer: A case-control study and meta-analysis.International journal of cancer · 2022Pooled it
- Bicarbonate defective CFTR variants increase risk for chronic pancreatitis: A meta-analysis.PloS one · 2022Pooled it
- Scale and Scope of Gene-Alcohol Interactions in Chronic Pancreatitis: A Systematic Review.Genes · 2021Pooled it
- Mutations in the pancreatic secretory enzymesProceedings of the National Academy of Sciences of the United States of America · 2018Trial
- Reevaluating the role of TRPV6 deficiency in human and mouse pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Early-Onset and Rapidly Progressive Hereditary Pancreatitis Associated with PRSS1 Mutations in a Romanian Pediatric Cohort.Maedica · 2026Article
- Personalizing treatment of pancreatitis-associated chronic pain: the need for an integrated omics approach.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- High-fat diet accelerates pancreas pathology in theFrontiers in physiology · 2026Article
- Advancing Gene Therapy for Pancreatitis: From Genetic Insights to Clinical Translation.Research (Washington, D.C.) · 2026Review
- Distinct chronic Pancreatitis Genetic Variants CPA1 N256K and PNLIP T221M Share Common Pathological Grounds.Cellular and molecular gastroenterology and hepatology · 2026Article
- Advancing the Diagnosis and Treatment of Early Chronic Pancreatitis Through Innovation in Imaging and Biomarker Profiling-A Narrative Review.Life (Basel, Switzerland) · 2025Review
- MisfoldingAmerican journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Chymotrypsin B2 (CTRB2) Deletion Variant Induces Endoplasmic Reticulum Stress but does not Increase Risk for Chronic Pancreatitis.Pancreas · 2025Article
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- Genetics and clinical implications of SPINK1 in the pancreatitis continuum and pancreatic cancer.Human genomics · 2025Review
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- Misfolding PRSS1 variant p.Ala61Val in a case of suspected intrauterine pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2025Article
- Carboxyl ester lipase hybrid 1 (CEL-HYB1) haplotypes confer varying risk for chronic pancreatitis.Scientific reports · 2024Article
- Genotypes of carboxypeptidase A1 and gamma-glutamyltransferase 1 may be useful tools for the diagnosis and the predictor of worrisome features of intraductal papillary mucinous neoplasm in Japan.JGH open : an open access journal of gastroenterology and hepatology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
purpose of reviewGenetic risk in chronic pancreatitis is partly due to mutations that cause misfolding of digestive enzymes and elicit endoplasmic reticulum stress. This review examines recent developments in this concept. RECENT
findingsThe best characterized misfolding variants in the highly expressed digestive proteases cationic trypsinogen (PRSS1) and carboxypeptidase A1 (CPA1) are strong, causative risk factors for chronic pancreatitis and may be associated with autosomal dominant hereditary pancreatitis. SUMMARY: Properties of misfolding digestive enzyme mutants indicate that endoplasmic reticulum stress is a highly relevant pathological mechanism and a potential therapeutic target in chronic pancreatitis.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.