ArticleMolecular medicine (Cambridge, Mass.)2019
PRSS1 mutation: a possible pathomechanism of pancreatic carcinogenesis and pancreatic cancer.
Article in Molecular medicine (Cambridge, Mass.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
19 citing papers in PubMed, 28 citations in OpenAlex.
- Targeting CYBA inhibits hepatic metastasis of pancreatic cancer through AKT/MLC2 pathway.Acta pharmacologica Sinica · 2026Article
- RNA methyltransferase 3 drives pancreatic acinar cell carcinoma growth and is a therapeutic target.Signal transduction and targeted therapy · 2026Article
- PRSS1 promotes gastric cancer invasion and metastasis by induction of the epithelial-mesenchymal transition and activation of the MAPK/ERK pathway.Translational cancer research · 2026Article
- NHE7-Driven endoplasmic reticulum stress signaling transmission promotes malignant progression of endometrial cancer via c-Fos/PRSS1/ERP27 axis.Journal of experimental & clinical cancer research : CR · 2026Article
- CSIE: cancer subtyping via inference and ensemble.Briefings in bioinformatics · 2026Article
- OSBPL3 promotes LUAD metastasis and glycolysis through transcriptional upregulation of PLAU via NFE2L2.Translational oncology · 2026Article
- Using transcriptomics and molecular docking to uncover the pharmacological targets and its associated biological mechanisms of paeoniflorigenone in treating bladder cancer.Discover oncology · 2026Article
- Mechanism of trypsin-mediated differentiation of pancreatic progenitor cells into functional islet-like clusters.World journal of diabetes · 2025Article
- Emerging roles of ADAM6 and PRSS1 as novel diagnostic/prognostic biomarkers for acute lymphoblastic and myeloid leukemia in adults.BMC cancer · 2025Article
- Targeting sphingosine 1-phosphate and sphingosine kinases in pancreatic cancer: mechanisms and therapeutic potential.Cancer cell international · 2024Review
- PAR2: The Cornerstone of Pancreatic Diseases.Physiological research · 2022Review
- SPCS: a spatial and pattern combined smoothing method for spatial transcriptomic expression.Briefings in bioinformatics · 2022Article
- Therapeutic siRNAs Targeting the JAK/STAT Signalling Pathway in Inflammatory Bowel Diseases.Journal of Crohn's & colitis · 2022Article
- Risk Factors for Pancreatic Cancer: Emerging Role of Viral Hepatitis.Journal of personalized medicine · 2022Review
- CGRP: A New Endogenous Cell Stemness Maintenance Molecule.Oxidative medicine and cellular longevity · 2022Review
- Human Tumor Targeted Cytotoxic Mast Cells for Cancer Immunotherapy.Frontiers in oncology · 2022Article
- Combination of Urine Exosomal mRNAs and lncRNAs as Novel Diagnostic Biomarkers for Bladder Cancer.Frontiers in oncology · 2021Article
- The Landscape of Genetic Alterations Stratified Prognosis in Oriental Pancreatic Cancer Patients.Frontiers in oncology · 2021Article
- Is There a Trojan Horse to Aggressive Pancreatic Cancer Biology? A Review of the Trypsin-PAR2 Axis to Proliferation, Early Invasion, and Metastasis.Journal of pancreatic cancer · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious studies revealed somatic mutations of the cationic trypsinogen gene (PRSS1) in patients with chronic pancreatitis and pancreatic cancer. However, whether PRSS1 mutations trigger pancreatic cancer and/or promote malignant proliferation and metastasis in pancreatic cancer remains largely unclear, as well as the potential underlying mechanisms.
methodsIn the present study, whole-exome sequencing was applied for screening, and the R116C mutation was validated by Sanger sequencing. Phosphorylation antibody array, RNA-Seq, and RT-qPCR were adopted to screen and validate that R116C mutation promoted pancreatic cancer progression via the JAK1-STAT5 pathway.
resultsIt showed that migration and invasion were significantly increased in R116C-bearing PANC-1 cells compared with wild type counterparts. In a transgenic mouse model of iZEG-PRSS1_R116C, primary pancreatic intraepithelial neoplasia (PanINs) was observed in the pancreatic duct.
conclusionsThese findings suggested a novel pathway mediating pancreatic cancer development, with PRSS1 mutation and overexpression playing an "inside job" role in pancreatic carcinogenesis and tumor development.
Indexed as
Identifiers
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.