Evidence map›Paper›PMID 41419303›Full record

ArticleGut2026

Hereditary chronic pancreatitis induced plasticity cooperates with mutant Kras in early pancreatic carcinogenesis.

Tanvi Vikrant Inamdar, Ferdinand Krannich, Nico Hesselbarth, Atul Verma, Teresa Vauti, Mariami Helena Jasaszwili, Ghanem El Kassem, Jasmine Hillmer, Tom Kaune, Michael Boettcher and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gut, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors.

Tanvi Vikrant Inamdar *Department of Internal Medicine I, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Ferdinand Krannich *Department of Internal Medicine I, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Nico Hesselbarth *Department of Internal Medicine I, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Atul VermaDepartment of Internal Medicine I, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Teresa VautiDepartment of Internal Medicine I, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Mariami Helena JasaszwiliDepartment of Internal Medicine I, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.ORCID 0000-0002-2821-5076
Ghanem El KassemInstitute of Molecular Medicine, Section for Molecular Medicine of Signal Transduction, Faculty of Medicine, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Jasmine HillmerInstitute of Molecular Medicine, Section for Molecular Medicine of Signal Transduction, Faculty of Medicine, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Tom KauneDepartment of Internal Medicine I, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.ORCID 0000-0002-7684-4598
Michael BoettcherInstitute of Molecular Medicine, Section for Molecular Medicine of Signal Transduction, Faculty of Medicine, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Ivonne RegelDepartment of Medicine II, University Hospital, Ludwig Maximilian University of Munich, Munich, Germany.ORCID 0000-0002-0206-4441
Heidi GriesmannDepartment of Internal Medicine I, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Irene EspositoInstitute of Pathology, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University, Düsseldorf, Germany.ORCID 0000-0002-0554-2402
Markus GlaßInstitute of Molecular Medicine, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Monika HämmerleInstitute of Pathology, Martin Luther University Halle-Wittenberg, University Medical Center, Halle (Saale), Germany.
Patrick MichlDept. of Internal Medicine IV, Heidelberg University Hospital, Heidelberg, Germany.ORCID 0000-0002-0401-5600
Helmut Laumen *Department of Internal Medicine I, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany jonas.rosendahl@uk-halle.de helmut.laumen@medizin.uni-halle.de.ORCID 0000-0002-5885-5242
Jonas Rosendahl *Department of Internal Medicine I, University Medicine Halle, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany jonas.rosendahl@uk-halle.de helmut.laumen@medizin.uni-halle.de.ORCID 0000-0003-4513-0506

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic pancreatitis (CP) is a risk factor for pancreatic cancer, with inherited cases conferring a markedly increased risk. The underlying mechanisms driving malignant transformation by CP remain poorly understood.

objectiveCombining a recently developed mouse model of CP carrying the human carboxypeptidase A1 (

designWe crossed

resultsKC-Cpa1 pancreata displayed a stark increase in remodelling, fibrosis and formation of metaplastic lesions as compared with KC.

conclusionsThe humanised KC-Cpa1 mouse model reveals the interplay of inflammation in hereditary CP and carcinogenesis.

Indexed as

Pancreatic NeoplasmsPancreatitis, ChronicProto-Oncogene Proteins p21(ras)Acinar CellsAnimalsCarboxypeptidases ACarcinogenesisCell Transformation, NeoplasticDisease Models, AnimalHumansMetaplasiaMiceMutationCarboxypeptidases AHras protein, mouseProto-Oncogene Proteins p21(ras)Pancreatic CancerPancreatic DamagePancreatic DiseasePancreatitis

Identifiers

PMID41419303
PMCPMC13151493

What OpenQuestion holds

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Registered trials

None linked

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.