Evidence map›Paper›PMID 42601023›Full record

ArticleCellular and molecular gastroenterology and hepatology2026

Evolutionarily Conserved Epigenetic Regulation of Transcriptional Cell States During Vertebrate Pancreatic Tumorigenesis.

Somer M Matar, Sandra Blázquez-Araguás, Andrea Diéguez-Docampo, Xiaoying Liu, Annie Katanga, Jordan E Magurk, Nicole F Gallien, Michael J Dong, Maria Lao, Nuray Tezcan and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

16 authors.

Somer M MatarDepartment of Molecular and Systems Biology and Dartmouth Cancer Center, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire.
Sandra Blázquez-AraguásInstitute for Research in Biomedicine (IRB), The Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Andrea Diéguez-DocampoInstitute for Research in Biomedicine (IRB), The Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Xiaoying LiuDepartment of Molecular and Systems Biology and Dartmouth Cancer Center, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire; Department of Pathology and Laboratory Medicine, Dartmouth Hitchcock Medical Center, Hanover, New Hampshire.
Annie KatangaDepartment of Molecular and Systems Biology and Dartmouth Cancer Center, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire.
Jordan E MagurkDepartment of Molecular and Systems Biology and Dartmouth Cancer Center, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire.
Nicole F GallienDepartment of Molecular and Systems Biology and Dartmouth Cancer Center, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire.
Michael J DongDepartment of Molecular and Systems Biology and Dartmouth Cancer Center, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire.
Maria LaoRubenstein Center for Pancreatic Cancer Research, Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York.
Nuray TezcanRubenstein Center for Pancreatic Cancer Research, Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York.
Zeynep TarcanRubenstein Center for Pancreatic Cancer Research, Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York.
Robert TsengDepartment of Surgery, Yale University, New Haven, Connecticut; Department of Therapeutic Radiology, Yale University, New Haven, Connecticut.
Luisa Escobar-HoyosDepartment of Therapeutic Radiology, Yale University, New Haven, Connecticut; Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut; Division of Oncology, Department of Medicine, Yale University, New Haven, Connecticut.
Direna Alonso-CurbeloInstitute for Research in Biomedicine (IRB), The Barcelona Institute of Science and Technology (BIST), Barcelona, Spain. Electronic address: direna.alonso-curbelo@irbbarcelona.org.
Britton C GoodaleDepartment of Molecular and Systems Biology and Dartmouth Cancer Center, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire. Electronic address: britton.c.goodale@dartmouth.edu.
Steven D LeachDepartment of Molecular and Systems Biology and Dartmouth Cancer Center, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire. Electronic address: steven.d.leach@dartmouth.edu.

Funding

Translational Engineering in Cancer (TEC)P30CA023108 · NCI · DARTMOUTH COLLEGE · PI Fred W Kolling IV · 1985 to 2026
$91.3M
Unleashing T-cell anti-tumor response through repair of altered RNA splicing and antigen mimicry recognitionDP2CA280625 · NCI · YALE UNIVERSITY · PI ESCOBAR HOYOS, LUISA · 2022 to 2025
$2.5M
Understanding and targeting mutant splicing factors in pancreatic cancerR01CA274355 · NCI · YALE UNIVERSITY · PI ESCOBAR HOYOS, LUISA · 2022 to 2025
$2.4M
Program for Oncology Workforce Education and Research Experience at DartmouthR25CA250956 · NCI · DARTMOUTH COLLEGE · PI FIERING, STEVEN · 2020 to 2024
$841k
Altered mRNA splicing dependent on mutant p53 identifies novel therapeutic vulnerability in pancreatic cancerR00CA226342 · NCI · YALE UNIVERSITY · PI ESCOBAR HOYOS, LUISA · 2020 to 2022
$741k
NCI NIH HHS DP2 CA280625NCI NIH HHS P30 CA023108NCI NIH HHS R00 CA226342NCI NIH HHS R01 CA274355NCI NIH HHS R25 CA250956
6 · The paper itself

Abstract

BACKGROUND &

aimsAlthough the majority of human pancreatic cancers are classified as pancreatic ductal adenocarcinomas, tumors are comprised of diverse dedifferentiated tumor cell states that dynamically interact with an equally complex microenvironment, making it imperative to understand, in vivo, how normal epithelial identity is (dys)regulated during tumorigenesis.

methodsHere, we integrate data from mouse and human pancreatic ductal adenocarcinoma with a unique zebrafish model of pancreatic cancer to elucidate evolutionarily conserved mechanisms regulating dedifferentiation during pancreatic tumorigenesis.

resultsHistologic and single-cell transcriptional profiling of heterogeneous tumors developing in dual-transgenic ptf1a:Gal4-VP16; UAS:mKO2- KRAS

conclusionsThese findings suggest a highly conserved role for HDAC9 and class IIA histone deacetylases in vertebrate pancreatic tumorigenesis and may lead to new strategies for reactivating (normal acinar-epithelial) differentiation programs to intercept and treat pancreatic ductal adenocarcinoma.

Indexed as

Acinar-to-DuctalDiversityKRAS MutantMetaplasiaProgenitorptf1a

Identifiers

PMID42601023
PMCPMC13654501

What OpenQuestion holds

Textmetadata
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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.