Evidence map›Paper›PMID 25792600›Full record

ArticleGenes & development2015

Brg1 promotes both tumor-suppressive and oncogenic activities at distinct stages of pancreatic cancer formation.

Nilotpal Roy, Shivani Malik, Karina E Villanueva, Atsushi Urano, Xinyuan Lu, Guido Von Figura, E Scott Seeley, David W Dawson, Eric A Collisson, Matthias Hebrok

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 1 pooled it
–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

107 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. RNA-Seq Profiling Reveals Transcriptional Changes in Phosphorylation-Site Mutants of Brg1.Genes to cells : devoted to molecular & cellular mechanisms · 2026
    Article
  7. Review
  8. Article
  9. The role of SMARCA4 in lung cancer.Scientific reports · 2025
    Review
  10. Article
  11. Development of an orally bioavailable mSWI/SNF ATPase degrader and acquired mechanisms of resistance in prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. (mis)-Targeting of SWI/SNF complex(es) in cancer.Cancer metastasis reviews · 2023
    Review
  18. Article
  19. Article
  20. Review

47 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Nilotpal RoyDiabetes Center, Department of Medicine, University of California at San Francisco, San Francisco, California 94143, USA;
Shivani MalikDepartment of Medicine/Hematology and Oncology, University of California at San Francisco, San Francisco, California 94143, USA;
Karina E VillanuevaDiabetes Center, Department of Medicine, University of California at San Francisco, San Francisco, California 94143, USA;
Atsushi UranoDiabetes Center, Department of Medicine, University of California at San Francisco, San Francisco, California 94143, USA;
Xinyuan LuDepartment of Medicine/Hematology and Oncology, University of California at San Francisco, San Francisco, California 94143, USA;
Guido Von FiguraII. Medizinische Klinik und Poliklinik, Klinikum Rechts der Isar der Technischen Universität München, 81675 Munich, Germany;
E Scott SeeleyDepartment of Pathology, University of California at San Francisco, San Francisco, California 94143, USA;
David W DawsonDepartment of Pathology and Laboratory Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA.
Eric A CollissonDepartment of Medicine/Hematology and Oncology, University of California at San Francisco, San Francisco, California 94143, USA;
Matthias HebrokDiabetes Center, Department of Medicine, University of California at San Francisco, San Francisco, California 94143, USA; mhebrok@diabetes.ucsf.edu.
University of California, San Francisco · USNuklearmedizinische Klinik des Klinikums rechts der Isar · DEUniversity of California, Los Angeles · US

Funding

Targeting diet-induced promotion of Kras-initiated pancreatic adenocarcinomaP01CA163200 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PANDOL, STEPHEN J. · 2012 to 2016
$6.2M
Embryonic Signaling Pathways in Pancreatic CancerR01CA112537 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HEBROK, MATTHIAS · 2004 to 2014
$2.7M
Epigenetic regulation of pancreatic cancerR01CA172045 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HEBROK, MATTHIAS · 2014 to 2018
$1.6M
Crucial Microenvironmental Cofactors for Pancreatic Cancer PathogenesisR01CA178015 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI COLLISSON, ERIC · 2014 to 2018
$1.5M
A Model for Preclinical Biomarker Discovery in Pancreatic Ductal AdenocarcinomaK08CA137153 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI COLLISSON, ERIC · 2010 to 2014
$815k
NCI NIH HHS K08 CA137153NCI NIH HHS K08CA137153NCI NIH HHS R01 CA112537NCI NIH HHS R01CA112537NCI NIH HHS R01 CA172045NCI NIH HHS R01CA172045NCI NIH HHS R01 CA178015NCI NIH HHS R01CA178015
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDA) develops predominantly through pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous neoplasm (IPMN) precursor lesions. Pancreatic acinar cells are reprogrammed to a "ductal-like" state during PanIN-PDA formation. Here, we demonstrate a parallel mechanism operative in mature duct cells during which functional cells undergo "ductal retrogression" to form IPMN-PDA. We further identify critical antagonistic roles for Brahma-related gene 1 (Brg1), a catalytic subunit of the SWI/SNF complexes, during IPMN-PDA development. In mature duct cells, Brg1 inhibits the dedifferentiation that precedes neoplastic transformation, thus attenuating tumor initiation. In contrast, Brg1 promotes tumorigenesis in full-blown PDA by supporting a mesenchymal-like transcriptional landscape. We further show that JQ1, a drug that is currently being tested in clinical trials for hematological malignancies, impairs PDA tumorigenesis by both mimicking some and inhibiting other Brg1-mediated functions. In summary, our study demonstrates the context-dependent roles of Brg1 and points to potential therapeutic treatment options based on epigenetic regulation in PDA.

Indexed as

AnimalsAzepinesCarcinoma, Pancreatic DuctalCell Transformation, NeoplasticDNA HelicasesGene Expression Regulation, NeoplasticHumansMiceNuclear ProteinsPancreatic NeoplasmsProto-Oncogene Proteins p21(ras)SOX9 Transcription FactorTranscription FactorsTriazolesTumor Cells, CulturedAzepinesDNA HelicasesHras protein, mouse(+)-JQ1 compoundNuclear ProteinsProto-Oncogene Proteins p21(ras)Smarca4 protein, mouseSox9 protein, mouseSOX9 Transcription FactorTranscription FactorsTriazolesBrg1dedifferentiationEMTIPMNKraspancreatic cancer

Identifiers

PMID25792600
PMCPMC4378197
OpenAlexW2112350662

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.