Evidence map›Paper›PMID 32156729›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

Men1 maintains exocrine pancreas homeostasis in response to inflammation and oncogenic stress.

Amanda R Wasylishen, Chang Sun, Gilda P Chau, Yuan Qi, Xiaoping Su, Michael P Kim, Jeannelyn S Estrella, Guillermina Lozano

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.9field-weighted citation impact, top 6% of its field
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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Vitamin BMedComm · 2024
    Article
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  5. Article
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  7. Review
  8. Article
  9. Article
  10. Insights into Mechanisms of Tumorigenesis in Neuroendocrine Neoplasms.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Article
  13. Article
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

8 authors at 1 institution in 1 country.

Amanda R WasylishenDepartment of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX 77030.ORCID 0000-0002-1940-5169
Chang SunDepartment of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Gilda P ChauDepartment of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Yuan QiDepartment of Bioinformatics and Computational Biology, University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Xiaoping SuDepartment of Bioinformatics and Computational Biology, University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Michael P KimDepartment of Surgical Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Jeannelyn S EstrellaDepartment of Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Guillermina LozanoDepartment of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX 77030; gglozano@mdanderson.org.ORCID 0000-0001-8985-4886
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Defining diverse roles of p53 in pancreatic cancerK08CA218690 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KIM, MICHAEL PAUL · 2017 to 2021
$853k
(PQ4) Mutations in the histone chaperone DAXX drive pancreatic neuroendocrine tumors not ductal adenocarcinomasR21CA208463 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOZANO, GUILLERMINA · 2016 to 2017
$383k
CIHRNCI NIH HHS K08 CA218690NCI NIH HHS P30 CA016672NCI NIH HHS R21 CA208463
6 · The paper itself

Abstract

A more comprehensive understanding of the molecular mechanisms underlying pancreatic diseases, including pancreatitis and cancer, is essential to improve clinical management. MEN1 has established roles in epigenetic regulation and tumor suppression in the endocrine pancreas; however, intriguing recent data suggest MEN1 may also function in the exocrine pancreas. Using physiologically relevant genetic mouse models, we provide direct evidence that Men1 is essential for exocrine pancreas homeostasis in response to inflammation and oncogenic stress. Men1 loss causes increased injury and impaired regeneration following acute caerulein-induced pancreatitis, leading to more severe damage, loss of the normal acinar compartment, and increased cytokeratin 19-positive metaplasias and immune cell infiltration. We further demonstrate the Men1 protein is stabilized in response to insult, and loss of Men1 is associated with the overexpression of proinflammatory Jund target genes, suggesting that loss of Men1-mediated repression of Jund activity is, at least in part, responsible for the impaired response. Finally, we demonstrate that

Indexed as

HomeostasisAnimalsBiomarkersCarcinogenesisCarcinoma, Pancreatic DuctalCell DifferentiationFemaleGene Expression RegulationHigh-Throughput Nucleotide SequencingInflammationMaleMiceMice, Inbred C57BLMice, KnockoutMutationPancreas, ExocrineBiomarkersHras protein, mousejunD protein, mouseMen1 protein, mouseProto-Oncogene ProteinsProto-Oncogene Proteins c-junProto-Oncogene Proteins p21(ras)acute pancreatitisJundMen1MLL

Identifiers

PMID32156729
PMCPMC7104337
OpenAlexW3012353851

What OpenQuestion holds

Textmetadata
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.