Evidence map›Paper›PMID 27801610›Full record

ArticleCancer biology & therapy2016

Kmt2a cooperates with menin to suppress tumorigenesis in mouse pancreatic islets.

Wenchu Lin, Joshua M Francis, Hong Li, Xiaoping Gao, Chandra Sekhar Pedamallu, Patricia Ernst, Matthew Meyerson

Open access · hybridAbstract read
In one paragraph

Article in Cancer biology & therapy, 2016. 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
1.7field-weighted citation impact, top 15% 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, 27 citations in OpenAlex.

  1. Article
  2. Menin in Cancer.Genes · 2024
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. MENIN loss as a tissue-specific driver of tumorigenesis.Molecular and cellular endocrinology · 2018
    Review
  12. Review
  13. 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

7 authors at 3 institutions in 2 countries.

Wenchu Lina High Magnetic Field Laboratory, Chinese Academy of Sciences , Hefei , Anhui , P.R. China.
Joshua M Francisb Department of Medical Oncology & Center for Cancer Genome Discovery , Dana-Farber Cancer Institute, Harvard Medical School , Boston , MA , USA.
Hong Lia High Magnetic Field Laboratory, Chinese Academy of Sciences , Hefei , Anhui , P.R. China.
Xiaoping Gaoa High Magnetic Field Laboratory, Chinese Academy of Sciences , Hefei , Anhui , P.R. China.
Chandra Sekhar Pedamallub Department of Medical Oncology & Center for Cancer Genome Discovery , Dana-Farber Cancer Institute, Harvard Medical School , Boston , MA , USA.
Patricia Ernstd Department of Pediatrics , The University of Colorado Anschutz Medical Campus , Aurora , USA.
Matthew Meyersonb Department of Medical Oncology & Center for Cancer Genome Discovery , Dana-Farber Cancer Institute, Harvard Medical School , Boston , MA , USA.
Harvard University · USHigh Magnetic Field Laboratory · CNUniversity of Colorado Anschutz Medical Campus · US

Funding

MLL Function in the Maintenance of the Blood Forming SystemR01HL090036 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ERNST, PATRICIA · 2007 to 2015
$3.8M
NHLBI NIH HHS R01 HL090036
6 · The paper itself

Abstract

The reported incidence of pancreatic neuroendocrine tumors (PanNETs) has increased, due in large part to improvements in detection and awareness. However, therapeutic options are limited and a critical need exists for understanding a more thorough characterization of the molecular pathology underlying this disease. The Men1 knockout mouse model recapitulates the early stage of human PanNET development and can serve as a foundation for the development of advanced mouse models that are necessary for preclinical testing. Menin, the product of the MEN1 gene, has been shown to physically interact with the KMT2A and KMT2B histone methyltransferases. Both the KMT2A and MEN1 genes are located on chromosome 11q, which frequently undergoes loss of heterozygosity (LOH) in PanNETs. We report herein that inactivation of Kmt2a in Men1-deficient mice accelerated pancreatic islet tumorigenesis and shortened the average life span. Increases in cell proliferation were observed in mouse pancreatic islet tumors upon inactivation of both Kmt2a and Men1. The Kmt2a/Men1 double knockout mouse model can be used as a mouse model to study advanced PanNETs.

Indexed as

AnimalsCarcinogenesisCell ProliferationHistone-Lysine N-MethyltransferaseIslets of LangerhansLoss of HeterozygosityMiceMice, KnockoutMyeloid-Lymphoid Leukemia ProteinNeoplasms, ExperimentalNeuroendocrine TumorsPancreatic NeoplasmsProto-Oncogene ProteinsHistone-Lysine N-MethyltransferaseKmt2a protein, mouseMen1 protein, mouseMyeloid-Lymphoid Leukemia ProteinProto-Oncogene ProteinsKmt2aMen1methyltransferasePanNETstumorigenesis

Identifiers

PMID27801610
PMCPMC5199165
OpenAlexW2547221042

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.