Evidence map›Paper›PMID 20555035›Full record

ArticleEndocrinology2010

Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice.

H-C Jennifer Shen, Kris Ylaya, Klaus Pechhold, Arianne Wilson, Asha Adem, Stephen M Hewitt, Steven K Libutti

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 54 citations in OpenAlex.

  1. Molecular Basis of Pancreatic Neuroendocrine Tumors.International journal of molecular sciences · 2024
    Review
  2. Alternative splicing generates isoform diversity inEndocrine oncology (Bristol, England) · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Pancreatic Neuroendocrine Neoplasms in Multiple Endocrine Neoplasia Type 1.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Men1 maintains exocrine pancreas homeostasis in response to inflammation and oncogenic stress.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. Article
  17. MENIN loss as a tissue-specific driver of tumorigenesis.Molecular and cellular endocrinology · 2018
    Review
  18. Review
  19. Review
  20. Pathophysiology of Gastric NETs: Role of Gastrin and Menin.Current gastroenterology reports · 2017
    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 4 institutions in 1 country.

H-C Jennifer ShenTissue Array Research Program, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-8322, USA.
Kris Ylaya
Klaus Pechhold
Arianne Wilson
Asha Adem
Stephen M Hewitt
Steven K Libutti
National Institutes of Health · USNational Institute of Diabetes and Digestive and Kidney Diseases · USAlbert Einstein College of Medicine · USMontefiore Medical Center · US

Funding

Tissue Array Research ProgramZICBC010923 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HEWITT, STEPHEN · 2009 to 2014
$4.7M
Intramural NIH HHS
6 · The paper itself

Abstract

The pancreatic alpha- and beta-cells are critical components in regulating blood glucose homeostasis via secretion of glucagon and insulin, respectively. Both cell types are typically localized in the islets of Langerhans. However, little is known about the roles of paracrine interactions that contribute to their physiological functions. The lack of suitable cell lines to study alpha- and beta-cells interactions have led us to develop an alpha-cell-specific Cre-expressing transgenic line utilizing a glucagon promoter sequence, the Glu-Cre transgenic mouse. Here, we demonstrate that the Glu-Cre could specifically and efficiently excise floxed target genes in adult islet alpha-cells. We further showed that deletion of the tumor suppressor gene, multiple endocrine neoplasia type 1 (Men1), in alpha-cells led to tumorigenesis. However, to our surprise, the lack of Men1 in alpha-cells did not result in glucagonomas but rather beta-cell insulinomas. Because deletion of the Men1 alleles was only present in alpha-cells, our data suggested that cross communication between alpha- and beta-cells contributes to tumorigenesis in the absence of Men1. Together, we believed that the new model systems described here will allow future studies to decipher cellular interactions between islet alpha- and beta-cells in a physiological context.

Indexed as

AnimalsCells, CulturedGene DeletionGene Knockdown TechniquesGlucagonGlucagon-Secreting CellsInsulinomaMiceMice, TransgenicOrgan SpecificityPancreatic NeoplasmsProto-Oncogene ProteinsGlucagonMen1 protein, mouseProto-Oncogene Proteins

Identifiers

PMID20555035
PMCPMC2940531
OpenAlexW2073548652

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.