Evidence map›Paper›PMID 18636077›Full record

ArticleCell death and differentiation2008

The intestinal epithelium compensates for p53-mediated cell death and guarantees organismal survival.

Y A Valentin-Vega, H Okano, G Lozano

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Funerals and Feasts: The Immunological Rites of Cell Death.The Yale journal of biology and medicine · 2019
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Mouse modelling of the MDM2/MDMX-p53 signalling axis.Journal of molecular cell biology · 2017
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. The p53 control of apoptosis and proliferation: lessons from Drosophila.Apoptosis : an international journal on programmed cell death · 2014
    Review
  16. Article
  17. Animal models of colorectal cancer.Cancer metastasis reviews · 2013
    Review
  18. Review
  19. Article
  20. 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

3 authors at 3 institutions in 2 countries.

Y A Valentin-VegaDepartment of Genetics, Program in Genes and Development, The Graduate School of Biomedical Sciences, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
H Okano
G Lozano
Keio University · JPThe Graduate Center, CUNY · USThe University of Texas Health Science Center at Houston · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
PATHWAY OF TUMOR SUPPRESSIONR01CA047296 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GUILLERMINA LOZANO · 1993 to 2026
$8.0M
RELATION OF P53 AND OTHER FACTORS IN TRANSGENIC MICER29CA047296 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI LOZANO, GUILLERMINA · 1988 to 1992
–
NCI NIH HHS CA16672NCI NIH HHS CA47296NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA047296
6 · The paper itself

Abstract

Mdm2 is the major inhibitor of the p53 tumor suppressor. Loss of Mdm2 in mice or in specific tissues of the mouse always yields p53-dependent lethal phenotypes. However, the role of Mdm2 in tissues with high turnover capacity is unknown. We have engineered mice lacking Mdm2 in the intestinal epithelium using the Cre/LoxP system. Loss of Mdm2 (Mdm2(intDelta)) results in viable animals, but neonates display multiple intestinal abnormalities such as hyperplasia, enterocyte vacuolization, and inflammation. These defects correlate with a drastic increase in p53-dependent apoptosis in highly proliferative and differentiated cells. Unexpectedly, the observed phenotypes disappear with age. The tissue selects against Mdm2-null cells and increases its proliferative capacity. Additionally, the intestinal stem and progenitor cell populations are enriched leading to an increase in crypt fission events. Enhanced proliferation is achieved by activation of the canonical Wnt and EGFR-mediated Ras/MAPK pathways. While Mdm2 is a critical inhibitor of p53 in the intestinal epithelium, the tissue employs a series of processes that compensate for cell death.

Indexed as

AnimalsCell DeathCell DifferentiationCell ProliferationDNAEpithelial CellsErbB ReceptorsIntestinal MucosaMAP Kinase Signaling SystemMiceProto-Oncogene Proteins c-mdm2ras ProteinsSurvival AnalysisTumor Suppressor Protein p53Wnt ProteinsDNAErbB ReceptorsMdm2 protein, mouseProto-Oncogene Proteins c-mdm2ras ProteinsTumor Suppressor Protein p53Wnt Proteins

Identifiers

PMID18636077
PMCPMC2742618
OpenAlexW2061031835

What OpenQuestion holds

Textmetadata
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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.