Evidence map›Paper›PMID 21425406›Full record

ArticleStem cells (Dayton, Ohio)2011

Ets2 regulates colonic stem cells and sensitivity to tumorigenesis.

Jorge Múnera, Grace Ceceña, Paul Jedlicka, Miriam Wankell, Robert G Oshima

Open access · greenAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Goblet cell differentiation subgroups in colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Article
  6. Prenatal stress induces changes in PAR2- and M3-dependent regulation of colon primitive cells.American journal of physiology. Gastrointestinal and liver physiology · 2022
    Article
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  20. ETS2 mediated tumor suppressive function and MET oncogene inhibition in human non-small cell lung cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    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

5 authors at 3 institutions in 1 country.

Jorge MúneraTumor Development Program, Cancer Research Center, Sanford-Burnham Medical Research Institute, La Jolla, California 92037, USA.
Grace Ceceña
Paul Jedlicka
Miriam Wankell
Robert G Oshima
Sanford Burnham Prebys Medical Discovery Institute · USCancer Research Center · USUniversity of Colorado Denver · US

Funding

Tumor Microenvironment and Cancer ImmunologyP30CA030199 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI Michael Jackson · 1985 to 2026
$107.2M
Signaling Interactions in Cell Survival and InvasionP01CA102583 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI FENG, GEN-SHENG · 2004 to 2008
$11.4M
Tumor repressive role of Ets2 in the intestineR01DK092084 · NIDDK · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI OSHIMA, ROBERT GLEN · 2010 to 2012
$1.3M
NCI NIH HHS P01 CA102583NCI NIH HHS P01-CA102583-05S1NCI NIH HHS P30 CA030199NCI NIH HHS P30 CA30199NIDDK NIH HHS R01 DK092084
6 · The paper itself

Abstract

Ets2 has both tumor repressive and supportive functions for different types of cancer. We have investigated the role of Ets2 within intestinal epithelial cells in postnatal mouse colon development and tumorigenesis. Conditional inactivation of Ets2 within intestinal epithelial cells results in over representation of Ets2-deficient colon crypts within young and adult animals. This preferential representation is associated with an increased number of proliferative cells within the stem cell region and an increased rate of crypt fission in young mice that result in larger patches of Ets2-deficient crypts. These effects are consistent with a selective advantage of Ets2-deficient intestinal stem cells in colonizing colonic crypts and driving crypt fission. Ets2-deficient colon crypts have an increased mucosal thickness, an increased number of goblet cells, and an increased density. Mice with Ets2-deficient intestinal cells develop more colon tumors in response to treatment with azoxymethane and dextran sulfate sodium. The selective population of colon crypts, the altered differentiation state and increased sensitivity to carcinogen-induced tumors all indicate that Ets2 deficiency alters colon stem cell number or behavior. Ets2-dependent, epithelial cell-autonomous repression of intestinal tumors may contribute to protection from colon cancer of persons with increased dosage of chromosome 21.

Indexed as

AdenomaAdult Stem CellsAnimalsCell ProliferationCells, CulturedCell Transformation, NeoplasticColonColonic NeoplasmsDown-RegulationFemaleGenetic Predisposition to DiseaseIntestinal MucosaMiceMice, Inbred C57BLMice, TransgenicOrgan SpecificityEts2 protein, mouseProto-Oncogene Protein c-ets-2

Identifiers

PMID21425406
PMCPMC3339631
OpenAlexW1997238736

What OpenQuestion holds

Textmetadata
LicenceTDM
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.