Evidence map›Paper›PMID 19852727›Full record

ReviewFuture oncology (London, England)2009

Mechanisms of the epithelial-mesenchymal transition by TGF-beta.

Michael K Wendt, Tressa M Allington, William P Schiemann

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Future oncology (London, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 3 pooled it
8.9field-weighted citation impact, top 2% 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

175 citing papers in PubMed, 3 syntheses or guidelines pooled it, 308 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Plasminogen activator inhibitor-1 promotes the proliferation and blocks TGF-β1-dependent growth inhibition of cholesteatoma keratinocytes by ERK signaling.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026
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  18. MicroRNAs regulating signaling pathways in cardiac fibrosis: potential role of the exercise training.American journal of physiology. Heart and circulatory physiology · 2024
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115 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Michael K WendtDepartment of Pharmacology, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado 80045, USA.
Tressa M Allington
William P Schiemann
University of Colorado Anschutz Medical Campus · US

Funding

Integrin-Mediated Regulation of TGF-Beta Signaling and TumorigenesisR01CA129359 · NCI · UNIVERSITY OF COLORADO DENVER · PI SCHIEMANN, WILLIAM · 2007 to 2016
$2.9M
Use of Cystatin C to Combat TGF-Beta TumorigenesisR01CA114039 · NCI · UNIVERSITY OF COLORADO DENVER · PI SCHIEMANN, WILLIAM · 2005 to 2009
$1.3M
NCI NIH HHS CA114039NCI NIH HHS CA129359NCI NIH HHS R01 CA114039NCI NIH HHS R01 CA129359
6 · The paper itself

Abstract

The formation of epithelial cell barriers results from the defined spatiotemporal differentiation of stem cells into a specialized and polarized epithelium, a process termed mesenchymal-epithelial transition. The reverse process, epithelial-mesenchymal transition (EMT), is a metastable process that enables polarized epithelial cells to acquire a motile fibroblastoid phenotype. Physiological EMT also plays an essential role in promoting tissue healing, remodeling or repair in response to a variety of pathological insults. On the other hand, pathophysiological EMT is a critical step in mediating the acquisition of metastatic phenotypes by localized carcinomas. Although metastasis clearly is the most lethal aspect of cancer, our knowledge of the molecular events that govern its development, including those underlying EMT, remain relatively undefined. Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine that oversees and directs all aspects of cell development, differentiation and homeostasis, as well as suppresses their uncontrolled proliferation and transformation. Quite dichotomously, tumorigenesis subverts the tumor suppressing function of TGF-beta, and in doing so, converts TGF-beta to a tumor promoter that stimulates pathophysiological EMT and metastasis. It therefore stands to reason that determining how TGF-beta induces EMT in developing neoplasms will enable science and medicine to produce novel pharmacological agents capable of preventing its ability to do so, thereby improving the clinical course of cancer patients. Here we review the cellular, molecular and microenvironmental mechanisms used by TGF-beta to mediate its stimulation of EMT in normal and malignant cells.

Indexed as

AnimalsCell DifferentiationCell Transformation, NeoplasticEpitheliumHumansMesodermMetaplasiaTransforming Growth Factor betaTransforming Growth Factor beta

Identifiers

PMID19852727
PMCPMC2858056
OpenAlexW1991973226

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.