Evidence map›Paper›PMID 20012924›Full record

ReviewCancer metastasis reviews2009

Role of epithelial-to-mesenchymal transition (EMT) in drug sensitivity and metastasis in bladder cancer.

David J McConkey, Woonyoung Choi, Lauren Marquis, Frances Martin, Michael B Williams, Jay Shah, Robert Svatek, Aditi Das, Liana Adam, Ashish Kamat and 2 more

Open access · greenAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 222 papers.

0numbers the graph read from it
0cells of the map it votes in
222citing papers in PubMed
7.7field-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

222 citing papers in PubMed, 374 citations in OpenAlex.

  1. Treatment Efficacy and Molecular Dynamics of Neoadjuvant Durvalumab and Olaparib in Resectable Urothelial Bladder Cancer: The NEODURVARIB Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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162 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

12 authors at 1 institution in 1 country.

David J McConkeyDepartment of Urology, U.T. M.D. Anderson Cancer Center, P.O. Box 1373, 1515 Holcombe Boulevard, Houston, TX 77030, USA. dmcconke@mdanderson.org
Woonyoung Choi
Lauren Marquis
Frances Martin
Michael B Williams
Jay Shah
Robert Svatek
Aditi Das
Liana Adam
Ashish Kamat
Arlene Siefker-Radtke
Colin Dinney
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Epithelial-to-mesenchymal transition (EMT) is a process that plays essential roles in development and wound healing that is characterized by loss of homotypic adhesion and cell polarity and increased invasion and migration. At the molecular level, EMT is characterized by loss of E-cadherin and increased expression of several transcriptional repressors of E-cadherin expression (Zeb-1, Zeb-2, Twist, Snail, and Slug). Early work established that loss of E-cadherin and increased expression of MMP-9 was associated with a poor clinical outcome in patients with urothelial tumors, suggesting that EMT might also be associated with bladder cancer progression and metastasis. More recently, we have used global gene expression profiling to characterize the molecular heterogeneity in human urothelial cancer cell lines (n = 20) and primary patient tumors, and unsupervised clustering analyses revealed that the cells naturally segregate into two discrete "epithelial" and "mesenchymal" subsets, the latter consisting entirely of muscle-invasive tumors. Importantly, sensitivity to inhibitors of the epidermal growth factor receptor (EGFR) or type-3 fibroblast growth factor receptor (FGFR3) was confined to the "epithelial" subset, and sensitivity to EGFR inhibitors could be reestablished by micro-RNA-mediated molecular reversal of EMT. The results suggest that EMT coordinately regulates drug resistance and muscle invasion/metastasis in urothelial cancer and is a dominant feature of overall cancer biology.

Indexed as

Drug Resistance, NeoplasmCadherinsCarcinoma, Transitional CellCell Line, TumorCell TransdifferentiationDisease ProgressionEpitheliumErbB ReceptorsFibroblast Growth Factor 3Gene Expression ProfilingGene Expression Regulation, DevelopmentalGene Expression Regulation, NeoplasticHumansMesodermMicroRNAsModels, BiologicalCadherinsEGFR protein, humanErbB ReceptorsFGF3 protein, humanFibroblast Growth Factor 3MicroRNAsNeoplasm ProteinsTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, human

Identifiers

PMID20012924
PMCPMC5915353
OpenAlexW2078134150

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.