Evidence map›Paper›PMID 20490631›Full record

ReviewJournal of mammary gland biology and neoplasia2010

Epithelial-mesenchymal transition in cancer: parallels between normal development and tumor progression.

Douglas S Micalizzi, Susan M Farabaugh, Heide L Ford

Abstract readReview
In one paragraph

Review in Journal of mammary gland biology and neoplasia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 512 papers.

0numbers the graph read from it
0cells of the map it votes in
512citing papers in PubMed
–field-weighted citation impact
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

512 citing papers in PubMed.

  1. Article
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  4. Review
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  11. The effect ofArchives of medical science : AMS · 2026
    Article
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  20. Recent Advances in Cancer Immunotherapy Aided by Regulatory Non-Coding RNA: A Review.Asian Pacific journal of cancer prevention : APJCP · 2025
    Review

452 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.

Douglas S MicalizziDepartment of Obstetrics and Gynecology, University of Colorado School of Medicine, Aurora, CO 80045, USA.
Susan M Farabaugh
Heide L Ford

Funding

Role of Six1 in EMT and Tumor ProgressionR01CA095277 · NCI · UNIVERSITY OF COLORADO DENVER · PI FORD, HEIDE L. · 2002 to 2017
$4.3M
NCI NIH HHS 2R01-CA095277NCI NIH HHS R01 CA095277
6 · The paper itself

Abstract

From the earliest stages of embryonic development, cells of epithelial and mesenchymal origin contribute to the structure and function of developing organs. However, these phenotypes are not always permanent, and instead, under the appropriate conditions, epithelial and mesenchymal cells convert between these two phenotypes. These processes, termed Epithelial-Mesenchymal Transition (EMT), or the reverse Mesenchymal-Epithelial Transition (MET), are required for complex body patterning and morphogenesis. In addition, epithelial plasticity and the acquisition of invasive properties without the full commitment to a mesenchymal phenotype are critical in development, particularly during branching morphogenesis in the mammary gland. Recent work in cancer has identified an analogous plasticity of cellular phenotypes whereby epithelial cancer cells acquire mesenchymal features that permit escape from the primary tumor. Because local invasion is thought to be a necessary first step in metastatic dissemination, EMT and epithelial plasticity are hypothesized to contribute to tumor progression. Similarities between developmental and oncogenic EMT have led to the identification of common contributing pathways, suggesting that the reactivation of developmental pathways in breast and other cancers contributes to tumor progression. For example, developmental EMT regulators including Snail/Slug, Twist, Six1, and Cripto, along with developmental signaling pathways including TGF-beta and Wnt/beta-catenin, are misexpressed in breast cancer and correlate with poor clinical outcomes. This review focuses on the parallels between epithelial plasticity/EMT in the mammary gland and other organs during development, and on a selection of developmental EMT regulators that are misexpressed specifically during breast cancer.

Indexed as

Cell TransdifferentiationEmbryonic DevelopmentAnimalsBreast NeoplasmsCell DedifferentiationCell DifferentiationDisease ProgressionEpithelial CellsFemaleHumansMammary Glands, AnimalMammary Glands, HumanMammary Neoplasms, ExperimentalMesenchymal Stem CellsNeoplasm InvasivenessNeoplasm Metastasis

Identifiers

PMID20490631
PMCPMC2886089

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.