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Title: CANCELLED EMT and back again: does cellular plasticity fuelneoplasticprogressi on?

Abstract

Epithelial-mesenchymal transition (EMT) is a cellular transdifferentiation program that facilitates organ morphogenesis and tissue remodeling in physiological processes such as embryonic development and wound healing. However, a similar phenotypic conversion is also detected in fibrotic diseases and neoplasia, in which it is associated with disease progression. EMT in cancer epithelial cells often appears to be an incomplete and bi-directional process. Here we discuss the phenomenon of EMT as it pertains to tumor development, focusing on exceptions to the commonly held rule that EMT promotes invasion and metastasis. We also highlight the role of the Ras-controlled signaling mediators, ERK1, ERK2 and PI3-kinase, as microenvironmental responsive regulators of EMT.

Authors:
; ; ;
Publication Date:
Research Org.:
Ernest Orlando Lawrence Berkeley NationalLaboratory, Berkeley, CA (US)
Sponsoring Org.:
USDOE Director. Office of Science. Biological andEnvironmental Research
OSTI Identifier:
928784
Report Number(s):
LBNL-62604
R&D Project: 443180; BnR: KP1104010; TRN: US200811%%335
DOE Contract Number:  
DE-AC02-05CH11231
Resource Type:
Journal Article
Resource Relation:
Journal Name: Nature Clinical Practice Oncology; Journal Volume: 5; Related Information: Journal Publication Date: 05/01/2008
Country of Publication:
United States
Language:
English
Subject:
60; DISEASES; FOCUSING; HEALING; MORPHOGENESIS; NEOPLASMS; ONTOGENESIS; ORGANS; PLASTICITY

Citation Formats

Turley, Eva A., Veiseh, Mandana, Radisky, Derek C., and Bissell, MinaJ. CANCELLED EMT and back again: does cellular plasticity fuelneoplasticprogressi on?. United States: N. p., 2007. Web.
Turley, Eva A., Veiseh, Mandana, Radisky, Derek C., & Bissell, MinaJ. CANCELLED EMT and back again: does cellular plasticity fuelneoplasticprogressi on?. United States.
Turley, Eva A., Veiseh, Mandana, Radisky, Derek C., and Bissell, MinaJ. Sat . "CANCELLED EMT and back again: does cellular plasticity fuelneoplasticprogressi on?". United States. doi:. https://www.osti.gov/servlets/purl/928784.
@article{osti_928784,
title = {CANCELLED EMT and back again: does cellular plasticity fuelneoplasticprogressi on?},
author = {Turley, Eva A. and Veiseh, Mandana and Radisky, Derek C. and Bissell, MinaJ.},
abstractNote = {Epithelial-mesenchymal transition (EMT) is a cellular transdifferentiation program that facilitates organ morphogenesis and tissue remodeling in physiological processes such as embryonic development and wound healing. However, a similar phenotypic conversion is also detected in fibrotic diseases and neoplasia, in which it is associated with disease progression. EMT in cancer epithelial cells often appears to be an incomplete and bi-directional process. Here we discuss the phenomenon of EMT as it pertains to tumor development, focusing on exceptions to the commonly held rule that EMT promotes invasion and metastasis. We also highlight the role of the Ras-controlled signaling mediators, ERK1, ERK2 and PI3-kinase, as microenvironmental responsive regulators of EMT.},
doi = {},
journal = {Nature Clinical Practice Oncology},
number = ,
volume = 5,
place = {United States},
year = {Sat Feb 24 00:00:00 EST 2007},
month = {Sat Feb 24 00:00:00 EST 2007}
}