ELF5, normal mammary development and the heterogeneous phenotypes of breast cancer

Gallego-Ortega, D; Oakes, SR; Lee, HJ; Piggin, CL; Ormandy, CJ

ELF5, normal mammary development and the heterogeneous phenotypes of breast cancer

Gallego-Ortega, D Oakes, SR Lee, HJ Piggin, CL Ormandy, CJ

Permalink

Publisher:: Future Science Group
Publication Type:: Journal Article
Citation:: Breast Cancer Management, 2013, 2, (6), pp. 489-498
Issue Date:: 2013-11

Closed Access

	Filename	Description	Size
	bmt.13.50.pdf	Published version	3.02 MB	Adobe PDF	View/Open

Copyright Clearance Process

Recently Added
In Progress
Closed Access

This item is closed access and not available.

Full metadata record

Field	Value	Language
dc.contributor.author	Gallego-Ortega, D
dc.contributor.author	Oakes, SR
dc.contributor.author	Lee, HJ
dc.contributor.author	Piggin, CL
dc.contributor.author	Ormandy, CJ
dc.date.accessioned	2023-02-27T19:25:04Z
dc.date.available	2023-02-27T19:25:04Z
dc.date.issued	2013-11
dc.identifier.citation	Breast Cancer Management, 2013, 2, (6), pp. 489-498
dc.identifier.issn	1758-1923
dc.identifier.issn	1758-1931
dc.identifier.uri	http://hdl.handle.net/10453/166469
dc.description.abstract	<jats:p> SUMMARY The ETS transcription factor ELF5 specifies the formation of the secretory cell lineage of the mammary gland during pregnancy, by directing cell fate decisions of the mammary progenitor cells. The decision-making activity continues in breast cancer, where in luminal breast cancer cells forced ELF5 expression suppresses estrogen sensitivity and shifts gene expression toward the basal molecular subtype. The development of anti-estrogen resistance in luminal breast cancer is accompanied by increased expression of ELF5 and acquired dependence on ELF5 for continued proliferation, providing a potential new therapeutic target or prognostic marker to improve the treatment of this stage of the disease. Forced ELF5 expression suppresses the mesenchymal phenotype, making cells more epithelial and producing lower rates of invasion and motility. Conversely, loss of ELF5 promotes metastasis, with a clear corollary in the claudin-low subtype of breast cancer, which does not express ELF5 and is highly metastatic, or during the final stages of tumor progression, where loss of ELF5 expression may be involved in the acquisition of the lethal phenotype. In circumstances where ELF5 expression increases in parallel with metastatic potential, such as anti-estrogen resistant luminal breast cancers and basal breast cancer, there is much more to be understood about ELF5 and metastasis. </jats:p>
dc.language	en
dc.publisher	Future Science Group
dc.relation.ispartof	Breast Cancer Management
dc.relation.isbasedon	10.2217/bmt.13.50
dc.rights	info:eu-repo/semantics/closedAccess
dc.title	ELF5, normal mammary development and the heterogeneous phenotypes of breast cancer
dc.type	Journal Article
utslib.citation.volume	2
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Engineering and Information Technology
pubs.organisational-group	/University of Technology Sydney/Faculty of Engineering and Information Technology/School of Biomedical Engineering
pubs.organisational-group	/University of Technology Sydney/Centre for Health Technologies (CHT)
utslib.copyright.status	closed_access	*
dc.date.updated	2023-02-27T19:25:03Z
pubs.issue	6
pubs.publication-status	Published
pubs.volume	2
utslib.citation.issue	6

Abstract:

SUMMARY The ETS transcription factor ELF5 specifies the formation of the secretory cell lineage of the mammary gland during pregnancy, by directing cell fate decisions of the mammary progenitor cells. The decision-making activity continues in breast cancer, where in luminal breast cancer cells forced ELF5 expression suppresses estrogen sensitivity and shifts gene expression toward the basal molecular subtype. The development of anti-estrogen resistance in luminal breast cancer is accompanied by increased expression of ELF5 and acquired dependence on ELF5 for continued proliferation, providing a potential new therapeutic target or prognostic marker to improve the treatment of this stage of the disease. Forced ELF5 expression suppresses the mesenchymal phenotype, making cells more epithelial and producing lower rates of invasion and motility. Conversely, loss of ELF5 promotes metastasis, with a clear corollary in the claudin-low subtype of breast cancer, which does not express ELF5 and is highly metastatic, or during the final stages of tumor progression, where loss of ELF5 expression may be involved in the acquisition of the lethal phenotype. In circumstances where ELF5 expression increases in parallel with metastatic potential, such as anti-estrogen resistant luminal breast cancers and basal breast cancer, there is much more to be understood about ELF5 and metastasis.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/166469