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Tumour-promoting role of EMT-inducing transcription factor ZEB1 in mantle cell lymphoma

Tumour-promoting role of EMT-inducing transcription factor ZEB1 in mantle cell lymphoma
Tumour-promoting role of EMT-inducing transcription factor ZEB1 in mantle cell lymphoma
Epithelial–mesenchymal transition (EMT) is an embryonic trans-differentiation programme that is implicated in organ formation by facilitating the formation of highly motile cells with stem cell capabilities. Most tissues of cells derived from ectoderm or mesoderm retain certain elements of EMT and mesenchymal properties are their differentiation markers. On the other hand, cells of organs derived from endoderm only experience EMT and its reversal (mesenchymal-epithelial transition) at certain phases of development and become differentiated secretory epithelial cells. As de-differentiation is a common feature of cancer progression, acquisition of mesenchymal markers accompanied with the loss of epithelial features can be observed in most carcinomas and considered as the reason of cancer spread (metastasis). For the reasons that (1) more than 85% of all cancers are of epithelial origin and (2) epithelial (differentiated) and mesenchymal (undifferentiated) carcinoma cells are morphologically very different, EMT has been mostly studied in carcinoma setting. However, there is growing evidence suggesting that cancers of organs derived from mesoderm (e.g., hematopoietic malignancies and sarcomas) or ectoderm (e.g., glioblastomas and melanomas) also activate EMT programs to acquire an undifferentiated state and become resistant to conventional therapies.
1350-9047
194-195
Sayan, A. E.
d1dbbcad-9c53-47c1-8b7e-1b45cc56e077
Sayan, A. E.
d1dbbcad-9c53-47c1-8b7e-1b45cc56e077

Sayan, A. E. (2014) Tumour-promoting role of EMT-inducing transcription factor ZEB1 in mantle cell lymphoma. Cell Death and Differentiation, 21 (2), 194-195. (doi:10.1038/cdd.2013.178). (PMID:24413199)

Record type: Article

Abstract

Epithelial–mesenchymal transition (EMT) is an embryonic trans-differentiation programme that is implicated in organ formation by facilitating the formation of highly motile cells with stem cell capabilities. Most tissues of cells derived from ectoderm or mesoderm retain certain elements of EMT and mesenchymal properties are their differentiation markers. On the other hand, cells of organs derived from endoderm only experience EMT and its reversal (mesenchymal-epithelial transition) at certain phases of development and become differentiated secretory epithelial cells. As de-differentiation is a common feature of cancer progression, acquisition of mesenchymal markers accompanied with the loss of epithelial features can be observed in most carcinomas and considered as the reason of cancer spread (metastasis). For the reasons that (1) more than 85% of all cancers are of epithelial origin and (2) epithelial (differentiated) and mesenchymal (undifferentiated) carcinoma cells are morphologically very different, EMT has been mostly studied in carcinoma setting. However, there is growing evidence suggesting that cancers of organs derived from mesoderm (e.g., hematopoietic malignancies and sarcomas) or ectoderm (e.g., glioblastomas and melanomas) also activate EMT programs to acquire an undifferentiated state and become resistant to conventional therapies.

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e-pub ahead of print date: 13 January 2014
Published date: February 2014
Organisations: Cancer Sciences

Identifiers

Local EPrints ID: 396734
URI: http://eprints.soton.ac.uk/id/eprint/396734
ISSN: 1350-9047
PURE UUID: a40188e3-0b7f-482d-9509-f36f3bb6dfc6
ORCID for A. E. Sayan: ORCID iD orcid.org/0000-0002-5291-1485

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Date deposited: 13 Jun 2016 08:56
Last modified: 15 Mar 2024 03:37

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