Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-12-15
pubmed:abstractText
Identification of molecular pathways essential for cancer stem cells is critical for understanding the underlying biology and designing effective cancer therapeutics. Here, we demonstrated that ?-catenin was activated during development of MLL leukemic stem cells (LSCs). Suppression of ?-catenin reversed LSCs to a pre-LSC-like stage and significantly reduced the growth of human MLL leukemic cells. Conditional deletion of ?-catenin completely abolished the oncogenic potential of MLL-transformed cells. In addition, established MLL LSCs that have acquired resistance against GSK3 inhibitors could be resensitized by suppression of ?-catenin expression. These results unveil previously unrecognized multifaceted functions of ?-catenin in the establishment and drug-resistant properties of MLL stem cells, highlighting it as a potential therapeutic target for an important subset of AMLs.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1878-3686
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
14
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
606-18
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
?-Catenin mediates the establishment and drug resistance of MLL leukemic stem cells.
pubmed:affiliation
Department of Haematological Medicine, King's College London, Denmark Hill, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't