File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: The Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice

TitleThe Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice
Authors
Issue Date2006
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/leu
Citation
Leukemia, 2006, v. 20 n. 10, p. 1829-1839 How to Cite?
AbstractRearrangement of the mixed lineage leukaemia (MLL) gene with extra eleven nineteen (EEN) was previously identified in an infant with acute myeloid leukaemia. Using homologous recombination, we have created a mouse equivalent of the human MLL-EEN allele and showed that when MllEen/+ embryonic stem (ES) cells were induced to differentiate in vitro into haemopoietic cells, there was increased proliferation of myeloid progenitors with self-renewal property. We also generated MllEen/+ chimeric mice, which developed leukaemia displaying enlarged livers, spleens, thymuses and lymph nodes owing to infiltration of MllEen/+-expressing leukemic cells. Immunophenotyping of cells from enlarged organs and bone marrow (BM) of the MllEen/+ chimeras revealed an accumulation of Mac-1+/Gr-1- immature myeloid cells and a reduction in normal B- and T-cell populations. We observed differential regulation of Hox genes between myeloid cells derived from MllEen/+ ES cells and mouse BM leukemic cells which suggested different waves of Hox expression may be activated by MLL fusion proteins for initiation (in ES cells) and maintenance (in leukemic cells) of the disease. We believe studies of MLL fusion proteins in ES cells combined with in vivo animal models offer new approaches to the dissection of molecular events in multistep pathogenesis of leukaemia.
Persistent Identifierhttp://hdl.handle.net/10722/68058
ISSN
2015 Impact Factor: 12.104
2015 SCImago Journal Rankings: 5.142
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKong, CTen_HK
dc.contributor.authorSham, MHen_HK
dc.contributor.authorSo, CWEen_HK
dc.contributor.authorCheah, KSEen_HK
dc.contributor.authorChen, SJen_HK
dc.contributor.authorChan, LCen_HK
dc.date.accessioned2010-09-06T06:00:56Z-
dc.date.available2010-09-06T06:00:56Z-
dc.date.issued2006en_HK
dc.identifier.citationLeukemia, 2006, v. 20 n. 10, p. 1829-1839en_HK
dc.identifier.issn0887-6924en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68058-
dc.description.abstractRearrangement of the mixed lineage leukaemia (MLL) gene with extra eleven nineteen (EEN) was previously identified in an infant with acute myeloid leukaemia. Using homologous recombination, we have created a mouse equivalent of the human MLL-EEN allele and showed that when MllEen/+ embryonic stem (ES) cells were induced to differentiate in vitro into haemopoietic cells, there was increased proliferation of myeloid progenitors with self-renewal property. We also generated MllEen/+ chimeric mice, which developed leukaemia displaying enlarged livers, spleens, thymuses and lymph nodes owing to infiltration of MllEen/+-expressing leukemic cells. Immunophenotyping of cells from enlarged organs and bone marrow (BM) of the MllEen/+ chimeras revealed an accumulation of Mac-1+/Gr-1- immature myeloid cells and a reduction in normal B- and T-cell populations. We observed differential regulation of Hox genes between myeloid cells derived from MllEen/+ ES cells and mouse BM leukemic cells which suggested different waves of Hox expression may be activated by MLL fusion proteins for initiation (in ES cells) and maintenance (in leukemic cells) of the disease. We believe studies of MLL fusion proteins in ES cells combined with in vivo animal models offer new approaches to the dissection of molecular events in multistep pathogenesis of leukaemia.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/leuen_HK
dc.relation.ispartofLeukemiaen_HK
dc.subject.meshAmino Acid Sequenceen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCell Division - physiologyen_HK
dc.subject.meshChimeraen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Profilingen_HK
dc.subject.meshGene Expression Regulation, Leukemicen_HK
dc.subject.meshGenes, Homeobox - physiologyen_HK
dc.subject.meshHematopoietic Stem Cells - pathology - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInfanten_HK
dc.subject.meshIntracellular Signaling Peptides and Proteins - geneticsen_HK
dc.subject.meshLeukemia, Myeloid - genetics - pathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshMyeloid Cells - pathology - physiologyen_HK
dc.subject.meshMyeloid-Lymphoid Leukemia Protein - geneticsen_HK
dc.subject.meshTranslocation, Geneticen_HK
dc.titleThe Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0887-6924&volume=20&spage=1829–1839&epage=&date=2006&atitle=The+Mll-Een+knockin+fusion+gene+enhances+proliferation+of+myeloid+progenitors+derived+from+mouse+embryonic+stem+cells+and+causes+myeloid+leukaemia+in+chimeric+miceen_HK
dc.identifier.emailSham, MH:mhsham@hkucc.hku.hken_HK
dc.identifier.emailCheah, KSE:hrmbdkc@hku.hken_HK
dc.identifier.emailChan, LC:chanlc@hkucc.hku.hken_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.identifier.authorityCheah, KSE=rp00342en_HK
dc.identifier.authorityChan, LC=rp00373en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.leu.2404342en_HK
dc.identifier.pmid16888613-
dc.identifier.scopuseid_2-s2.0-33750076358en_HK
dc.identifier.hkuros123786en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33750076358&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume20en_HK
dc.identifier.issue10en_HK
dc.identifier.spage1829en_HK
dc.identifier.epage1839en_HK
dc.identifier.eissn1476-5551-
dc.identifier.isiWOS:000241381000023-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridKong, CT=7102017292en_HK
dc.identifier.scopusauthoridSham, MH=7003729109en_HK
dc.identifier.scopusauthoridSo, CWE=23395387500en_HK
dc.identifier.scopusauthoridCheah, KSE=35387746200en_HK
dc.identifier.scopusauthoridChen, SJ=13310288700en_HK
dc.identifier.scopusauthoridChan, LC=7403540707en_HK
dc.identifier.citeulike786782-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats