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dc.contributor.authorSchulte, CE
dc.contributor.authorvon Lindern, M
dc.contributor.authorSteinlein, P
dc.contributor.authorBeug, H
dc.contributor.authorWiedemann, LM
dc.identifier.citationEMBO JOURNAL, 2002, 21 pp. 4297 - 4306
dc.description.abstractThe MLL gene is targeted by chromosomal translocations, which give rise to heterologous MLL fusion proteins and are associated with distinct types of acute lymphoid and myeloid leukaemia. To determine how MLL fusion proteins alter the proliferation and/or differentiation of primary haematopoietic progenitors, we introduced the MLL-AF9 and MLL-ENL fusion proteins into primary chicken bone marrow cells. Both fusion proteins caused the sustained outgrowth of immature haematopoietic cells, which was strictly dependent on stem cell factor (SCF). The renewing cells have a long in vitro lifespan exceeding the Hayflick limit of avian cells. Analysis of clonal cultures identified the renewing cells as immature, multipotent progenitors, expressing erythroid, myeloid, lymphoid and stem cell surface markers. Employing a two-step commitment/differentiation protocol involving the controlled withdrawal of SCF, the MLL-ENL-transformed progenitors could be induced to terminal erythroid or myeloid differentiation. Finally, in cooperation with the weakly leukaemogenic receptor tyrosine kinase v-Sea, the MLL-ENL fusion protein gave rise to multilineage leukaemia in chicks, suggesting that other activated, receptor tyrosine kinases can substitute for ligand-activated c-Kit in vivo.
dc.format.extent4297 - 4306
dc.titleMLL-ENL cooperates with SCF to transform primary avian multipotent cells
dc.typeJournal Article
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfEMBO JOURNAL
pubs.notesresearcherid-numbers: Wiedemann, Leanne/E-3316-2010 orcid-numbers: Wiedemann, Leanne/0000-0002-0964-4676 unique-id: ISI:000177355300010
pubs.notesNot known
pubs.embargo.termsNot known
dc.contributor.icrauthorSchulte, Cathleenen

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