Transformation from committed progenitor to leukaemia stem cell initiated by MLL–AF9 View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2006-08

AUTHORS

Andrei V. Krivtsov, David Twomey, Zhaohui Feng, Matthew C. Stubbs, Yingzi Wang, Joerg Faber, Jason E. Levine, Jing Wang, William C. Hahn, D. Gary Gilliland, Todd R. Golub, Scott A. Armstrong

ABSTRACT

Leukaemias and other cancers possess a rare population of cells capable of the limitless self-renewal necessary for cancer initiation and maintenance. Eradication of these cancer stem cells is probably a critical part of any successful anti-cancer therapy, and may explain why conventional cancer therapies are often effective in reducing tumour burden, but are only rarely curative. Given that both normal and cancer stem cells are capable of self-renewal, the extent to which cancer stem cells resemble normal tissue stem cells is a critical issue if targeted therapies are to be developed. However, it remains unclear whether cancer stem cells must be phenotypically similar to normal tissue stem cells or whether they can retain the identity of committed progenitors. Here we show that leukaemia stem cells (LSC) can maintain the global identity of the progenitor from which they arose while activating a limited stem-cell- or self-renewal-associated programme. We isolated LSC from leukaemias initiated in committed granulocyte macrophage progenitors through introduction of the MLL-AF9 fusion protein encoded by the t(9;11)(p22;q23). The LSC were capable of transferring leukaemia to secondary recipient mice when only four cells were transferred, and possessed an immunophenotype and global gene expression profile very similar to that of normal granulocyte macrophage progenitors. However, a subset of genes highly expressed in normal haematopoietic stem cells was re-activated in LSC. LSC can thus be generated from committed progenitors without widespread reprogramming of gene expression, and a leukaemia self-renewal-associated signature is activated in the process. Our findings define progression from normal progenitor to cancer stem cell, and suggest that targeting a self-renewal programme expressed in an abnormal context may be possible. More... »

PAGES

818

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature04980

DOI

http://dx.doi.org/10.1038/nature04980

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1030873412

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16862118


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