Molecular signature of CD34+ hematopoietic stem and progenitor cells of patients with CML in chronic phase View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2007-01-25

AUTHORS

E Diaz-Blanco, I Bruns, F Neumann, J C Fischer, T Graef, M Rosskopf, B Brors, S Pechtel, S Bork, A Koch, A Baer, U-P Rohr, G Kobbe, A von Haeseler, N Gattermann, R Haas, R Kronenwett

ABSTRACT

In this study, we provide a molecular signature of highly enriched CD34+ cells from bone marrow of untreated patients with chronic myelogenous leukemia (CML) in chronic phase in comparison with normal CD34+ cells using microarrays covering 8746 genes. Expression data reflected several BCR-ABL-induced effects in primary CML progenitors, such as transcriptional activation of the classical mitogen-activated protein kinase pathway and the phosphoinositide-3 kinase/AKT pathway as well as downregulation of the proapoptotic gene IRF8. Moreover, novel transcriptional changes in comparison with normal CD34+ cells were identified. These include upregulation of genes involved in the transforming growth factorβ pathway, fetal hemoglobin genes, leptin receptor, sorcin, tissue inhibitor of metalloproteinase 1, the neuroepithelial cell transforming gene 1 and downregulation of selenoprotein P. Additionally, genes associated with early hematopoietic stem cells (HSC) and leukemogenesis such as HoxA9 and MEIS1 were transcriptionally activated. Differential expression of differentiation-associated genes suggested an altered composition of the CD34+ cell population in CML. This was confirmed by subset analyses of chronic phase CML CD34+ cells showing an increase of the proportion of megakaryocyte-erythroid progenitors, whereas the proportion of HSC and granulocyte–macrophage progenitors was decreased in CML. In conclusion, our results give novel insights into the biology of CML and could provide the basis for identification of new therapeutic targets. More... »

PAGES

494-504

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  • Journal

    TITLE

    Leukemia

    ISSUE

    3

    VOLUME

    21

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/sj.leu.2404549

    DOI

    http://dx.doi.org/10.1038/sj.leu.2404549

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1043862344

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/17252012


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