Cited by 150Chronic Myeloid Leukemia TreatmentsAcute Myeloid Leukemia ResearchRetinoids in leukemia and cellular processes

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

Diaz-Blanco, E, Bruns, I, Neumann, F, Fischer, J C, Graef, T, Rosskopf, M, Brors, B, Pechtel, S, Bork, S, Koch, A, Baer, A, Rohr, U-P, Kobbe, G, Haeseler, A von, Gattermann, N, Haas, R, Kronenwett, R·2007·Leukemia

DOI 10.1038/sj.leu.2404549

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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 factorbeta 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.

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Authors: Diaz-Blanco, E., Bruns, I., Neumann, F., Fischer, J. C., Graef, T., Rosskopf, M., Brors, B., Pechtel, S., Bork, S., Koch, A., Baer, A., Rohr, U.-P., Kobbe, G., Haeseler, A. V., Gattermann, N., Haas, R., & Kronenwett, R.
Affiliations: Heinrich Heine University Düsseldorf (DE)
German Cancer Research Center (DE)
University of Vienna (AT)
Corresponding author: Kronenwett, R
ORCID: Bruns, I
Neumann, F
Fischer, J C
Graef, T
Brors, B
Kobbe, G
Haeseler, A von
Gattermann, N
Haas, R
Kronenwett, R
Venue: Leukemia
Publisher: Springer Science and Business Media LLC
Published: 2007-01-25
Volume: 21
Issue: 3
Pages: 494-504
ISSN: 0887-6924 (ISSN-L)
1476-5551
DOI: 10.1038/sj.leu.2404549
OpenAlex: W2564723484
Cited by: 148
References: 78
Citations by year: 2026: 4 · 2025: 3 · 2024: 6 · 2023: 5 · 2022: 4 · 2021: 10 · 2020: 6 · 2019: 6 · 2018: 2 · 2017: 8 · 2016: 4 · 2015: 10 · 2014: 5 · 2013: 12 · 2012: 7
FWCI: 9.58
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Leukemia (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Hematology › Chronic Myeloid Leukemia Treatments
Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
Keywords: chronic myeloid leukemia, chronic phase, CD34+ hematopoietic stem and progenitor cells, BCR-ABL, gene expression signatures, MAPK signaling, phosphoinositide 3-kinase/Akt pathway, IRF8, HOXA9, MEIS1, megakaryocyte-erythroid progenitors, CFU-GM, fetal hemoglobin, selenoprotein P, leukemogenesis, therapeutic target
MeSH terms: Cell Adhesion, Cell Differentiation, Cell Division, DNA, Neoplasm, Hematopoietic Stem Cells, Humans, Neoplasm Proteins, Receptors, Cell Surface, RNA, Messenger, RNA, Neoplasm, Neoplastic Stem Cells, Signal Transduction, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Leukemia, Myeloid, Chronic-Phase, Up-Regulation, Gene Expression Regulation, Leukemic, Fusion Proteins, bcr-abl, Apoptosis, Receptors, Growth Factor, DNA, Complementary, Antigens, CD34, Gene Expression Profiling, Intercellular Signaling Peptides and Proteins, Receptors, Leptin

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

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