Characterization of stage progression in chronic myeloid leukemia by DNA microarray with purified hematopoietic stem cells

Ohmine, Ken; Ota, Jun; Ueda, Masuzu; Ueno, Shu‐ichi; Yoshida, Kōji; Yamashita, Yuichi; Kirito, Keita; Imagawa, Shigehiko; Nakamura, Yūichi; Saito, Kenji; Akutsu, Miyuki; Mitani, Kinuko; Kano, Yasuhiko; Komatsu, Norio; Ozawa, Keiya; Mano, Hiroyuki

doi:10.1038/sj.onc.1205029

Cited by 73 publications

(56 citation statements)

References 22 publications

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“…This cell population was compared with fully differentiated normal control cells. In another study, CD133 was used to enrich hematopoietic progenitor cells from patients with CML for gene expression analyses (Ohmine et al, 2001). This study focused on the identification of molecular events associated with disease progression.…”

Section: Discussionmentioning

confidence: 99%

“…Large-scale gene expression analyses of leukemic cells from patients with Ph þ CML have been used to investigate a genomic profile associated with response to therapy with the tyrosine kinase inhibitor imatinib (McLean et al, 2004) and have broadened the knowledge about alterations of gene expression in BCR-ABLpositive cells in comparison with normal cells (Ohmine et al, 2001;Nowicki et al, 2003). While Ohmine and coworkers examined CD133 þ hematopoietic progenitor cells in the study of Nowicki and co-workers mononuclear CML cells were used.…”

Section: Introductionmentioning

confidence: 99%

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Distinct molecular phenotype of malignant CD34+ hematopoietic stem and progenitor cells in chronic myelogenous leukemia

et al. 2005

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Chronic myelogenous leukemia (CML) is a malignant disorder of the hematopoietic stem cell characterized by the BCR-ABL oncogene. We examined gene expression profiles of highly enriched CD34 þ hematopoietic stem and progenitor cells from patients with CML in chronic phase using cDNA arrays covering 1.185 genes. Comparing CML CD34 þ cells with normal CD34 þ cells, we found 158 genes which were significantly differentially expressed. Gene expression patterns reflected BCR-ABLinduced functional alterations such as increased cell-cycle and proteasome activity. Detoxification enzymes and DNA repair proteins were downregulated in CML CD34 þ cells, which might contribute to genetic instability. Decreased expression of junction plakoglobulin and CXC chemokine receptor 4 (CXCR-4) might facilitate the release of immature precursors from bone marrow in CML. GATA-2 was upregulated in CML CD34 þ cells, suggesting an increased self-renewal in comparison with normal CD34 þ cells. Moreover, we found upregulation of the proto-oncogene SKI and of receptors for neuromediators such as opioid l1 receptor, GABA B receptor, adenosine A1 receptor, orexin 1 and 2 receptors and corticotropine-releasing hormone receptor. Treatment of CML progenitor cells with the selective adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) resulted in a dose-dependent significant inhibition of clonogenic growth by 40% at a concentration of 10 À5 M, which could be reversed by the equimolar addition of the receptor agonist 2-chloro-N6-cyclopentyladenosine (Po0.05). The incubation of normal progenitor cells with DPCPX resulted in an inhibition of clonogenic growth to a significantly lesser extent in comparison with CML cells (Po0.05), suggesting that the adenosine A1 receptor is of functional relevance in CML hematopoietic progenitor cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Distinct molecular phenotype of malignant CD34+ hematopoietic stem and progenitor cells in chronic myelogenous leukemia

et al. 2005

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“…26,27 Total RNA extracted from freshly isolated and cultured cells by the acid guanidinium method was used to synthesize double-stranded cDNA. Biotin-labeled cRNA was prepared from each cDNA by ENZO BioArray High-Yield RNA Transcript Labeling kit (Affymetrix, Santa Clara, CA), and hybridized with a GeneChip HGU133A microarray (Affymetrix) harboring more than 22 000 human probe sets.…”

Section: Microarraymentioning

confidence: 99%

Reprogramming of human postmitotic neutrophils into macrophages by growth factors

Araki

Katayama

Yamashita

et al. 2004

Blood

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It is generally recognized that postmitotic neutrophils give rise to polymorphonuclear neutrophils alone. We obtained evidence for a lineage switch of human postmitotic neutrophils into macrophages in culture. When the CD15 ؉ CD14 ؊ cell population, which predominantly consists of band neutrophils, was cultured with granulocyte macrophage-colonystimulating factor, tumor necrosis factor-␣, interferon-␥, and interleukin-4, and subsequently with macrophage colonystimulating factor alone, the resultant cells had morphologic, cytochemical, and phenotypic features of macrophages. In contrast to the starting population, they were negative for myeloperoxidase, specific esterase, and lactoferrin, and they upregulated nonspecific esterase activity and the expression of macrophage colony-stimulating factor receptor, mannose receptor, and HLA-DR. CD15 ؉ CD14 ؊ cells proceeded to macrophages through the CD15 ؊ CD14 ؊ cell population. Microarray analysis of gene expression also disclosed the lineage conversion from neutrophils to macrophages. Macrophages derived from CD15 ؉ CD14 ؊ neutrophils had phagocytic function. Data obtained using 3 different techniques, including Ki-67 staining, bromodeoxyuridine incorporation, and cytoplasmic dye labeling, together with the yield of cells, indicated that the generation of macrophages from CD15 ؉ CD14 ؊ neutrophils did not result from a contamination of progenitors for macrophages. Our data show that in response to cytokines, postmitotic neutrophils can become macrophages. This may represent another differentiation pathway toward macrophages in human postnatal

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“…Previous approaches to elucidate mechanisms of disease transformation with similar techniques as described by us found downregulation of, among others, PIASy, a potential inhibitor of the STAT proteins with apoptosis-promoting and growth suppressive properties 35 and upregulation of PRAME 36 in blast crisis progenitor cells derived from the bone marrow. In another, probably less appropriate experiment, overexpression of ribosomal proteins, of a c-myc-related protein and of a cellular adhesion molecule was found in K562 cells, serving as a model of CML blast crisis, compared to primary CML spleen cells.…”

Section: Other Genesmentioning

confidence: 99%

Identification of genes potentially involved in disease transformation of CML

et al. 2005

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Characterization of stage progression in chronic myeloid leukemia by DNA microarray with purified hematopoietic stem cells

Cited by 73 publications

References 22 publications

Distinct molecular phenotype of malignant CD34+ hematopoietic stem and progenitor cells in chronic myelogenous leukemia

Distinct molecular phenotype of malignant CD34+ hematopoietic stem and progenitor cells in chronic myelogenous leukemia

Reprogramming of human postmitotic neutrophils into macrophages by growth factors

Identification of genes potentially involved in disease transformation of CML

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