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FIP1L1-PDGFRA in chronic eosinophilic leukemia and BCR-ABL1 in chronic myeloid leukemia affect different leukemic cells

FIP1L1-PDGFRA in chronic eosinophilic leukemia and BCR-ABL1 in chronic myeloid leukemia affect different leukemic cells
FIP1L1-PDGFRA in chronic eosinophilic leukemia and BCR-ABL1 in chronic myeloid leukemia affect different leukemic cells
We investigated genetically affected leukemic cells in FIP1L1-PDGFRA+ chronic eosinophilic leukemia (CEL) and in BCR-ABL1+ chronic myeloid leukemia (CML), two myeloproliferative disorders responsive to imatinib. Fluorescence in situ hybridization specific for BCR-ABL1 and for FIP1L1-PDGFRA was combined with cytomorphology or with lineage-restricted monoclonal antibodies and applied in CML and CEL, respectively. In CEL the amount of FIP1L1-PDGFRA+ cells among CD34+ and CD133+ cells, B and T lymphocytes, and megakaryocytes were within normal ranges. Positivity was found in eosinophils, granulo-monocytes and varying percentages of erythrocytes. In vitro assays with imatinib showed reduced survival of peripheral blood mononuclear cells but no reduction in colony-forming unit growth medium (CFU-GM) growth. In CML the BCR-ABL1 fusion gene was detected in CD34+/CD133+ cells, granulo-monocytes, eosinophils, erythrocytes, megakaryocytes and B-lymphocytes. Growth of both peripheral blood mononuclear cells and CFU-GM was inhibited by imatinib. This study provided evidence for marked differences in the leukemic masses which are targeted by imatinib in CEL or CML, as harboring FIP1L1-PDGFRA or BCR-ABL1.
lymphocytes, eosinophils, glycophorin, receptor, growth, antigens, myeloproliferative disorders, protein kinase inhibitors, granulocytes, fusion proteins, in vitro, agents, oncogene proteins, cd34, bone marrow, comparative study, protein, bone marrow transplantation, research support, piperazines, chronic disease, leukemia, myelogenous, affect, t-lymphocytes, platelet-derived growth factor, genetics, blood, hypereosinophilic syndrome, tumor stem cell assay, mrna cleavage and polyadenylation factors, fluorescence, x chromosome inactivation, alpha, b-lymphocytes, antagonists & inhibitors, bcr-abl positive, drug therapy, hematopoietic stem cells, glycoproteins, multicenter studies, human, lymphocyte subsets, in-vitro, therapeutic use, clone cells, drug resistance, fusion, cell lineage, antibodies, pathology, platelet-derived growth factor alpha, cd, neoplastic stem cells, antineoplastic agents, myeloid cells, survival, megakaryocytes, monocytes, chronic, bcr-abl, research, enzymology, analysis, transplantation, immunophenotyping, humans, bone, in situ hybridization, proteins, erythrocytes, pyrimidines, peptides
0887-6924
397-402
Crescenzi, B.
a48526a2-1af0-4304-92d5-35f61aa90886
Chase, A.
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Starza, R.L.
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Beacci, D.
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Rosti, V.
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Galli, A.
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Specchia, G.
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Martelli, M.F.
4447aca8-62bb-437b-8044-3436da788f22
Vandenberghe, P.
382c88a8-a6c9-4527-a390-af7d1cbc4341
Cools, J.
ca24d9ad-d95b-46a8-b92c-bb49e896aab2
Jones, A.V.
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Cross, N.C.
f87650da-b908-4a34-b31b-d62c5f186fe4
Marynen, P.
fe45b010-1c84-4514-bd51-c97be31a498e
Mecucci, C.
2bd5a6ae-507a-438f-b8fa-ea67e67b0d5b
Crescenzi, B.
a48526a2-1af0-4304-92d5-35f61aa90886
Chase, A.
a40a09c2-3073-4655-ba0b-a802e34914b5
Starza, R.L.
8a5c03cb-8f60-4ccb-94f9-cec3cbec10dd
Beacci, D.
da36e6b1-b19a-4db3-ba32-3536d9d5e3ce
Rosti, V.
686e0159-b5eb-44b8-8ee1-4c45c93e5cab
Galli, A.
4da0ed72-21ac-4d40-8165-88e8bfcb0127
Specchia, G.
618085e0-281f-4bab-a361-58d833175c74
Martelli, M.F.
4447aca8-62bb-437b-8044-3436da788f22
Vandenberghe, P.
382c88a8-a6c9-4527-a390-af7d1cbc4341
Cools, J.
ca24d9ad-d95b-46a8-b92c-bb49e896aab2
Jones, A.V.
daa5d0cf-4454-48c3-abb8-daf03aa21e8b
Cross, N.C.
f87650da-b908-4a34-b31b-d62c5f186fe4
Marynen, P.
fe45b010-1c84-4514-bd51-c97be31a498e
Mecucci, C.
2bd5a6ae-507a-438f-b8fa-ea67e67b0d5b

Crescenzi, B., Chase, A., Starza, R.L., Beacci, D., Rosti, V., Galli, A., Specchia, G., Martelli, M.F., Vandenberghe, P., Cools, J., Jones, A.V., Cross, N.C., Marynen, P. and Mecucci, C. (2007) FIP1L1-PDGFRA in chronic eosinophilic leukemia and BCR-ABL1 in chronic myeloid leukemia affect different leukemic cells. Leukemia, 21 (3), 397-402. (doi:10.1038/sj.leu.2404510).

Record type: Article

Abstract

We investigated genetically affected leukemic cells in FIP1L1-PDGFRA+ chronic eosinophilic leukemia (CEL) and in BCR-ABL1+ chronic myeloid leukemia (CML), two myeloproliferative disorders responsive to imatinib. Fluorescence in situ hybridization specific for BCR-ABL1 and for FIP1L1-PDGFRA was combined with cytomorphology or with lineage-restricted monoclonal antibodies and applied in CML and CEL, respectively. In CEL the amount of FIP1L1-PDGFRA+ cells among CD34+ and CD133+ cells, B and T lymphocytes, and megakaryocytes were within normal ranges. Positivity was found in eosinophils, granulo-monocytes and varying percentages of erythrocytes. In vitro assays with imatinib showed reduced survival of peripheral blood mononuclear cells but no reduction in colony-forming unit growth medium (CFU-GM) growth. In CML the BCR-ABL1 fusion gene was detected in CD34+/CD133+ cells, granulo-monocytes, eosinophils, erythrocytes, megakaryocytes and B-lymphocytes. Growth of both peripheral blood mononuclear cells and CFU-GM was inhibited by imatinib. This study provided evidence for marked differences in the leukemic masses which are targeted by imatinib in CEL or CML, as harboring FIP1L1-PDGFRA or BCR-ABL1.

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Published date: 11 January 2007
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Keywords: lymphocytes, eosinophils, glycophorin, receptor, growth, antigens, myeloproliferative disorders, protein kinase inhibitors, granulocytes, fusion proteins, in vitro, agents, oncogene proteins, cd34, bone marrow, comparative study, protein, bone marrow transplantation, research support, piperazines, chronic disease, leukemia, myelogenous, affect, t-lymphocytes, platelet-derived growth factor, genetics, blood, hypereosinophilic syndrome, tumor stem cell assay, mrna cleavage and polyadenylation factors, fluorescence, x chromosome inactivation, alpha, b-lymphocytes, antagonists & inhibitors, bcr-abl positive, drug therapy, hematopoietic stem cells, glycoproteins, multicenter studies, human, lymphocyte subsets, in-vitro, therapeutic use, clone cells, drug resistance, fusion, cell lineage, antibodies, pathology, platelet-derived growth factor alpha, cd, neoplastic stem cells, antineoplastic agents, myeloid cells, survival, megakaryocytes, monocytes, chronic, bcr-abl, research, enzymology, analysis, transplantation, immunophenotyping, humans, bone, in situ hybridization, proteins, erythrocytes, pyrimidines, peptides
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Identifiers

Local EPrints ID: 59615
URI: http://eprints.soton.ac.uk/id/eprint/59615
DOI: doi:10.1038/sj.leu.2404510
ISSN: 0887-6924
PURE UUID: 9138d537-e540-4d16-a6e3-33305921ac06
ORCID for A. Chase: ORCID iD orcid.org/0000-0001-6617-9953
ORCID for N.C. Cross: ORCID iD orcid.org/0000-0001-5481-2555

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Date deposited: 04 Sep 2008
Last modified: 16 Mar 2024 03:23

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Contributors

Author: B. Crescenzi
Author: A. Chase ORCID iD
Author: R.L. Starza
Author: D. Beacci
Author: V. Rosti
Author: A. Galli
Author: G. Specchia
Author: M.F. Martelli
Author: P. Vandenberghe
Author: J. Cools
Author: A.V. Jones
Author: N.C. Cross ORCID iD
Author: P. Marynen
Author: C. Mecucci

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