author_facet Oehler, Leopold
Jaeger, Eva
Eser, Alexander
Sillaber, Christian
Gisslinger, Heinz
Geissler, Klaus
Oehler, Leopold
Jaeger, Eva
Eser, Alexander
Sillaber, Christian
Gisslinger, Heinz
Geissler, Klaus
author Oehler, Leopold
Jaeger, Eva
Eser, Alexander
Sillaber, Christian
Gisslinger, Heinz
Geissler, Klaus
spellingShingle Oehler, Leopold
Jaeger, Eva
Eser, Alexander
Sillaber, Christian
Gisslinger, Heinz
Geissler, Klaus
Blood
Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
Cell Biology
Hematology
Immunology
Biochemistry
author_sort oehler, leopold
spelling Oehler, Leopold Jaeger, Eva Eser, Alexander Sillaber, Christian Gisslinger, Heinz Geissler, Klaus 0006-4971 1528-0020 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood-2003-03-0676 <jats:title>Abstract</jats:title> <jats:p>The overproduction of red blood cells in patients with polycythemia vera (PV) is reflected in vitro by the formation of erythroid burst-forming units (BFU-Es) in the absence of exogenous erythropoietin. In contrast to other myeloproliferative disorders, the molecular mechanism of PV is unknown and no specific chromosomal abnormality has been described. We speculated that imatinib mesylate may reverse the pathological overproduction of red cells by inhibition of autonomous erythropoiesis. In the present study, imatinib mesylate was found to either block or strongly inhibit autonomous BFU-E formation in vitro in all patients tested. Moreover, autonomous BFU-E growth was also markedly reduced by exposure of PV cells to imatinib mesylate prior to cultivation in semisolid medium. The profound effect of imatinib mesylate on autonomous erythropoiesis suggests the involvement of an as yet unidentified kinase in the pathogenesis of PV and should provide the rationale for a forthcoming clinical trial.</jats:p> Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro Blood
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title Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_unstemmed Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_full Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_fullStr Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_full_unstemmed Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_short Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_sort imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
topic Cell Biology
Hematology
Immunology
Biochemistry
url http://dx.doi.org/10.1182/blood-2003-03-0676
publishDate 2003
physical 2240-2242
description <jats:title>Abstract</jats:title> <jats:p>The overproduction of red blood cells in patients with polycythemia vera (PV) is reflected in vitro by the formation of erythroid burst-forming units (BFU-Es) in the absence of exogenous erythropoietin. In contrast to other myeloproliferative disorders, the molecular mechanism of PV is unknown and no specific chromosomal abnormality has been described. We speculated that imatinib mesylate may reverse the pathological overproduction of red cells by inhibition of autonomous erythropoiesis. In the present study, imatinib mesylate was found to either block or strongly inhibit autonomous BFU-E formation in vitro in all patients tested. Moreover, autonomous BFU-E growth was also markedly reduced by exposure of PV cells to imatinib mesylate prior to cultivation in semisolid medium. The profound effect of imatinib mesylate on autonomous erythropoiesis suggests the involvement of an as yet unidentified kinase in the pathogenesis of PV and should provide the rationale for a forthcoming clinical trial.</jats:p>
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author Oehler, Leopold, Jaeger, Eva, Eser, Alexander, Sillaber, Christian, Gisslinger, Heinz, Geissler, Klaus
author_facet Oehler, Leopold, Jaeger, Eva, Eser, Alexander, Sillaber, Christian, Gisslinger, Heinz, Geissler, Klaus, Oehler, Leopold, Jaeger, Eva, Eser, Alexander, Sillaber, Christian, Gisslinger, Heinz, Geissler, Klaus
author_sort oehler, leopold
container_issue 6
container_start_page 2240
container_title Blood
container_volume 102
description <jats:title>Abstract</jats:title> <jats:p>The overproduction of red blood cells in patients with polycythemia vera (PV) is reflected in vitro by the formation of erythroid burst-forming units (BFU-Es) in the absence of exogenous erythropoietin. In contrast to other myeloproliferative disorders, the molecular mechanism of PV is unknown and no specific chromosomal abnormality has been described. We speculated that imatinib mesylate may reverse the pathological overproduction of red cells by inhibition of autonomous erythropoiesis. In the present study, imatinib mesylate was found to either block or strongly inhibit autonomous BFU-E formation in vitro in all patients tested. Moreover, autonomous BFU-E growth was also markedly reduced by exposure of PV cells to imatinib mesylate prior to cultivation in semisolid medium. The profound effect of imatinib mesylate on autonomous erythropoiesis suggests the involvement of an as yet unidentified kinase in the pathogenesis of PV and should provide the rationale for a forthcoming clinical trial.</jats:p>
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imprint American Society of Hematology, 2003
imprint_str_mv American Society of Hematology, 2003
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spelling Oehler, Leopold Jaeger, Eva Eser, Alexander Sillaber, Christian Gisslinger, Heinz Geissler, Klaus 0006-4971 1528-0020 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood-2003-03-0676 <jats:title>Abstract</jats:title> <jats:p>The overproduction of red blood cells in patients with polycythemia vera (PV) is reflected in vitro by the formation of erythroid burst-forming units (BFU-Es) in the absence of exogenous erythropoietin. In contrast to other myeloproliferative disorders, the molecular mechanism of PV is unknown and no specific chromosomal abnormality has been described. We speculated that imatinib mesylate may reverse the pathological overproduction of red cells by inhibition of autonomous erythropoiesis. In the present study, imatinib mesylate was found to either block or strongly inhibit autonomous BFU-E formation in vitro in all patients tested. Moreover, autonomous BFU-E growth was also markedly reduced by exposure of PV cells to imatinib mesylate prior to cultivation in semisolid medium. The profound effect of imatinib mesylate on autonomous erythropoiesis suggests the involvement of an as yet unidentified kinase in the pathogenesis of PV and should provide the rationale for a forthcoming clinical trial.</jats:p> Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro Blood
spellingShingle Oehler, Leopold, Jaeger, Eva, Eser, Alexander, Sillaber, Christian, Gisslinger, Heinz, Geissler, Klaus, Blood, Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro, Cell Biology, Hematology, Immunology, Biochemistry
title Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_full Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_fullStr Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_full_unstemmed Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_short Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_sort imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
title_unstemmed Imatinib mesylate inhibits autonomous erythropoiesis in patients with polycythemia vera in vitro
topic Cell Biology, Hematology, Immunology, Biochemistry
url http://dx.doi.org/10.1182/blood-2003-03-0676