Myelodysplastic, myeloproliferative diseases associated with platelet-derived growth factor receptor

Myelodysplastic/myeloproliferative diseases associated with platelet-derived growth factor receptor (PDGFR) gene rearrangements are rare clonal hematologic malignancies that affect the hematopoietic stem and progenitor cells of the bone marrow These disorders exhibit hybrid features of both myelodysplasia—manifesting as cytopenias, morphologic dysplasia, and ineffective hematopoiesis—and myeloproliferation, characterized by leukocytosis, persistent eosinophilia, and hepatosplenomegaly

Myelodysplastic/myeloproliferative diseases associated with platelet-derived growth factor receptor (PDGFR) gene rearrangements are rare clonal hematologic malignancies that affect the hematopoietic stem and progenitor cells of the bone marrow Driven pathophysiologically by chromosomal translocations that cause constitutive activation of PDGFR receptor tyrosine kinases, the disease leads to aberrant intracellular signaling, autonomous cellular proliferation, and a heightened risk of transformati...

Myelodysplastic/myeloproliferative diseases associated with platelet-derived growth factor receptor (PDGFR) gene rearrangements are rare clonal hematologic malignancies that affect the hematopoietic stem and progenitor cells of the bone marrow These disorders exhibit hybrid features of both myelodysplasia—manifesting as cytopenias, morphologic dysplasia, and ineffective hematopoiesis—and myeloproliferation, characterized by leukocytosis, persistent eosinophilia, and hepatosplenomegaly Driven pat...

These disorders exhibit hybrid features of both myelodysplasia—manifesting as cytopenias, morphologic dysplasia, and ineffective hematopoiesis—and myeloproliferation, characterized by leukocytosis, persistent eosinophilia, and hepatosplenomegaly

These disorders exhibit hybrid features of both myelodysplasia—manifesting as cytopenias, morphologic dysplasia, and ineffective hematopoiesis—and myeloproliferation, characterized by leukocytosis, persistent eosinophilia, and hepatosplenomegaly

Driven pathophysiologically by chromosomal translocations that cause constitutive activation of PDGFR receptor tyrosine kinases, the disease leads to aberrant intracellular signaling, autonomous cellular proliferation, and a heightened risk of transformation to acute myeloid leukemia

Driven pathophysiologically by chromosomal translocations that cause constitutive activation of PDGFR receptor tyrosine kinases, the disease leads to aberrant intracellular signaling, autonomous cellular proliferation, and a heightened risk of transformation to acute myeloid leukemia