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• W4235964300 abstract "Major progress in understanding the pathogenesis in patients with thrombocytosis has been made by identifying mutations in the key regulators of thrombopoietin: the thrombopoietin receptor MPL and JAK2. Together, these mutations can be found in 50% to 60% of patients with essential thrombocythemia or primary myelofibrosis and in 10% to 20% of hereditary thrombocytosis. A decrease in expression of the Mpl protein can cause thrombocytosis even in the absence of mutations in the coding sequence, due to a shift in the balance between stimulation of signaling in megakaryopoiesis and removal of thrombopoietin by receptor mediated internalization in platelets. When present in a heterozygous state the JAK2-V617F mutation preferentially stimulates megakaryopoiesis and in most cases manifests as essential thrombocythemia (ET), whereas homozygous JAK2-V617F reduces megakaryopoiesis in favor of increased erythropoiesis, resulting in polycythemia vera and/or myelofibrosis. In 30% to 40% of patients with ET or primary myelofibrosis (PMF) and in 80% to 90% of pedigrees with hereditary thrombocytosis the disease-causing gene remains unknown. Ongoing genetic and genomic screens have identified genes that, when mutated, can cause thrombocytosis in mouse models. A more complete picture of the pathways that regulate megakaryopoisis and platelet production will be important for finding new ways of controlling platelet production in patients with thrombocytosis." @default.
• W4235964300 created "2022-05-12" @default.
• W4235964300 creator A5050358937 @default.
• W4235964300 date "2009-01-01" @default.
• W4235964300 modified "2023-10-15" @default.
• W4235964300 title "Thrombocytosis" @default.
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• W4235964300 doi "https://doi.org/10.1182/asheducation-2009.1.159" @default.
• W4235964300 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20008195" @default.
• W4235964300 hasPublicationYear "2009" @default.
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