We have previously reported that HDAC enzyme activities were elevated in patients with agnogenic myeloid metaplasia (AMM) as compared with patients with other myeloproliferative disorders including essential thrombocytosis (ET) and polycythemia vera (PV) and normal volunteer controls (

Exp hematol 33:105 2005
). Jak 2 mutations were found in 35–50% patients with AMM. The present study was designed to see if the elevated HDAC activities in AMM are related to JAK 2 mutations. 9 patients of AMM, and 17 of other MPD, and 10 normal volunteer controls were studied. Detection of Jak 2 mutation was using Bsa X1 digestion of the PCR product (
Lancet 365: 1054, 2005
). 4 patients with AMM were found to have elevated HDAC enzyme activities (defined as more than 2 SD of controls) and only one patient was found to have an heterozygous mutation of Jak2 mutation.. We conclude that enhanced HDAC activities in AMM are not related to the Jak-2 mutation and enhanced HDAC activities may represent another mechanism than JAK2 mutations in the pathogenesis of AMM.

Topics:
enzymes, histone deacetylase, mutation, myelofibrosis, idiopathic, chronic, myeloproliferative disease, polycythemia vera, polymerase chain reaction, thrombocythemia, hemorrhagic

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2005, The American Society of Hematology
2005
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