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1 ion of genes that are somatically mutated in essential thrombocytosis.
2 tive disorder, that is, polycythemia vera or essential thrombocytosis.
3 receptor in JAK2-negative myelofibrosis and essential thrombocytosis.
4 st trauma and in the other in the setting of essential thrombocytosis.
5 del of Jak2-V617F-mediated polycythemia vera/essential thrombocytosis.
6 ic myelofibrosis, but not in 4 patients with essential thrombocytosis, 3 with chronic myelogenous leu
8 ifferences between PMF and polycythemia vera/essential thrombocytosis and reveal methylomic signature
9 ML, and JAK2 mutations in polycythemia vera, essential thrombocytosis, and chronic idiopathic myelofi
10 tive neoplasms, including polycythemia vera, essential thrombocytosis, and myelofibrosis, are disorde
11 enome-wide methylation in polycythemia vera, essential thrombocytosis, and PMF samples compared with
12 loproliferative disorders polycythemia vera, essential thrombocytosis, and primary myelofibrosis are
13 We determined that polycythemia vera and essential thrombocytosis are characterized by aberrant p
14 models of the MPN polycythemia vera (PV) and essential thrombocytosis (ET) by disrupting JAK2 protein
16 is (PMF) has a markedly worse prognosis than essential thrombocytosis or polycythemia vera, the molec
17 lassical myeloproliferative neoplasms (MPNs) essential thrombocytosis, polycythemia vera, and primary
18 The classic myeloproliferative neoplasms--essential thrombocytosis, polycythemia vera, and primary
19 ood cells, an often indolent course, and (in essential thrombocytosis) usually a normal life span.
20 ly methylated genes in polycythemia vera and essential thrombocytosis were involved predominantly in
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