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1 tial thrombocythemia, and myelofibrosis with myeloid metaplasia.
2 II(-/-) mice may contribute to their extreme myeloid metaplasia.
4 studied 25 patients with myelofibrosis with myeloid metaplasia and 19 patients with secondary myelof
7 ssential thrombocythemia, myelofibrosis with myeloid metaplasia, and, less commonly, chronic myelomon
8 es in the pathogenesis of myelofibrosis with myeloid metaplasia are expected to facilitate the develo
9 e distinctive features of myelofibrosis with myeloid metaplasia but not of secondary myelofibrosis du
10 , the presence of JAK2 in myelofibrosis with myeloid metaplasia has not been shown to have prognostic
11 an integral component of myelofibrosis with myeloid metaplasia (MMM) and may be classified into 3 di
12 /d) has been evaluated in myelofibrosis with myeloid metaplasia (MMM) based on its antiangiogenic pro
13 ian age, 64.8 years) with myelofibrosis with myeloid metaplasia (MMM) had therapeutic splenectomy at
16 rimary disease process in myelofibrosis with myeloid metaplasia (MMM) is clonal myeloproliferation wi
18 consecutive patients with myelofibrosis with myeloid metaplasia (MMM) seen at our institution, 91 ful
19 lood from 4 patients with myelofibrosis with myeloid metaplasia (MMM) that was associated with either
22 total of 21 patients with myelofibrosis with myeloid metaplasia (MMM), with a median age of 54 years
26 e evaluated patients with myelofibrosis with myeloid metaplasia (MMM; n=25) for the gene mutation pri
29 2 study, 23 patients with myelofibrosis with myeloid metaplasia were treated with imatinib mesylate a
32 ative disorders including myelofibrosis with myeloid metaplasia with the reported mutational frequenc
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