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1 nsient myeloproliferative disorder and acute megakaryocytic leukemia.
2 e A (AURKA) is a therapeutic target in acute megakaryocytic leukemia.
3  not only lymphoid leukemia but also erythro-megakaryocytic leukemia.
4 7.5 years, respectively; P <.001), with more megakaryocytic leukemia (70% v 6%; P <.001).
5                                        Acute megakaryocytic leukemia (AMegL) is a rare subtype of acu
6 ty to develop leukemia, in particular, acute megakaryocytic leukemia (AMkL) associated with somatic G
7 ion of mature megakaryocyte markers in acute megakaryocytic leukemia (AMKL) blasts and displayed pote
8            We observed that a specific acute megakaryocytic leukemia (AMKL) cell line (6133) derived
9 ptional regulation of the CBS gene in the DS megakaryocytic leukemia (AMkL) cell line, CMK, character
10  Children with Down syndrome (DS) with acute megakaryocytic leukemia (AMkL) have very high survival r
11 ts in Down syndrome (DS) children with acute megakaryocytic leukemia (AMkL) were 4.4-fold (P < .001)
12 ient myeloproliferative disease (TMD), acute megakaryocytic leukemia (AMKL), and acute lymphoid leuke
13 ncreased in ML-DS compared with non-DS acute megakaryocytic leukemias (AMKLs).
14 esin mutations are highly prevalent in acute megakaryocytic leukemia associated with Down syndrome (D
15            We used a bcr-abl-deficient human megakaryocytic leukemia cell line MO7E and an isogenic M
16                However, MB-02 cells, a human megakaryocytic leukemia cell line which can be infected
17                          Erythroleukemic and megakaryocytic leukemia cell lines (n = 5) bound little
18 CD34(+), CD61(+) cells, blood platelets, and megakaryocytic leukemia cell lines all expressed the CXC
19 eration, and autocrine production of IL-3 by megakaryocytic leukemia cell lines and bone marrow-deriv
20 scriptional regulation of IL-3 expression in megakaryocytic leukemia cell lines is similar, but not i
21 ecule probes that induce polyploidization of megakaryocytic leukemia cells and serve as perturbagens
22 lanoma cells, lymphoblastoid cell lines, and megakaryocytic leukemia cells by reverse transcriptase p
23                           We used DAMI human megakaryocytic leukemia cells to study transmembrane ion
24 pharyngeal carcinoma) cells, and M07e (human megakaryocytic leukemia) cells were infected with vCMVp-
25                        To characterize acute megakaryocytic leukemia (FAB M7 AML), we identified 37 p
26  and a 500-fold increased risk of developing megakaryocytic leukemia; however, the specific effects o
27 nsient myeloproliferative disorder and acute megakaryocytic leukemia in children with Down syndrome a
28 ormalities and underlies the pathogenesis of megakaryocytic leukemia in Down syndrome.
29 a fusion partner in t(1;22)-associated acute megakaryocytic leukemia, is also essential for maintaini
30 ted in Mks lacking Mkl1, which is mutated in megakaryocytic leukemia, is via elevated GEF-H1 expressi
31  and the aberrant erythroid phenotype of the megakaryocytic leukemias of DS.
32 elp elucidate the mechanism of t(1,22) acute megakaryocytic leukemia pathogenesis, a conditional alle
33 e uniform detection of GATA1 mutations in DS megakaryocytic leukemia suggested the potential role of
34 restricted to newborns with trisomy 21, is a megakaryocytic leukemia that although lethal in some is
35                         In a subset of human megakaryocytic leukemias, the transcription factor GATA1
36 re congenital malformations, including acute megakaryocytic leukemia, transient myeloproliferative di
37 ose being the rare but uniformly fatal acute megakaryocytic leukemia type 7.
38 nique occurrence of myelodysplasia and acute megakaryocytic leukemia type 7.
39 me NUP98 fusions, such as NUP98::KDM5A acute megakaryocytic leukemia with RB1 loss or T-ALL with NOTC
40 n to the presence of few mutations was acute megakaryocytic leukemias, with the majority of these leu