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1 in children with CBL syndrome and transient juvenile myelomonocytic leukemia.
2 cure a relevant proportion of children with juvenile myelomonocytic leukemia.
3 2AF35, and SRSF2 in 371 children with MDS or juvenile myelomonocytic leukemia.
4 A 3-year-old boy was treated for juvenile myelomonocytic leukemia.
5 alignancies, including an increased risk for juvenile myelomonocytic leukemia.
7 occurs in specific human cancers, including juvenile myelomonocytic leukemia, an aggressive myelopro
8 some mutations are rare in pediatric MDS and juvenile myelomonocytic leukemia and are unlikely to ope
9 suppressor gene is frequently inactivated in juvenile myelomonocytic leukemia, and Nf1 mutant mice mo
10 s associated with marked thrombocytosis, and juvenile myelomonocytic leukemia, are clonal hematologic
12 y contributing to the pathogenesis of NS and juvenile myelomonocytic leukemia caused by PTPN11 gain-o
13 e retrospectively analyzed 110 patients with juvenile myelomonocytic leukemia, given single-unit, unr
17 RAS family members are frequently mutated in juvenile myelomonocytic leukemia (JMML) and acute myeloi
18 boratory features that overlap with those of juvenile myelomonocytic leukemia (JMML) and chronic myel
19 a (AML), acute lymphoblastic leukemia (ALL), juvenile myelomonocytic leukemia (JMML) and LEOPARD synd
21 human hematopoietic malignancies, including juvenile myelomonocytic leukemia (JMML) and T-cell lymph
22 Overactive RAS signaling is prevalent in juvenile myelomonocytic leukemia (JMML) and the myelopro
23 Chronic myelomonocytic leukemia (CMML) and juvenile myelomonocytic leukemia (JMML) are myelodysplas
24 r (GM-CSF) hypersensitivity is a hallmark of juvenile myelomonocytic leukemia (JMML) but has not been
25 re that individuals with Noonan syndrome and juvenile myelomonocytic leukemia (JMML) have germline mu
43 f mononuclear cells from five of seven (71%) juvenile myelomonocytic leukemia (JMML) patients and fro
44 dren with myelodysplastic syndrome (MDS) and juvenile myelomonocytic leukemia (JMML) treated in a uni
45 of validating the molecular underpinnings of juvenile myelomonocytic leukemia (JMML) with the generat
46 way is known to underlie the pathogenesis of juvenile myelomonocytic leukemia (JMML), a fatal childho
47 redisposes individuals to the development of juvenile myelomonocytic leukemia (JMML), a fatal myelopr
48 osphatase PTPN11 (SHP-2) are associated with juvenile myelomonocytic leukemia (JMML), a myeloprolifer
49 fibromatosis type 1 (NF1) are predisposed to juvenile myelomonocytic leukemia (JMML), an aggressive m
50 ype myelodysplastic syndrome (A-MDS), 60 had juvenile myelomonocytic leukemia (JMML), and 6 infants w
51 oodwin et al investigate the pathogenesis of juvenile myelomonocytic leukemia (JMML), demonstrating t
52 id in acute promyelocytic leukemia (APL) and juvenile myelomonocytic leukemia (JMML), we evaluated UA
53 in childhood acute leukemias, in addition to juvenile myelomonocytic leukemia (JMML), which is a myel
63 11 mutations occur in children with sporadic juvenile myelomonocytic leukemia, myelodysplasic syndrom
67 identified in human leukemias, particularly juvenile myelomonocytic leukemia, which is characterized
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