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1 ere represent likely drivers or modifiers of myeloproliferative disease.
2 ng survival in animal models of FLT3-induced myeloproliferative disease.
3 not required or redundant in Bcr-Abl-induced myeloproliferative disease.
4 s essential for Bcr-Abl to induce a CML-like myeloproliferative disease.
5 e Abl kinase alone is sufficient to induce a myeloproliferative disease.
6 ergoing treatment for leukemia, lymphoma, or myeloproliferative disease.
7 the first oligonucleotide-based treatment to myeloproliferative disease.
8 the older mice developed a nontransplantable myeloproliferative disease.
9 in mice leads to increased susceptibility to myeloproliferative disease.
10 an paradigm with therapeutic implications in myeloproliferative disease.
11 cell/C3H/HeJ mouse model of FLT3 ITD-driven myeloproliferative disease.
12 fluences the development of FLT3-ITD-induced myeloproliferative disease.
13 eloid progenitors, and consequently an acute myeloproliferative disease.
14 gulation of NF-kappaB is responsible for the myeloproliferative disease.
15 erates, and differentiates to give rise to a myeloproliferative disease.
16 cial abnormalities, and an increased risk of myeloproliferative disease.
17 of NQO1(-/-) mice to gamma-radiation led to myeloproliferative disease.
18 oietic stem cells lead to the development of myeloproliferative disease.
19 sulted in increased mortality accompanied by myeloproliferative disease.
20 graftment and impaired induction of CML-like myeloproliferative disease.
21 e transplantation model of a bcr/abl-induced myeloproliferative disease.
22 leles may have functional complementation in myeloproliferative disease.
23 lymphoma associated TEL-FGFR3 fusion-induced myeloproliferative disease.
24 ies similar to those in Noonan syndrome, and myeloproliferative disease.
25 patients with acute and chronic leukemia and myeloproliferative diseases.
26 ene in mice leads to gamma radiation-induced myeloproliferative diseases.
27 strategy for the treatment of CML and other myeloproliferative diseases.
28 f therapeutic value in both inflammatory and myeloproliferative diseases.
29 in-deleted KIT(D816V) uniformly caused fatal myeloproliferative diseases.
30 c plaque, and in thrombotic complications of myeloproliferative diseases.
32 ence of cancer, including myelodysplastic or myeloproliferative diseases, after a first pregnancy wit
33 in the risk of myelodysplastic syndromes or myeloproliferative diseases (AHR, 2.43; 95% CI, 1.46-4.0
34 ional T and B cells, leads to a lethal acute myeloproliferative disease (AMD) and to high levels of v
35 GATA1s-producing mutations promote transient myeloproliferative disease and acute megakaryoblastic le
36 eas somatic PTPN11 mutations cause childhood myeloproliferative disease and contribute to some solid
38 anus kinase 2 (JAK2) abrogates initiation of myeloproliferative disease and substantial disease regre
39 he Abl SH3 domain of Bcr-Abl in induction of myeloproliferative disease and tested whether c-Abl acti
40 lts, including associations with infections, myeloproliferative diseases and associated conditions, s
41 We treated four patients who had chronic myeloproliferative diseases and chromosomal translocatio
42 rease in the incidence of myelodysplastic or myeloproliferative diseases and kidney cancer and a decr
44 ten in mice lacking G-CSF, the splenomegaly, myeloproliferative disease, and splenic HSC accumulation
45 e BM cells and the development of a CML-like myeloproliferative disease, and treatment of mice with t
46 ic mutations in JAK2 are frequently found in myeloproliferative diseases, and gain-of-function JAK3 a
47 s durable responses in patients with chronic myeloproliferative diseases associated with activation o
48 bl-transduced bone marrow cells succumb to a myeloproliferative disease between 3 and 5 weeks after b
49 in Bcr-Abl play additional roles in inducing myeloproliferative disease beyond simply activating the
50 nstrated the efficient induction of CML-like myeloproliferative disease by BCR/ABL in a murine bone m
51 ired for the efficient induction of CML-like myeloproliferative disease by oncogenic Abl proteins.
53 murine transplant model, JAK2T875N induced a myeloproliferative disease characterized by features of
54 human chronic myelogenous leukemia (CML), a myeloproliferative disease characterized by massive expa
58 ITD significantly shortened the latency of a myeloproliferative disease compared with FLT3-ITD alone
60 ntaneously developed transplantable CML-like myeloproliferative disease due to increased cellular pro
61 ecome a useful, but nonspecific biomarker of myeloproliferative diseases, especially polycythemia ver
64 A small proportion of patients with chronic myeloproliferative diseases have constitutive activation
65 including the associations between JAK2 and myeloproliferative disease, HOXB13 and cancer of prostat
66 g-mutant of AE developed a nontransplantable myeloproliferative disease identical to that induced by
68 ls to IL-3 independence and induces a murine myeloproliferative disease in a bone marrow transplantat
69 etaR is necessary and sufficient to induce a myeloproliferative disease in a murine BMT model, and PD
71 ransduction of T/T(L) causes a rapidly fatal myeloproliferative disease in a murine bone marrow trans
74 etroviral transduction efficiently induces a myeloproliferative disease in mice resembling human CML.
75 l targeted Kras(G12D) allele induces a fatal myeloproliferative disease in mice that closely models j
76 on with NPM1c rapidly leads to an aggressive myeloproliferative disease in mice with a latency of 31.
77 hat deregulated expression of Id1 leads to a myeloproliferative disease in mice, and immortalizes mye
78 sults showed that SHP-2 E76K mutation caused myeloproliferative disease in mice, while overexpression
85 /c (H-2(d)) BM, inducing mixed chimerism and myeloproliferative disease in recipients resembling rela
86 hat full-length Tel-Abl induced two distinct myeloproliferative diseases in mice: CML-like leukemia s
87 ent of a chronic myeloid leukemia (CML)-like myeloproliferative disease; in contrast, a significantly
88 e kinase oncogenes have been associated with myeloproliferative diseases, including Bcr/Abl, Tel/Abl,
89 The Y177F mutation greatly attenuates the myeloproliferative disease induced by BCR/ABL, with mice
90 icant shortening in the latency of the fatal myeloproliferative disease induced by retroviral-mediate
91 plantation assay, AMN107 effectively treated myeloproliferative disease induced by TEL-PDGFRbeta and
93 R1 fusion kinase associated with an atypical myeloproliferative disease is constitutively activated a
94 er, mutant IDH1 greatly accelerated onset of myeloproliferative disease-like myeloid leukemia in mice
97 loid leukemia [sAML], and 47 myelodysplastic/myeloproliferative disease [MDS/MPD]) and 76 controls.
100 which mice with an FLT3/ITD mutation develop myeloproliferative disease (MPD) and a block in early B-
101 rleukin (IL)-3 plasma levels are elevated in myeloproliferative disease (MPD) caused by the TEL/tyros
102 isplay persistent macrocytosis and develop a myeloproliferative disease (MPD) characterized by profou
103 -ITD in vivo model, SYK is indispensable for myeloproliferative disease (MPD) development, and SYK ov
104 Cbl RING finger mutant mouse as a model of a myeloproliferative disease (MPD) driven by wild-type Flt
107 n Shp2D61G enhances HSC activity and induces myeloproliferative disease (MPD) in vivo by HSC transfor
109 h juvenile myelomonocytic leukemia (JMML), a myeloproliferative disease (MPD) of early childhood.
111 sing bone marrow cells exclusively develop a myeloproliferative disease (MPD) resembling human CML.
112 h Nf1-/- fetal hematopoietic cells develop a myeloproliferative disease (MPD) that models the human d
113 ted for a suspicion of Philadelphia-negative myeloproliferative disease (MPD), were retrospectively e
114 After marked decrease of AML blast cells, myeloproliferative disease (MPD)-like AML relapsed chara
121 ogenesis of acute myeloid leukemia (AML) and myeloproliferative diseases (MPD) and have led to the de
123 ession of CD177 is an important biomarker of myeloproliferative diseases, NB1 glycoprotein is a ligan
125 nd IL-3, but not SCF, rapidly caused a fatal myeloproliferative disease rather than acute myeloid leu
127 na (+/-) mice spontaneously develop a lethal myeloproliferative disease resembling human atypical chr
128 l transduction efficiently induces in mice a myeloproliferative disease resembling human CML and that
129 pproximately 95% of recipient mice develop a myeloproliferative disease resembling the myeloprolifera
130 2 V617F mutant, found at high frequencies in myeloproliferative diseases, retains the ability to bind
131 IR = 16.1), myelodysplastic syndrome/chronic myeloproliferative diseases (SIR = 6.0), lower gastroint
132 inst unconventional Ag MPD6 in patients with myeloproliferative diseases suggests MPD6 as a potential
133 stoylated AKT1 (myr-AKT), recipients develop myeloproliferative disease, T-cell lymphoma, or AML.
134 roviral transduction, caused a rapidly fatal myeloproliferative disease that closely recapitulated hu
135 is phenotype culminates in a Stat5-dependent myeloproliferative disease that is accompanied by M2 mac
136 marrow cells from patients with an atypical myeloproliferative disease that is associated with perip
137 L-RARA expressed in myeloid cells leads to a myeloproliferative disease that ultimately evolves into
138 dence to indicate that Nf1 gene loss induces myeloproliferative disease through a Ras-mediated hypers
139 nts, and an increased incidence of transient myeloproliferative disease (TMD), acute megakaryocytic l
140 ein induced 2 distinct illnesses: a CML-like myeloproliferative disease very similar to that induced
142 olonies in methylcellulose cultures, but the myeloproliferative disease was not transplantable into s
146 o clathrin, resulted in the development of a myeloproliferative disease, whereas inclusion of this do
147 kemia/lymphoma syndrome (SCLL) presents as a myeloproliferative disease which can progress to acute m
148 g (HH) ligand secretion and loss of PTCH2 in myeloproliferative disease, which drives canonical and n
149 between stem cell quiescence/homeostasis and myeloproliferative disease while also giving novel insig
150 a useful drug for treatment of patients with myeloproliferative disease who harbor these kinase fusio
151 of TEL2 alone in mouse bone marrow causes a myeloproliferative disease with a long latency period bu
152 bone marrow cells, whereas FLT3-ITD induced myeloproliferative disease with a median latency of 50 d
153 of vav-FLT3-ITD transgenic mice developed a myeloproliferative disease with high penetrance and a di
154 overexpress CREB in myeloid cells develop a myeloproliferative disease with splenomegaly and aberran
155 p210 forms of BCR/ABL induce fatal CML-like myeloproliferative disease within 4 weeks, p210 SH2 muta