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1 nous leukemia, myelodysplastic syndrome, and myeloproliferative disorders).
2 aling can translate into the occurrence of a myeloproliferative disorder.
3 lomonocytic leukemia (JMML) is a rare clonal myeloproliferative disorder.
4 s noted in more than half of patients with a myeloproliferative disorder.
5 smic tyrosine kinase JAK2 in patients with a myeloproliferative disorder.
6 atory features that were characteristic of a myeloproliferative disorder.
7 osinophilic syndrome (HES) and an underlying myeloproliferative disorder.
8 a retroviral transduction assay results in a myeloproliferative disorder.
9 nsion of repopulating cells accompanied by a myeloproliferative disorder.
10 ype 1 in patients with an atypical stem cell myeloproliferative disorder.
11 Chronic myelogenous leukemia is a myeloproliferative disorder.
12 ematopoiesis that can best be described as a myeloproliferative disorder.
13 n in Jak2 is associated with a proportion of myeloproliferative disorders.
14 w discusses how this process is unfolding in myeloproliferative disorders.
15 ne investigated as a potential treatment for myeloproliferative disorders.
16 ling in the Philadelphia chromosome negative myeloproliferative disorders.
17 derstanding of the molecular pathogenesis of myeloproliferative disorders.
18 2 have been identified in JAK2V617F negative myeloproliferative disorders.
19 veloping a specifically targeted therapy for myeloproliferative disorders.
20 se 2, found in the majority of patients with myeloproliferative disorders.
21 use for diseases such as leukemias and other myeloproliferative disorders.
22 eatment of JAK2(V617F)-positive PV and other myeloproliferative disorders.
23 on in Jak2 has recently been associated with myeloproliferative disorders.
24 derstanding of the molecular pathogenesis of myeloproliferative disorders.
25 V617F, and the pathogenesis of JAK2-negative myeloproliferative disorders.
26 patients with myelodysplastic syndromes and myeloproliferative disorders.
27 diagnosis, classification, and treatment of myeloproliferative disorders.
28 has recently been shown for the JAK2 gene in myeloproliferative disorders.
29 onocytic hyperplasia and progressed to fatal myeloproliferative disorders.
30 the BM niche and affects the development of myeloproliferative disorders.
31 myelopoiesis under normal conditions and in myeloproliferative disorders.
32 RAPL expression is widely abrogated in human myeloproliferative disorders.
33 odysplastic characteristics with features of myeloproliferative disorders.
34 ell as methylation of these genes in several myeloproliferative disorders.
35 gulated protein tyrosine kinases involved in myeloproliferative disorders.
36 signaling pathway may contribute to various myeloproliferative disorders.
37 ntial use in the treatment of thrombotic and myeloproliferative disorders.
38 es to treat the energy imbalance observed in myeloproliferative disorders.
39 sions observed in patients with leukemia and myeloproliferative disorders.
40 ausal role of an activating JAK2 mutation in myeloproliferative disorders.
41 cilitates progression to the blast phases of myeloproliferative disorders.
42 cell disease, myelodysplastic syndromes, and myeloproliferative disorders.
43 potentially vascular events) associated with myeloproliferative disorders.
46 mia (CML), the phenotype closely resembles a myeloproliferative disorder affecting the megakaryocytic
47 22 of 26 patients with clinical evidence of myeloproliferative disorder and 1 patient with clinicall
48 n syndrome (trisomy 21)-associated transient myeloproliferative disorder and acute megakaryoblastic l
49 iscovered that nearly all cases of transient myeloproliferative disorder and acute megakaryocytic leu
50 eness of the role of trisomy 21 in transient myeloproliferative disorder and acute megakaryocytic leu
51 ts supports redefinition of the disease as a myeloproliferative disorder and provides opportunities t
52 rmed stem cells that give rise to a distinct myeloproliferative disorder and T-lymphoblastic leukemia
53 itors, including the Down syndrome-transient myeloproliferative disorder and the thrombocytopenia abs
56 roven beneficial effects in the treatment of myeloproliferative disorders and inflammatory conditions
58 antineoplastic agent commonly used to treat myeloproliferative disorders and other nonneoplastic con
59 resent in patients with myelofibrosis due to myeloproliferative disorders and that these features are
60 mice: it increases both the severity of the myeloproliferative disorders and the self-renewal proper
61 ce, displayed leukocytosis, a transplantable myeloproliferative disorder, and a dramatic expansion of
62 , acute megakaryoblastic leukemia, transient myeloproliferative disorder, and a group of related cong
63 pulation, reduced leukocytosis, reversed the myeloproliferative disorder, and accelerated atheroscler
64 ents with AML, DS infants with the transient myeloproliferative disorder, and Epstein-Barr Virus (EBV
65 er, a preleukemic condition termed transient myeloproliferative disorder, and increased incidence of
66 matory demyelinating polyradiculoneuropathy, myeloproliferative disorder, and monoclonal gammopathy o
67 of disorders including inherited cytopenias, myeloproliferative disorders, and erythromegakaryocytic
68 tribute to the pathogenesis of JAK2-negative myeloproliferative disorders, and led to the discovery o
69 617F)) in essential thrombocythemia, related myeloproliferative disorders, and the impact on clinical
70 n to alter the diagnostic criteria for these myeloproliferative disorders, and these changes are revi
75 this study, we have used the murine CML-like myeloproliferative disorder as a platform to characteriz
76 myeloid leukemia (CML) or polycythemia vera, myeloproliferative disorders associated with the BCR-ABL
79 Cre, LSL-Nras(G12D) mice develop an indolent myeloproliferative disorder but ultimately die of a dive
81 D mutant proteins are sufficient to induce a myeloproliferative disorder, but are insufficient to rec
83 oduct will contribute to progression of this myeloproliferative disorder by constitutive activation o
84 nt progress in the molecular pathogenesis of myeloproliferative disorders calls for a paradigm shift
86 romyelomonocyte leukemic cell line) and MPD (myeloproliferative disorder cell line), following differ
87 ogene causes chronic myelogenous leukemia, a myeloproliferative disorder characterized by clonal expa
88 causes chronic myelogenous leukemia (CML), a myeloproliferative disorder characterized by clonal expa
90 anded MDR1-transduced stem cells developed a myeloproliferative disorder characterized by high periph
91 Langerhans cell histiocytosis (LCH) is a myeloproliferative disorder characterized by lesions com
92 ile myelomonocytic leukemia is an aggressive myeloproliferative disorder characterized by malignant t
93 etic defects, aged Runx3 KO mice developed a myeloproliferative disorder characterized by myeloid-dom
94 I-expressing hematopoietic cells developed a myeloproliferative disorder characterized by overproduct
95 pathic hypereosinophilic syndrome (HES) is a myeloproliferative disorder characterized by persistent
97 myelodysplastic syndromes (MDSs) and chronic myeloproliferative disorders (CMDs) to population-based
99 drome (DS) infants are born with a transient myeloproliferative disorder (DS-TMD) that spontaneously
101 n mouse haematopoietic stem cells leads to a myeloproliferative disorder, followed by acute T-lymphob
103 n blood counts relative to mutation-negative myeloproliferative disorders; future preclinical researc
104 f Janus kinase 2 and associated mutations in myeloproliferative disorders (> 95% in polycythemia vera
105 sis of essential thrombocythemia as a clonal myeloproliferative disorder has been clearly established
106 the classic Philadelphia-chromosome negative myeloproliferative disorders has made it a much anticipa
107 ysiology of Philadelphia-chromosome negative myeloproliferative disorders has significantly advanced
108 ing acute megakaryocytic leukemia, transient myeloproliferative disorder, Hirschsprung disease, duode
109 I571-treated mice were cured of the CML-like myeloproliferative disorder, however, and STI571-treated
110 ripheral blood and bone marrow, suggesting a myeloproliferative disorder; however, granulocyte precur
111 ated kinase 2 (JAK2) mutations are common in myeloproliferative disorders; however, although they are
112 was first described in 1879, classified as a myeloproliferative disorder in 1951, and characterized a
113 CSF3R T618I, is sufficient to drive a lethal myeloproliferative disorder in a murine bone marrow tran
114 novel useful tool for establishing a clonal myeloproliferative disorder in JAK2 and MPL wt patients
115 Bone marrow chimeras confirmed that the myeloproliferative disorder in lal(-/-) mice was primari
116 etroviral transduction efficiently induces a myeloproliferative disorder in mice resembling human CML
119 ur results can explain the absence of clonal myeloproliferative disorders in mice (lifetime, 2 years)
120 has recently been described in a spectrum of myeloproliferative disorders including myelofibrosis wit
121 oid progenitors is a major characteristic of myeloproliferative disorders, including chronic myeloid
122 may contribute to phenotypic diversity among myeloproliferative disorders, including in the presence
125 ities in these processes are associated with myeloproliferative disorders, including thrombocytopenia
126 Mll5 did not alter the phenotype of a fatal myeloproliferative disorder induced by oncogenic Kras in
127 brafish embryos, including rhabdomyosarcoma, myeloproliferative disorder, intestinal hyperplasia, and
132 f pathologists and clinical investigators in myeloproliferative disorders; it was subsequently presen
133 matologic malignancies, including leukemias, myeloproliferative disorders, lymphomas, and multiple my
136 obstruction to hepatic venous outflow, with myeloproliferative disorder (MPD) accounting for up to 4
137 nsformed with BCR-ABL(P210) initiated both a myeloproliferative disorder (MPD) and B-lymphoid leukemi
138 ature T-cell lymphomas (CD4(+), CD8(+)) or a myeloproliferative disorder (MPD) at increased rates and
139 etroviral transduction efficiently induces a myeloproliferative disorder (MPD) in mice resembling hum
140 etroviral transduction efficiently induces a myeloproliferative disorder (MPD) in mice resembling hum
142 mpared the effects of inhibitors of MEK in a myeloproliferative disorder (MPD) initiated by inactivat
144 ation of JunB in postnatal mice results in a myeloproliferative disorder (MPD) resembling early human
145 emia/lymphoma syndrome usually presents as a myeloproliferative disorder (MPD) that evolves to acute
146 mphoma syndrome usually presents itself as a myeloproliferative disorder (MPD) that evolves to acute
147 /-) hematopoietic stem cells develop a fatal myeloproliferative disorder (MPD) that models JMML.
148 zyme 12/15-lipoxygenase (12/15-LO) develop a myeloproliferative disorder (MPD) that progresses to tra
150 murine models ICSBP deficiency results in a myeloproliferative disorder (MPD) with increased mature
151 terozygous Nf1 mutant mice develop a similar myeloproliferative disorder (MPD), and adoptive transfer
152 BCS patients are found to have an underlying myeloproliferative disorder (MPD), antiplatelet therapy
158 lso is associated with a risk for developing myeloproliferative disorders (MPD), including juvenile m
159 myelodysplastic syndromes (MDS), overlap MDS/myeloproliferative disorders (MPD), MPD, and acute myelo
163 an associated myelodysplastic syndrome (MDS)/myeloproliferative disorder [MPD]) based on in vitro stu
164 chromosomal abnormality associated with the myeloproliferative disorders (MPDs) and is also found in
165 is present in the majority of patients with myeloproliferative disorders (MPDs) and is implicated in
171 ffective therapeutic agent for patients with myeloproliferative disorders (MPDs) or sickle cell disea
172 alence of this mutation in either "atypical" myeloproliferative disorders (MPDs) or the myelodysplast
173 Janus kinase 2 (JAK2) tyrosine kinase in the myeloproliferative disorders (MPDs) polycythemia vera, e
174 heral blood CD34(+) cells of 2 patients with myeloproliferative disorders (MPDs) who acquired the JAK
177 7F) mutation was found in most patients with myeloproliferative disorders (MPDs), including polycythe
178 ation (JAK2 V617F) is present in the chronic myeloproliferative disorders (MPDs), polycythemia vera (
185 eloped a clinical picture closely resembling myeloproliferative disorders/neoplasms (MPNs), including
186 The chronic myelogenous leukemia (CML)-like myeloproliferative disorder observed in the BCR/ABL muri
187 Juvenile myelomonocytic leukemia (JMML) is a myeloproliferative disorder of childhood caused by mutat
191 me present with lymphoblastic lymphoma and a myeloproliferative disorder, often accompanied by pronou
193 on and differentiation can lead to leukemia, myeloproliferative disorders, or marrow failure; however
194 ocus on the pathophysiology of thrombosis in myeloproliferative disorders, particularly in terms of t
195 chromosome 20 is a recurrent abnormality in myeloproliferative disorders, particularly polycythemia
196 athogenesis, including a contribution to the myeloproliferative disorder phenotype by a gain-of-funct
197 Familial or childhood occurrence of the myeloproliferative disorder polycythemia vera are also d
198 occurs in the majority of patients with the myeloproliferative disorders polycythemia vera, essentia
200 molecular lesion in eosinophilia-associated myeloproliferative disorders, predicting a favorable res
202 topoietic stem cell transplantation (AHSCT), Myeloproliferative Disorder Research Consortium 101 tria
203 mutations in CSF3R are sufficient to drive a myeloproliferative disorder resembling aCML and CNL that
204 chromosomal aberrations and develop a fatal myeloproliferative disorder resembling chronic myelomono
206 ronic myelogenous leukemia (CML) is a clonal myeloproliferative disorder resulting from the neoplasti
207 onic myelomonocytic leukemia/myelodysplastic/myeloproliferative disorder similar to that seen in huma
208 Four out of 25 primary mice succumbed to myeloproliferative disorders, some of which progressed t
209 a sizeable proportion of patients with other myeloproliferative disorders such as essential thrombocy
210 ations in chronic myeloid leukemia and other myeloproliferative disorders suggested the possibility t
211 poietic cells into irradiated mice induces a myeloproliferative disorder that did not respond to L-74
212 ytogenetic abnormality seen in a nonspecific myeloproliferative disorder that is associated with T-ce
213 ous miRNA, miR-125b, caused a dose-dependent myeloproliferative disorder that progressed to a lethal
214 id differentiation, and the development of a myeloproliferative disorder that progresses to acute mye
215 on of HoxA10 in murine bone marrow induces a myeloproliferative disorder that progresses to AML over
216 nd that expression of Bcr-Abl/p210 induced a myeloproliferative disorder that resembled the chronic p
218 activity in eosinophilia-associated chronic myeloproliferative disorders that are characterized by a
219 a (ET) and polycythemia vera (PV) are clonal myeloproliferative disorders that are often difficult to
221 the diagnosis of an underlying Ph1-negative myeloproliferative disorder, that is, polycythemia vera
222 ribed in polycythemia vera and other BCR-ABL myeloproliferative disorders; the particular discovery h
223 derstanding of the molecular pathogenesis of myeloproliferative disorders, though many questions rema
224 2 related hematopoietic diseases: transient myeloproliferative disorder (TMD) and acute megakaryobla
225 al erythropoietic porphyria (CEP), transient myeloproliferative disorder (TMD) and acute megarakaryob
226 the pathogenesis of Down syndrome-transient myeloproliferative disorder (TMD) and Down syndrome-acut
227 th Down syndrome (DS) present with transient myeloproliferative disorder (TMD) at or shortly after bi
229 ) and in nearly every patient with transient myeloproliferative disorder (TMD), a "preleukemia" that
230 ividuals with DS who are born with transient myeloproliferative disorder (TMD), a clonal preleukemia,
231 a (AMKL); DS newborns present with transient myeloproliferative disorder (TMD), a preleukemic form of
232 are diagnosed with self-regressing transient myeloproliferative disorder (TMD), and 20% to 30% of tho
233 en reported in Down syndrome (DS), transient myeloproliferative disorder (TMD), and acute megakaryobl
237 ndividuals with Down syndrome with transient myeloproliferative disorder (TMD, also called transient
239 scriptional regulatory genes, whereas in the myeloproliferative disorders tyrosine kinases are freque
240 617F in the Philadelphia-chromosome negative myeloproliferative disorders, unlike bcr/abl tyrosine ki
241 atients were further subdivided into primary myeloproliferative disorders versus secondary thrombocyt
243 se levels are elevated in some patients with myeloproliferative disorders, we examined their utility
244 ral blood mononuclear cells of patients with myeloproliferative disorders, we isolated numerous genes
247 sent a novel in vivo model for a Myc-induced myeloproliferative disorder which can be controlled.
248 t mice, as they age, spontaneously develop a myeloproliferative disorder, which progresses from myelo
250 ogenous murine locus rapidly induces a fatal myeloproliferative disorder with 100% penetrance charact
253 ion studies, HoxA10 overexpression induces a myeloproliferative disorder with accumulation of mature
254 hrocytosis (familial polycythemia) is a rare myeloproliferative disorder with an autosomal dominant m
257 -formatted siRNA against SHIP1 resulted in a myeloproliferative disorder, with striking similarities
258 studies are needed to elucidate the cause of myeloproliferative disorders without known disease allel
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