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1 nd the role of inherited genetic variants in leukemogenesis.
2 ietary restriction and profoundly suppressed leukemogenesis.
3 t inactivation of CXXC5 might play a role in leukemogenesis.
4 K79 methylation and cooperates with DOT1L in leukemogenesis.
5 ts, implicating PRC2 dysregulation in WT1mut leukemogenesis.
6 red for hematopoietic stem cell function and leukemogenesis.
7 llaborator required for Hoxa9/Meis1-mediated leukemogenesis.
8 ents occurring in -7/del(7q) AMLs to promote leukemogenesis.
9 opoietic stem cell fate determination and in leukemogenesis.
10 of hematopoietic homeostasis, HSC aging, and leukemogenesis.
11 ss of Ikaros contributes to multistep B cell leukemogenesis.
12 liferation required for Hoxa9/Meis1-mediated leukemogenesis.
13 lation of NuRD during lymphopoiesis promotes leukemogenesis.
14 ne in inv(3)(q21;q26) inversions, leading to leukemogenesis.
15 t nodes of the Wnt pathway can contribute to leukemogenesis.
16 receptor checkpoint and a safeguard against leukemogenesis.
17 tors in the pathogenesis of autoimmunity and leukemogenesis.
18 ollaborate with the CBFB/MYH11 fusion during leukemogenesis.
19 oncogenic Nras signaling in HSC function and leukemogenesis.
20 e discovered a dual role of RUNX1 in myeloid leukemogenesis.
21 RV has not been definitively associated with leukemogenesis.
22 ivity, and are likely to exert a key role in leukemogenesis.
23 s morphogenetic pathway as a target in human leukemogenesis.
24 ired for PML-RARalpha-mediated initiation of leukemogenesis.
25 or that is necessary for MLL-fusion-mediated leukemogenesis.
26 L), and its aberrant activity contributes to leukemogenesis.
27 emic mice with an HDAC inhibitor accelerated leukemogenesis.
28 our knowledge of the role of NPM1 mutant in leukemogenesis.
29 for normal hematopoiesis but is required for leukemogenesis.
30 l self-renewal, Asxl2 loss promoted AML1-ETO leukemogenesis.
31 n of leukemia relevant genes, and eventually leukemogenesis.
32 y downstream effects on candidate drivers of leukemogenesis.
33 and unique role of this microRNA in myeloid leukemogenesis.
34 gnaling node of FLT3-ITD and MOZ-TIF2 driven leukemogenesis.
35 are suggested to contribute significantly to leukemogenesis.
36 o induce embryonic hematopoietic defects and leukemogenesis.
37 a promising strategy to block MLL1-mediated leukemogenesis.
38 unclear how Nras(G12D/+) signaling promotes leukemogenesis.
39 MLL1 is dispensable for MLL-fusion-mediated leukemogenesis.
40 ion on expression of 17 potential drivers of leukemogenesis.
41 such misspliced genes might be important in leukemogenesis.
42 pected prosurvival role for RUNX1 in myeloid leukemogenesis.
43 id and T-lymphoid cells, contribute to overt leukemogenesis.
44 e effects on lymphopoiesis and contribute to leukemogenesis.
45 target genes in MLL1 fusion protein mediated leukemogenesis.
46 2-mediated degradation and may contribute to leukemogenesis.
47 on between mutated KIT and CBFB-MYH11 during leukemogenesis.
48 Tel-PdgfRbeta oncoprotein may contribute to leukemogenesis.
49 ation may be a common oncogenic mechanism in leukemogenesis.
50 lted in clonal expansion, myelodysplasia, or leukemogenesis.
51 ng direct genetic evidence of TAK1's role in leukemogenesis.
52 m cell (HSC) function and is associated with leukemogenesis.
53 riptional coactivator CBP/p300, critical for leukemogenesis.
54 MYC in T-ALL, thereby contributing to T-cell leukemogenesis.
55 AL1 activity has been associated with T-cell leukemogenesis.
56 suggested to be aberrantly regulated during leukemogenesis.
57 genitor population and implicated in myeloid leukemogenesis.
58 hat disruption of endocytosis contributes to leukemogenesis.
59 promote HSC proliferation, HSC depletion, or leukemogenesis.
60 ly as secondary events to further potentiate leukemogenesis.
61 a gene that cooperates with CREB in myeloid leukemogenesis.
62 external cytokine control, thereby promoting leukemogenesis.
63 rentiation programs during hematopoiesis and leukemogenesis.
64 loss of which can lead to transformation and leukemogenesis.
65 1, the fusion gene generated by inv(16), for leukemogenesis.
66 ne, thereby possibly leading to enhanced AML leukemogenesis.
67 ually in all biological processes, including leukemogenesis.
68 cell (HSC) proliferation, HSC depletion, and leukemogenesis.
69 atekeeper and its repression is required for leukemogenesis.
70 which promotes oncogenic transformation and leukemogenesis.
71 mutated TIP60 may contribute to c-Myb-driven leukemogenesis.
72 atal hematopoiesis and the initiation of MLL leukemogenesis.
73 ollaborates with NRASG12D to promote myeloid leukemogenesis.
74 esults were seen in vivo during HOX-mediated leukemogenesis.
75 ys important roles in normal development and leukemogenesis.
76 ion of CBFA2T3-GLIS2 directly contributes to leukemogenesis.
77 ions in both genes have been associated with leukemogenesis.
78 are secondary events that occur later during leukemogenesis.
79 ions cooperate with biCEBPA mutations during leukemogenesis.
80 evidence for involvement of MUC1 in myeloid leukemogenesis.
81 patients, they cannot completely explain LGL leukemogenesis.
82 hat etoposide metabolites may be involved in leukemogenesis.
83 ctopic expression of Sox17 eventually led to leukemogenesis.
84 SEC, and how MLL fusion proteins can mediate leukemogenesis.
85 apoptosis and differentiation while delaying leukemogenesis.
86 igned to explore different aspects of MLL-FP leukemogenesis.
87 CHD7 is also critical for CBFB-MYH11-induced leukemogenesis.
88 GAB2-SHP2 pathway is essential for lymphoid leukemogenesis.
89 ew genes that promote cytokine signaling and leukemogenesis.
90 enic fusion transcription factors that drive leukemogenesis.
91 ietic stem cell (HSC) functions and promotes leukemogenesis.
92 VPS33B deficiency led to a dramatic delay in leukemogenesis.
93 S1 target gene that cooperates with Hoxa9 in leukemogenesis.
94 ulates normal B cell development or promotes leukemogenesis.
95 ent roles of EED in normal hematopoiesis and leukemogenesis.
96 f either Mll1 or Dot1l impaired MN1-mediated leukemogenesis.
97 ways nor shown to functionally contribute to leukemogenesis.
98 dently and at different time points prior to leukemogenesis.
99 ency on MLL1 function in NUP98-fusion-driven leukemogenesis.
100 how DNMT3B-mediated DNA methylation affects leukemogenesis.
101 lly collaborates with HOXA9 to drive myeloid leukemogenesis.
102 tool to unravel the pathogenesis of MLL-AF4 leukemogenesis.
103 as overexpression of activated AKT1 promoted leukemogenesis.
104 cing H3K27 methylation contributes to T-cell leukemogenesis.
105 insights each model has provided into MLL-FP leukemogenesis.
106 th these two important pathways, may promote leukemogenesis.
107 eukemia-initiating cells (LICs) and promotes leukemogenesis.
108 erentiation in AML stem cells and attenuated leukemogenesis.
109 ing 1) plays a pivotal role in acute myeloid leukemogenesis.
110 ies, we show that ZFP521 is not required for leukemogenesis, although its absence leads to a signific
111 lasmic (BAALC) gene is implicated in myeloid leukemogenesis and associated with poor outcome in both
113 argeting lymphoid development are central to leukemogenesis and contribute to the arrest in lymphoid
115 Determining the role of these lesions in leukemogenesis and drug resistance should provide import
116 Activation of beta-catenin was linked to CML leukemogenesis and drug resistance through its BCR-ABL-d
119 e nucleotide exchange factor Vav in lymphoid leukemogenesis and explore the roles of Vav proteins in
120 ghted the central role of DNA methylation in leukemogenesis and have led to clinical trials of epigen
122 4-MYB/MYC signaling axis in myelopoiesis and leukemogenesis and highlight the critical roles of METTL
123 Here we show that Rictor deletion prevents leukemogenesis and HSC depletion after Pten deletion in
124 veral genes previously implicated in myeloid leukemogenesis and HSC function as being regulated in a
126 wide analyses has provided new insights into leukemogenesis and identified many novel subtypes of leu
127 Dnmt1 was sufficient to delay progression of leukemogenesis and impair LSC self-renewal without alter
128 data suggest a role for Mer in acute myeloid leukemogenesis and indicate that targeted inhibition of
129 les for mTORC1 in hematopoietic function and leukemogenesis and inform clinical strategies based on c
130 ted patterns suggest different mechanisms of leukemogenesis and may underlie the differential outcome
131 revealed that these mutations occur early in leukemogenesis and often persist in clonal remissions.
132 sent a major advance in the understanding of leukemogenesis and prognosis, and have enabled the devel
135 Overexpression of FAS significantly inhibits leukemogenesis and reverses miR-196b-mediated phenotypes
136 nce of the c-Myb-p300 interaction in myeloid leukemogenesis and suggest disruption of this interactio
137 a molecular mechanism for SALL4 function in leukemogenesis and suggest that targeting of the SALL4/M
138 MEIS1, through induction of SYTL1, promotes leukemogenesis and supports leukemic cell homing and eng
141 aordinary advances into the genetic basis of leukemogenesis and treatment responsiveness in ALL.
142 establish a critical role for mutant IDH2 in leukemogenesis and tumor maintenance and identify an IDH
143 remains unclear how its loss contributes to leukemogenesis and whether ongoing PAX5 deficiency is re
144 ta revealed a multifaceted role for PAR-1 in leukemogenesis, and highlight this receptor as a potenti
145 ing factor-beta (CBFB) play pivotal roles in leukemogenesis, and inhibition of RUNX1 has now been wid
146 ic oncogene-mediated cell transformation and leukemogenesis, and inhibits all-trans-retinoic acid (AT
147 or engraftment of primary human AML LSCs and leukemogenesis, and it regulates LSC self-renewal predom
148 that PBX3 is a critical cofactor of HOXA9 in leukemogenesis, and targeting their interaction is a fea
149 ifferent stem and progenitor compartments in leukemogenesis are challenges for the identification of
150 ical studies indicate that hematopoiesis and leukemogenesis are dependent upon hypoxia-inducible fact
152 the first time, that Mll-PTD contributes to leukemogenesis as a gain-of-function mutation and descri
154 he dual importance of ETS factors in t(8;21) leukemogenesis, both as transcriptional regulators of th
155 ents that are important initiating events in leukemogenesis but are insufficient to explain the biolo
156 aled mechanisms of blood differentiation and leukemogenesis, but a similar analysis of HSC developmen
157 operate with antecedent molecular lesions in leukemogenesis, but have limited independent prognostic
158 ietic stem cells (HSCs) without induction of leukemogenesis, but requires frequent administration to
161 without gene fusions have been implicated in leukemogenesis by causing deregulation of proto-oncogene
163 We examined the contribution of G2DHE to leukemogenesis by creating a bacterial artificial chromo
164 gest that impaired Icsbp expression enhances leukemogenesis by deregulating processes that normally l
165 croenvironment and propose that ILK promotes leukemogenesis by enabling CLL cells to cope with centro
166 hat Chd7 is important for Cbfb-MYH11-induced leukemogenesis by facilitating RUNX1 regulation of trans
167 anine nucleotide exchange factor Vav3 delays leukemogenesis by p190-BCR-ABL and phenocopies the effec
169 Although this latter function may promote leukemogenesis, concurrent p53 activation also leads to
171 ly targeting two critical signaling nodes in leukemogenesis could represent a therapeutic breakthroug
173 nal EPOR on the cell surface and its role in leukemogenesis driven by ETV6-RUNX1 remains to be identi
174 gulation of both normal HSC functions and in leukemogenesis driven by the mixed lineage leukemia (MLL
175 fic advances have provided new insights into leukemogenesis, drug resistance, and host pharmacogenomi
176 mutations play a significant role in myeloid leukemogenesis due to selective missplicing of tumor-ass
177 interactions.IMPORTANCE During virus-induced leukemogenesis, ecotropic mouse leukemia viruses (MLVs)
178 o mutations in genes known to be involved in leukemogenesis (ETV6, NOTCH1, JAK1, and NF1), we identif
180 tractable signaling molecules essential for leukemogenesis facilitates the development of effective
181 cohesin mutations occur as an early event in leukemogenesis, facilitating the potential development o
182 of the role of IDH mutations and (R)-2HG in leukemogenesis has been hampered by a lack of appropriat
186 mTOR complexes (mTORCs) in hematopoiesis and leukemogenesis have not been adequately elucidated.
188 e whether GM-CSF signaling affects RUNX1-ETO leukemogenesis, hematopoietic stem/progenitor cells that
189 een increased levels of IL-15 expression and leukemogenesis, high-risk disease, and CNS relapse and s
191 of Cdk inhibitory nuclear functions enhances leukemogenesis in a murine CML model compared with compl
192 Importantly, MN1 cooperated with Mll-AF9 in leukemogenesis in an in vivo BM viral transduction and t
193 recognized mechanism of clonal selection and leukemogenesis in bone marrow failure syndromes and our
194 ity of Tet2 loss and PTPN11 D61Y to initiate leukemogenesis in concert with expression of AML1-ETO in
199 cific demethylase KDM5B negatively regulates leukemogenesis in murine and human MLL-rearranged AML ce
200 96b significantly delays MLL-fusion-mediated leukemogenesis in primary bone marrow transplantation th
202 leukaemic phenotypes and causes much faster leukemogenesis in secondary transplantation than MLL fus
203 ugh aberrant Notch activation contributes to leukemogenesis in T cells, its role in acute myelogenous
204 he transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overexpression
205 tantly, the role of ROCK in hematopoiesis or leukemogenesis in the context of whole organism remains
206 e a mechanistic insight into miR-155-induced leukemogenesis in the Emu-miR-155 mouse model through ge
207 berrant production of Fgf2 may contribute to leukemogenesis in the subset of AML with dysregulated Ho
211 ent mice has been critical for understanding leukemogenesis in vivo and defining self-renewing leukem
212 M1-mutated AML, the role of NPM1 mutation in leukemogenesis in vivo has not been fully elucidated.
213 ced PRDX2 expression inhibited c-Myc-induced leukemogenesis in vivo on BM transplantation in mice.
214 0(-/-) bone marrow and progression of B-cell leukemogenesis in vivo revealed no differences in diseas
215 is required for MLL fusion protein-mediated leukemogenesis in vivo, and this interaction has been va
221 emical networks connecting the Kit mutant to leukemogenesis, in the present study, we performed a glo
222 vation for several genes relevant to myeloid leukemogenesis, including DNA methyltransferases and rec
223 h reduced intensity myeloablation to inhibit leukemogenesis, indicating that TRC105 may represent a n
224 context of hematopoietic immortalization and leukemogenesis, individual HOX properties are governed a
225 kemia (ALL), where Notch activation promotes leukemogenesis, induction of Notch signaling in B-cell A
226 echanism by which DNMT3A loss contributes to leukemogenesis is altered DNA methylation and the attend
233 unctional importance of their interaction in leukemogenesis is unclear.We recently reported that over
235 cell growth and delayed MLL-fusion-mediated leukemogenesis, likely through targeting FLT3 and MYB an
236 of acute myeloid leukemia (AML) and promotes leukemogenesis, making CDX2, in principle, an attractive
237 igations of the pathologic role of Cited2 in leukemogenesis may yield useful information in developin
238 a conditional knockout mouse model inhibited leukemogenesis mediated by the MLL-AF6 fusion oncogene.
239 These findings uncover a novel mechanism of leukemogenesis mediated by the nuclear export pathway an
240 a cell lines derived from human experimental leukemogenesis models yielded 80 hits, of which 10 were
241 tients suggests a novel molecular pathway of leukemogenesis: mutations in the hematopoietic cytokine
243 es during the course of infection to promote leukemogenesis of infected T cells, our results indicate
244 ment of Dot1l in postnatal hematopoiesis and leukemogenesis of MLL translocation proteins has not bee
245 gest that defective self-renewal ability and leukemogenesis of MLL-Af4 myeloid cells could contribute
247 Whether constitutively active Ras promotes leukemogenesis on the t(8;21) background has not been de
248 ertain GATA-2 target genes are implicated in leukemogenesis, only recently have definitive insights e
250 ) or nuclear retention (p27(S10A)) attenuate leukemogenesis over wild-type p27, validating the tumor-
251 L, coexpression of IkappaBalphaSR attenuated leukemogenesis, prolonged survival, and reduced myeloid
252 Deletion of CD44 during TCL1-driven murine leukemogenesis reduced the tumor burden in peripheral bl
253 on of Mof in a mouse model of MLL-AF9-driven leukemogenesis reduced tumor burden and prolonged host s
254 hematopoietic compartment results in delayed leukemogenesis, reduced disease burden, and a loss of LS
261 so defective in homing and engraftment, with leukemogenesis rescued by coexpression of chimeric E/L-s
263 pathologic role of Shp2 in hematopoiesis and leukemogenesis, respectively, will yield information nee
264 cells following intravenous injection, with leukemogenesis restored by direct intrafemoral injection
265 of six miRNAs implicated in B and T lineage leukemogenesis, resulted in profound defects in T cell d
267 referentially at gene bodies.MLL-AF9-induced leukemogenesis showed much less pronounced DNA hypermeth
269 ection for oncogenically initiated cells and leukemogenesis specifically in the context of an aged he
270 /proliferation of leukemic cells and delayed leukemogenesis; such effects could be reversed by forced
271 CDK6 as critical effector of MLL fusions in leukemogenesis that might be targeted to overcome the di
273 cesses that appear to actively contribute to leukemogenesis, these models may not fully recapitulate
274 tic tumor-promoting gene that contributed to leukemogenesis through dysregulation of nuclear factor o
275 el of dual functional properties of SALL4 in leukemogenesis through inhibiting DNA damage repair and
276 for mixed lineage leukemia 1 (MLL1)-mediated leukemogenesis through its direct interaction with MLL1.
277 viral oncoprotein Tax functions pivotally in leukemogenesis through its potent activation of NF-kappa
281 how Dnmt3b-mediated DNA methylation affects leukemogenesis, we analyzed leukemia development under c
282 rectly elucidate the requirement of GRP78 in leukemogenesis, we created a biallelic conditional knock
283 luate whether LOS cooperates with t(8;21) in leukemogenesis, we first used a retroviral transduction/
284 y 92- overexpression induces lymphomagenesis/leukemogenesis, we generated a B-cell-specific transgeni
285 ovel genes that cooperate with ETV6-RUNX1 in leukemogenesis, we generated a mouse model that uses the
286 he role(s) of EED in adult hematopoiesis and leukemogenesis, we generated Eed conditional knockout (E
289 echanism by which RUNX1 disruption initiates leukemogenesis, we investigated its normal role in murin
290 To examine the role of PAX5 alterations in leukemogenesis, we performed mutagenesis screens of mice
291 tribution of DNMT3A-dependent methylation to leukemogenesis, we performed whole-genome bisulfite sequ
292 regions point to candidate genes involved in leukemogenesis, we used microarray-based comparative gen
293 the functional contribution of trisomy 21 to leukemogenesis, we used mouse and human cell models of D
294 in healthy cells and has been shown to drive leukemogenesis when mutated in patients with acute myelo
295 the direct relationship of such mutations to leukemogenesis, when they occur in cells of an apparentl
297 on, PI3Kgamma or PI3Kdelta alone can support leukemogenesis, whereas inactivation of both isoforms su
298 g how ECs and leukemia cells interact during leukemogenesis, which could be used to develop novel tre
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