ライフサイエンスコーパス: leukemogenesis

1 cyte colony-stimulating factor and increased leukemogenesis).

2 CHD7 is also critical for CBFB-MYH11-induced leukemogenesis.

3 GAB2-SHP2 pathway is essential for lymphoid leukemogenesis.

4 ew genes that promote cytokine signaling and leukemogenesis.

5 enic fusion transcription factors that drive leukemogenesis.

6 ietic stem cell (HSC) functions and promotes leukemogenesis.

7 VPS33B deficiency led to a dramatic delay in leukemogenesis.

8 S1 target gene that cooperates with Hoxa9 in leukemogenesis.

9 ulates normal B cell development or promotes leukemogenesis.

10 ent roles of EED in normal hematopoiesis and leukemogenesis.

11 on and that plays a well-established role in leukemogenesis.

12 f either Mll1 or Dot1l impaired MN1-mediated leukemogenesis.

13 ways nor shown to functionally contribute to leukemogenesis.

14 dently and at different time points prior to leukemogenesis.

15 ency on MLL1 function in NUP98-fusion-driven leukemogenesis.

16 how DNMT3B-mediated DNA methylation affects leukemogenesis.

17 -rearranged AML, associated with accelerated leukemogenesis.

18 lly collaborates with HOXA9 to drive myeloid leukemogenesis.

19 tool to unravel the pathogenesis of MLL-AF4 leukemogenesis.

20 as overexpression of activated AKT1 promoted leukemogenesis.

21 cing H3K27 methylation contributes to T-cell leukemogenesis.

22 th these two important pathways, may promote leukemogenesis.

23 eukemia-initiating cells (LICs) and promotes leukemogenesis.

24 erentiation in AML stem cells and attenuated leukemogenesis.

25 ing 1) plays a pivotal role in acute myeloid leukemogenesis.

26 ietary restriction and profoundly suppressed leukemogenesis.

27 t inactivation of CXXC5 might play a role in leukemogenesis.

28 K79 methylation and cooperates with DOT1L in leukemogenesis.

29 ts, implicating PRC2 dysregulation in WT1mut leukemogenesis.

30 red for hematopoietic stem cell function and leukemogenesis.

31 -repression model for CBFbeta-SMMHC-mediated leukemogenesis.

32 llaborator required for Hoxa9/Meis1-mediated leukemogenesis.

33 ents occurring in -7/del(7q) AMLs to promote leukemogenesis.

34 opoietic stem cell fate determination and in leukemogenesis.

35 of hematopoietic homeostasis, HSC aging, and leukemogenesis.

36 ss of Ikaros contributes to multistep B cell leukemogenesis.

37 liferation required for Hoxa9/Meis1-mediated leukemogenesis.

38 lation of NuRD during lymphopoiesis promotes leukemogenesis.

39 ne in inv(3)(q21;q26) inversions, leading to leukemogenesis.

40 t nodes of the Wnt pathway can contribute to leukemogenesis.

41 ancer progression, with an important role in leukemogenesis.

42 receptor checkpoint and a safeguard against leukemogenesis.

43 tors in the pathogenesis of autoimmunity and leukemogenesis.

44 ollaborate with the CBFB/MYH11 fusion during leukemogenesis.

45 oncogenic Nras signaling in HSC function and leukemogenesis.

46 e discovered a dual role of RUNX1 in myeloid leukemogenesis.

47 RV has not been definitively associated with leukemogenesis.

48 ivity, and are likely to exert a key role in leukemogenesis.

49 s morphogenetic pathway as a target in human leukemogenesis.

50 ired for PML-RARalpha-mediated initiation of leukemogenesis.

51 or that is necessary for MLL-fusion-mediated leukemogenesis.

52 L), and its aberrant activity contributes to leukemogenesis.

53 emic mice with an HDAC inhibitor accelerated leukemogenesis.

54 apoptosis, stem cell-related properties, and leukemogenesis.

55 our knowledge of the role of NPM1 mutant in leukemogenesis.

56 for normal hematopoiesis but is required for leukemogenesis.

57 n of leukemia relevant genes, and eventually leukemogenesis.

58 y downstream effects on candidate drivers of leukemogenesis.

59 and unique role of this microRNA in myeloid leukemogenesis.

60 gnaling node of FLT3-ITD and MOZ-TIF2 driven leukemogenesis.

61 are suggested to contribute significantly to leukemogenesis.

62 o induce embryonic hematopoietic defects and leukemogenesis.

63 a promising strategy to block MLL1-mediated leukemogenesis.

64 unclear how Nras(G12D/+) signaling promotes leukemogenesis.

65 ion on expression of 17 potential drivers of leukemogenesis.

66 such misspliced genes might be important in leukemogenesis.

67 pected prosurvival role for RUNX1 in myeloid leukemogenesis.

68 id and T-lymphoid cells, contribute to overt leukemogenesis.

69 e effects on lymphopoiesis and contribute to leukemogenesis.

70 target genes in MLL1 fusion protein mediated leukemogenesis.

71 2-mediated degradation and may contribute to leukemogenesis.

72 on between mutated KIT and CBFB-MYH11 during leukemogenesis.

73 Tel-PdgfRbeta oncoprotein may contribute to leukemogenesis.

74 ation may be a common oncogenic mechanism in leukemogenesis.

75 lted in clonal expansion, myelodysplasia, or leukemogenesis.

76 ng direct genetic evidence of TAK1's role in leukemogenesis.

77 m cell (HSC) function and is associated with leukemogenesis.

78 nhibition of TAL1 expression and TAL1-driven leukemogenesis.

79 cell-related properties, and is required for leukemogenesis.

80 E2A-PBX1-mediated target gene activation and leukemogenesis.

81 d differentiation and apoptosis, and delayed leukemogenesis.

82 of the endogenous GEF motif leads to reduced leukemogenesis.

83 promote transcription of genes important for leukemogenesis.

84 TAD and oncogenic transcription networks in leukemogenesis.

85 (m(6)A) demethylase, was reported to promote leukemogenesis.

86 epigenetic progress contributing to lineage leukemogenesis.

87 as a checkpoint in B lymphoid maturation and leukemogenesis.

88 f AE+ AML cells, thereby impairing AE driven leukemogenesis.

89 Myc as a co-operating factor in NPM1c-driven leukemogenesis.

90 ough downregulation of key genes involved in leukemogenesis.

91 ction is essential for Notch1-induced T-cell leukemogenesis.

92 ght cooperate with cyclin E hyperactivity in leukemogenesis.

93 nd the role of inherited genetic variants in leukemogenesis.

94 MLL1 is dispensable for MLL-fusion-mediated leukemogenesis.

95 to promote downstream survival signaling and leukemogenesis.

96 insights each model has provided into MLL-FP leukemogenesis.

97 l self-renewal, Asxl2 loss promoted AML1-ETO leukemogenesis.

98 MYC in T-ALL, thereby contributing to T-cell leukemogenesis.

99 ly as secondary events to further potentiate leukemogenesis.

100 atal hematopoiesis and the initiation of MLL leukemogenesis.

101 are secondary events that occur later during leukemogenesis.

102 patients, they cannot completely explain LGL leukemogenesis.

103 apoptosis and differentiation while delaying leukemogenesis.

104 igned to explore different aspects of MLL-FP leukemogenesis.

105 ies, we show that ZFP521 is not required for leukemogenesis, although its absence leads to a signific

106 lasmic (BAALC) gene is implicated in myeloid leukemogenesis and associated with poor outcome in both

107 This mutation is critical during leukemogenesis and constitutes a good prognostic factor

108 argeting lymphoid development are central to leukemogenesis and contribute to the arrest in lymphoid

109 AMPK deletion significantly delayed leukemogenesis and depleted LICs by reducing the express

110 Determining the role of these lesions in leukemogenesis and drug resistance should provide import

111 Activation of beta-catenin was linked to CML leukemogenesis and drug resistance through its BCR-ABL-d

112 e that SIRT1 plays a crucial role in myeloid leukemogenesis and drug resistance.

113 cancer, and provides profound insights into leukemogenesis and drug response.

114 ne system for studying early events of human leukemogenesis and for evaluating efficacy and mechanism

115 HOXA9 plays a relevant role in leukemogenesis and hematopoiesis.

116 4-MYB/MYC signaling axis in myelopoiesis and leukemogenesis and highlight the critical roles of METTL

117 veral genes previously implicated in myeloid leukemogenesis and HSC function as being regulated in a

118 ether, our findings reveal a role of TAF1 in leukemogenesis and identify TAF1 as a potential therapeu

119 data suggest a role for Mer in acute myeloid leukemogenesis and indicate that targeted inhibition of

120 les for mTORC1 in hematopoietic function and leukemogenesis and inform clinical strategies based on c

121 ndings reveal crucial functions of ALKBH5 in leukemogenesis and LSC/LIC self-renewal/maintenance and

122 revealed that these mutations occur early in leukemogenesis and often persist in clonal remissions.

123 sent a major advance in the understanding of leukemogenesis and prognosis, and have enabled the devel

124 ia (CLL) cells, clear evidence for a role in leukemogenesis and progression in CLL is lacking.

125 Leukemogenesis and recovery under treatment may be a con

126 Overexpression of FAS significantly inhibits leukemogenesis and reverses miR-196b-mediated phenotypes

127 nce of the c-Myb-p300 interaction in myeloid leukemogenesis and suggest disruption of this interactio

128 a molecular mechanism for SALL4 function in leukemogenesis and suggest that targeting of the SALL4/M

129 MEIS1, through induction of SYTL1, promotes leukemogenesis and supports leukemic cell homing and eng

130 ween these states, i.e. critical drivers for leukemogenesis and targets for differentiation.

131 ne system for studying early events of human leukemogenesis and testing the efficacy of immunotherape

132 g how different mutations cooperate to drive leukemogenesis and the context-dependent effects of onco

133 This interaction is essential for leukemogenesis and thus is a promising drug target.

134 aordinary advances into the genetic basis of leukemogenesis and treatment responsiveness in ALL.

135 establish a critical role for mutant IDH2 in leukemogenesis and tumor maintenance and identify an IDH

136 remains unclear how its loss contributes to leukemogenesis and whether ongoing PAX5 deficiency is re

137 UP98-KDM5A and NUP98-BPTF fusions in driving leukemogenesis, and demonstrate that blocking this inter

138 inant-negative effect by DNMT3A(R882mut) for leukemogenesis, and describes an attractive strategy for

139 ta revealed a multifaceted role for PAR-1 in leukemogenesis, and highlight this receptor as a potenti

140 ing factor-beta (CBFB) play pivotal roles in leukemogenesis, and inhibition of RUNX1 has now been wid

141 ic oncogene-mediated cell transformation and leukemogenesis, and inhibits all-trans-retinoic acid (AT

142 or engraftment of primary human AML LSCs and leukemogenesis, and it regulates LSC self-renewal predom

143 CDK6 severely attenuated NUP98-fusion-driven leukemogenesis, and NUP98-fusion AML was sensitive to ph

144 MYC regulatory circuit that underlies T cell leukemogenesis, and provide a rationale for therapeutic

145 that PBX3 is a critical cofactor of HOXA9 in leukemogenesis, and targeting their interaction is a fea

146 ifferent stem and progenitor compartments in leukemogenesis are challenges for the identification of

147 ical studies indicate that hematopoiesis and leukemogenesis are dependent upon hypoxia-inducible fact

148 bserved, but downstream targets relevant for leukemogenesis are not known.

149 SOCS2 promoted leukemogenesis as well as the abundance, quiescence, and

150 ic suppression of MLL fusion protein-induced leukemogenesis both in vitro and in vivo.

151 ents that are important initiating events in leukemogenesis but are insufficient to explain the biolo

152 aled mechanisms of blood differentiation and leukemogenesis, but a similar analysis of HSC developmen

153 operate with antecedent molecular lesions in leukemogenesis, but have limited independent prognostic

154 ietic stem cells (HSCs) without induction of leukemogenesis, but requires frequent administration to

155 olar RNAs (snoRNAs), play important roles in leukemogenesis, but the relevant mechanisms remain incom

156 id leukemia (AML), and its inhibition delays leukemogenesis, but whether the metabolic function of AM

157 t GAB2 is essential for myeloid and lymphoid leukemogenesis by BCR-ABL1.

158 eta/IKK2 also inhibited lymphoid and myeloid leukemogenesis by BCR-ABL1.

159 without gene fusions have been implicated in leukemogenesis by causing deregulation of proto-oncogene

160 which have been proposed to be important for leukemogenesis by CBFbeta-SMMHC.

161 We examined the contribution of G2DHE to leukemogenesis by creating a bacterial artificial chromo

162 gest that impaired Icsbp expression enhances leukemogenesis by deregulating processes that normally l

163 croenvironment and propose that ILK promotes leukemogenesis by enabling CLL cells to cope with centro

164 hat Chd7 is important for Cbfb-MYH11-induced leukemogenesis by facilitating RUNX1 regulation of trans

165 anine nucleotide exchange factor Vav3 delays leukemogenesis by p190-BCR-ABL and phenocopies the effec

166 As a coreceptor, CD44 promotes leukemogenesis by regulating stimuli of MCL1 expression.

167 PHD finger-dependent mechanism that promotes leukemogenesis by this type of NUP98 fusions.

168 bes a novel mechanism of FLT3 involvement in leukemogenesis by upregulation via chromatin remodeling

169 unx1 is indispensable for Cbfb-MYH11-induced leukemogenesis by working together with CBFbeta-SMMHC to

170 Although this latter function may promote leukemogenesis, concurrent p53 activation also leads to

171 2D61Y and Shp2E76K in HSC transformation and leukemogenesis continue to be under investigation.

172 ly targeting two critical signaling nodes in leukemogenesis could represent a therapeutic breakthroug

173 ediates transcriptional effects that promote leukemogenesis driven by AML1-ETO.

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 vestigated the impact of NCAM1 expression on leukemogenesis, drug resistance, and its role as a bioma

177 mutations play a significant role in myeloid leukemogenesis due to selective missplicing of tumor-ass

178 terminated emergency granulopoiesis, delayed leukemogenesis during emergency granulopoiesis, and norm

179 interactions.IMPORTANCE During virus-induced leukemogenesis, ecotropic mouse leukemia viruses (MLVs)

180 Deletion of this GEF domain increased leukemogenesis, enhanced cell survival and proliferation

181 o mutations in genes known to be involved in leukemogenesis (ETV6, NOTCH1, JAK1, and NF1), we identif

182 cantly extends survival of mice in models of leukemogenesis evoked by Pten deficiency.

183 tractable signaling molecules essential for leukemogenesis facilitates the development of effective

184 cohesin mutations occur as an early event in leukemogenesis, facilitating the potential development o

185 ntial signaling pathways required in Ph-like leukemogenesis for improved therapeutic targeting.

186 of the role of IDH mutations and (R)-2HG in leukemogenesis has been hampered by a lack of appropriat

187 mediators of apoptosis in hematopoiesis and leukemogenesis has not been elucidated.

188 malignant hematopoiesis, but how it promotes leukemogenesis has not been elucidated.

189 box gene family members in hematopoiesis and leukemogenesis has not been extensively studied.

190 mTOR complexes (mTORCs) in hematopoiesis and leukemogenesis have not been adequately elucidated.

191 Insights into MLL fusion-mediated leukemogenesis have not yet translated into better thera

192 e whether GM-CSF signaling affects RUNX1-ETO leukemogenesis, hematopoietic stem/progenitor cells that

193 een increased levels of IL-15 expression and leukemogenesis, high-risk disease, and CNS relapse and s

194 olved in Mixed Lineage Leukemia (MLL) fusion leukemogenesis; however, its role in prostate cancer (PC

195 might subvert immunosurveillance and promote leukemogenesis in a cell-extrinsic manner.

196 of Cdk inhibitory nuclear functions enhances leukemogenesis in a murine CML model compared with compl

197 hymocyte development that is retained during leukemogenesis in a subset of T-ALLs and is reversible w

198 ity of Tet2 loss and PTPN11 D61Y to initiate leukemogenesis in concert with expression of AML1-ETO in

199 ht open up a novel approach in understanding leukemogenesis in future.

200 s of the 2 combinations on hematopoiesis and leukemogenesis in knock-in mice.

201 1alpha and Hif-2alpha at different stages of leukemogenesis in mice.

202 cific demethylase KDM5B negatively regulates leukemogenesis in murine and human MLL-rearranged AML ce

203 event in the progression of BCR-FGFR1-driven leukemogenesis in stem cell leukemia and lymphoma syndro

204 ugh aberrant Notch activation contributes to leukemogenesis in T cells, its role in acute myelogenous

205 he transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overexpression

206 tantly, the role of ROCK in hematopoiesis or leukemogenesis in the context of whole organism remains

207 P restores leukemic TADs, transcription, and leukemogenesis in the CTCF-boundary-attenuated AML cells

208 is known about the target genes that explain leukemogenesis in these mice.

209 he innate immune response and contributes to leukemogenesis in this AML subtype.

210 of Hdac1 and Hdac2 dramatically accelerates leukemogenesis in transgenic preleukemic mice.

211 armacological inhibition of BCL6 compromised leukemogenesis in transplant recipient mice and restored

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 ion and proliferation in vitro, and promotes leukemogenesis in vivo.

216 an significantly promote MLL fusion-mediated leukemogenesis in vivo.

217 n promoting cell transformation in vitro and leukemogenesis in vivo.

218 on-mediated cell transformation in vitro and leukemogenesis in vivo.

219 h reduced intensity myeloablation to inhibit leukemogenesis, indicating that TRC105 may represent a n

220 echanism by which DNMT3A loss contributes to leukemogenesis is altered DNA methylation and the attend

221 The mechanism of SALL4 in promoting leukemogenesis is at least in part mediated by its repre

222 Overall, our results indicate that leukemogenesis is driven by distinct evolutionary forces

223 JMML leukemogenesis is linked to a hyperactivated RAS pathway

224 ent samples, NUP98 fusion oncoprotein-driven leukemogenesis is mediated by changes in chromatin struc

225 mors; however, its role in hematopoiesis and leukemogenesis is not yet known.

226 Adrenergic signaling promoting leukemogenesis is transduced by the beta2, but not beta3

227 t extent the wild-type allele contributes to leukemogenesis is unclear.

228 unctional importance of their interaction in leukemogenesis is unclear.We recently reported that over

229 a regulatory role in normal HSC function and leukemogenesis is unknown.

230 cell growth and delayed MLL-fusion-mediated leukemogenesis, likely through targeting FLT3 and MYB an

231 of acute myeloid leukemia (AML) and promotes leukemogenesis, making CDX2, in principle, an attractive

232 igations of the pathologic role of Cited2 in leukemogenesis may yield useful information in developin

233 ced CpG hypomethylation, thereby suppressing leukemogenesis mediated by DNMT3A(R882mut).

234 a conditional knockout mouse model inhibited leukemogenesis mediated by the MLL-AF6 fusion oncogene.

235 These findings uncover a novel mechanism of leukemogenesis mediated by the nuclear export pathway an

236 a cell lines derived from human experimental leukemogenesis models yielded 80 hits, of which 10 were

237 tients suggests a novel molecular pathway of leukemogenesis: mutations in the hematopoietic cytokine

238 Leukemogenesis occurs under hypoxic conditions within th

239 gulated by chromatin state alteration during leukemogenesis of human acute myeloid leukemia (AML), an

240 es during the course of infection to promote leukemogenesis of infected T cells, our results indicate

241 gest that defective self-renewal ability and leukemogenesis of MLL-Af4 myeloid cells could contribute

242 HOTTIP loss attenuates leukemogenesis of transplanted mice, while reactivation

243 ertain GATA-2 target genes are implicated in leukemogenesis, only recently have definitive insights e

244 Cyclin E status did not impact leukemogenesis or oncogene activations.

245 erated and whether HSC heterogeneity affects leukemogenesis or treatment options.

246 ) or nuclear retention (p27(S10A)) attenuate leukemogenesis over wild-type p27, validating the tumor-

247 myeloid leukemia (AML), often necessary for leukemogenesis, persistent throughout the disease course

248 L, coexpression of IkappaBalphaSR attenuated leukemogenesis, prolonged survival, and reduced myeloid

249 Deletion of CD44 during TCL1-driven murine leukemogenesis reduced the tumor burden in peripheral bl

250 on of Mof in a mouse model of MLL-AF9-driven leukemogenesis reduced tumor burden and prolonged host s

251 hematopoietic compartment results in delayed leukemogenesis, reduced disease burden, and a loss of LS

252 lecular mechanisms through which it promotes leukemogenesis remain elusive.

253 nisms underlying the role of PML-RARalpha in leukemogenesis remain largely unknown.

254 teractome, and related mechanisms underlying leukemogenesis remain unclear.

255 c stem cell (HSC) function and contribute to leukemogenesis remains elusive.

256 However, the specific role of NOTCH1 in leukemogenesis remains to be established.

257 However, the precise role of CALM in leukemogenesis remains unclear.

258 a multifaceted effect of DNMT3A(R882mut) in leukemogenesis remains undetermined.

259 ning response to therapy and contribution to leukemogenesis remains unknown.

260 The long-term effect of this therapy on leukemogenesis remains unknown.

261 her this receptor plays a functional role in leukemogenesis remains unknown.

262 so defective in homing and engraftment, with leukemogenesis rescued by coexpression of chimeric E/L-s

263 ant implications for HSC-based therapies and leukemogenesis research.

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

266 NTRK1, the latter of which drives erythroid leukemogenesis sensitive to TRK inhibition.

267 representing distinct underlying pathways of leukemogenesis, show widely divergent outcomes.

268 referentially at gene bodies.MLL-AF9-induced leukemogenesis showed much less pronounced DNA hypermeth

269 in vitro colony forming activity and in vivo leukemogenesis, similar to MLL-AF9.

270 ection for oncogenically initiated cells and leukemogenesis specifically in the context of an aged he

271 including those essential for MLL-rearranged leukemogenesis, such as DOT1L and SETD1A.

272 /proliferation of leukemic cells and delayed leukemogenesis; such effects could be reversed by forced

273 CDK6 as critical effector of MLL fusions in leukemogenesis that might be targeted to overcome the di

274 stimuli are believed to play a major role in leukemogenesis, the critical determinants are not well d

275 Although critically important in leukemogenesis, the underlying pathogenetic mechanisms t

276 cesses that appear to actively contribute to leukemogenesis, these models may not fully recapitulate

277 el of dual functional properties of SALL4 in leukemogenesis through inhibiting DNA damage repair and

278 for mixed lineage leukemia 1 (MLL1)-mediated leukemogenesis through its direct interaction with MLL1.

279 Virus-induced leukemogenesis thus involves generation of complex recom

280 troduce a robust experimental model of human leukemogenesis to further elucidate key mechanisms invol

281 Nonetheless, leukemogenesis was delayed in both models with a shared

282 Leukemogenesis was restored by expression of GAB2 but no

283 how Dnmt3b-mediated DNA methylation affects leukemogenesis, we analyzed leukemia development under c

284 y 92- overexpression induces lymphomagenesis/leukemogenesis, we generated a B-cell-specific transgeni

285 he role(s) of EED in adult hematopoiesis and leukemogenesis, we generated Eed conditional knockout (E

286 To elucidate RUNX1 function(s) in leukemogenesis, we generated Tal1/Lmo2/Rosa26-CreER(T2)R

287 Here, using murine models of leukemogenesis, we have shown that MEIS1 promotes leukem

288 echanism by which RUNX1 disruption initiates leukemogenesis, we investigated its normal role in murin

289 To examine the role of PAX5 alterations in leukemogenesis, we performed mutagenesis screens of mice

290 tribution of DNMT3A-dependent methylation to leukemogenesis, we performed whole-genome bisulfite sequ

291 operties of leukemic stem cells (LSC) and on leukemogenesis were queried.

292 in healthy cells and has been shown to drive leukemogenesis when mutated in patients with acute myelo

293 the direct relationship of such mutations to leukemogenesis, when they occur in cells of an apparentl

294 Thus, Myc can substitute for Notch1 in leukemogenesis, whereas Akt cannot.

295 on, PI3Kgamma or PI3Kdelta alone can support leukemogenesis, whereas inactivation of both isoforms su

296 g how ECs and leukemia cells interact during leukemogenesis, which could be used to develop novel tre

297 All three MLV subgroups are linked to leukemogenesis, which involves generation of recombinant

298 , with both positive and negative impacts on leukemogenesis, which requires the action of cooperating

299 nt co-occurring mutations cooperate to drive leukemogenesis will be crucial for improving diagnostic

300 and co-downregulation of genes implicated in leukemogenesis (WT1, GATA2, MLL, DNMT3B, RUNX1).