ライフサイエンスコーパス: leukemic

1 oach is that miR-26a can elicit in vivo anti-leukemic activities mediated by increased apoptosis.

2 The antibodies exhibit potent anti-leukemic activity in cell lines and tumor xenografts har

3 how here that R-2HG also exerts a broad anti-leukemic activity in vitro and in vivo by inhibiting leu

4 ntly, only DAC potentiated HSPC-NK cell anti-leukemic activity in vivo.

5 The anti-leukemic agent asparaginase activates the integrated str

6 ncreases risk for liver toxicity by the anti-leukemic agent asparaginase, but the mechanism is unknow

7 Sezary syndrome is a leukemic and aggressive form of cutaneous T cell lymphom

8 HDACi causes distinct chromatin responses in leukemic and host CD4(+) T cells, reprogramming host T c

9 whole-genome bisulfite sequencing of primary leukemic and non-leukemic cells in patients with or with

10 Both leukemic and nonleukemic cells exhibit higher BMP4 level

11 entified gene expression differences between leukemic and nonleukemic LTHSCs.

12 ation group L) is downregulated in SALL4B Tg leukemic and pre-leukemic cells.

13 so exhibited improved capacity to graft both leukemic and solid tumor cells compared with NSI, NOG, a

14 cy and expression of PD-L1 and Gal-9 on both leukemic and stromal cells in the leukemic microenvironm

15 ration, survival, and tissue infiltration of leukemic B cells.

16 ng was therefore not sufficient to eliminate leukemic behavior.

17 mbinant EGFL7 in vitro leads to increases in leukemic blast cell growth and levels of phosphorylated

18 MDR(+) cells were frequently observed in leukemic blast cells in both pretherapy and relapsed sam

19 genetic and phenotypic heterogeneity between leukemic blast cells is a well-recognized phenomenon, th

20 This enabled categorization into leukemic blast cells with MDR activity (MDR(+)) and leuk

21 c blast cells with MDR activity (MDR(+)) and leukemic blast cells without MDR activity (MDR(-ve)).

22 related with Alox5 overexpression in MLL-AF9-leukemic blast cells; inhibition of the above signaling

23 the EMT regulator ZEB1 significantly reduced leukemic blast invasion.

24 riability in MDR activity between individual leukemic blasts are lacking.

25 ensitive to existing chemotherapy drugs than leukemic blasts because of a distinctive lower prolifera

26 Leukemic blasts could also be distinguished from benign

27 herapy samples from 20 adults with AML whose leukemic blasts had MDR activity against the anthracylin

28 In addition, leukemic blasts in one-fourth of JMML patients present w

29 an autocrine mechanism supporting growth of leukemic blasts in patients with AML.

30 gs indicate that targeting CD19 and CD123 on leukemic blasts represents an effective strategy for tre

31 at relapse was identified in populations of leukemic blasts that did not demonstrate this activity b

32 riability in functional MDR activity between leukemic blasts was observed, with MDR(+) cells not infr

33 stem cells, leukemic stem cells [LSCs], and leukemic blasts).

34 ned that CART123, but not CART19, recognized leukemic blasts, established protracted synapses, and er

35 0 complex is exposed on the cell membrane of leukemic blasts.

36 induction of myeloid differentiation of the leukemic blasts.

37 to identify heterogeneity in MDR activity in leukemic blasts.

38 analog that is used to treat preleukemic and leukemic blood disorders.

39 in vitro and led to a 2-log reduction in the leukemic burden in patient-derived xenograft mice.

40 7,8) resulted in substantial reductions in leukemic burden, specifically in isogenic mouse leukemia

41 opriate costimulation, correlated with lower leukemic burden.

42 unt an efficient recognition of the residual leukemic burden.

43 on of ALL cells, including patients with low leukemic burdens during and after therapy.

44 -7 signaling, was reduced in preleukemic and leukemic CD19-CreDeltaPB cells compared with controls.

45 In vivo, DHODH inhibitors reduced leukemic cell burden, decreased levels of leukemia-initi

46 protein responded with a greater decrease in leukemic cell count compared with those samples expressi

47 r, which in turn regulates genes that induce leukemic cell death.

48 udies on the mechanisms/pathways involved in leukemic cell differentiation revealed that binding of S

49 tant to clarify the mechanisms of incomplete leukemic cell eradication by vemurafenib and to explore

50 , miR-26a was the most effective in reducing leukemic cell expansion.

51 ML lines and primary patient cells decreased leukemic cell growth and chemoresistance via downregulat

52 on in acute myeloid leukemia (AML) and drive leukemic cell growth and survival.

53 trate that FOXP1 by itself supports HSPC and leukemic cell growth, thus mimicking PUM activities.

54 reover, we found that PUM1/2 sustain myeloid leukemic cell growth.

55 M1/2 and FOXP1 in regulating normal HSPC and leukemic cell growth.

56 as able to inhibit STAT5 phosphorylation and leukemic cell growth.

57 mogenesis, we have shown that MEIS1 promotes leukemic cell homing and engraftment in bone marrow and

58 SYTL1, promotes leukemogenesis and supports leukemic cell homing and engraftment, facilitating inter

59 BPDCN cell xenograft revealed a decrease of leukemic cell infiltration and BPDCN-induced cytopenia a

60 efforts to develop new models to study niche-leukemic cell interaction in human myeloid malignancies;

61 Using a leukemic cell line and diagnostic bone marrow cells from

62 eral blood mononuclear cells (PBMCs) to lyse leukemic cell lines and primary acute myeloid leukemia s

63 ed expression of GFI1 in several widely used leukemic cell lines inhibits their growth and decreases

64 ion therapies to better control the residual leukemic cell population.

65 AT mutations were not sufficient to initiate leukemic cell proliferation but rather only augmented si

66 oietic stem cells and summarizes its role on leukemic cell response to chemotherapy.

67 pt ( P < 1.0E(-6)) and with lower diagnostic leukemic cell surface CD33 intensity ( P < 1.0E(-6)).

68 re with 3 signaling pathways associated with leukemic cell survival, namely: NF-kappaB activation, as

69 would contribute to reducing the survival of leukemic cells and also tackling their chemoresistance.

70 findings suggest striking interplay between leukemic cells and AT to create a unique microenvironmen

71 graftment, facilitating interactions between leukemic cells and bone marrow stroma.

72 e, we used RNA-Seq-based analysis of patient leukemic cells and found that upregulation of the Tec fa

73 microenvironment to support the survival of leukemic cells and influence their response to therapeut

74 lly effective in promoting PBMC cytolysis of leukemic cells and is 1000- to 10 000-fold more potent a

75 wide suppression of Notch-activated genes in leukemic cells and other models.

76 In particular, leukemic cells are highly heterogeneous, and there is a

77 Finally, we observe that persistent residual leukemic cells are quiescent and can become responsive t

78 We analyzed global DNA binding of MEIS1 in leukemic cells as well as gene expression alterations in

79 to efficiently redirect killing of HLA-DR(+) leukemic cells by human CD5(+) cytokine-induced killer T

80 Leukemic cells can remodel the niche into a permissive e

81 -leukemic therapies, it has been elusive how leukemic cells could acquire the serious resistance agai

82 ore circadian transcription factors, wherein leukemic cells depend on the clock machinery for surviva

83 es in leukemia and potentially other cancers.Leukemic cells depend on the nucleotide synthesis pathwa

84 l regulatory proteins to induce apoptosis in leukemic cells derived from genetically engineered mouse

85 However, the mechanisms that render leukemic cells drug resistant remain largely undefined.

86 ow that JAM-C expression defines a subset of leukemic cells endowed with leukemia-initiating cell act

87 Patients' leukemic cells exposed ex vivo to BRAF inhibitors are sp

88 lfite sequencing of primary leukemic and non-leukemic cells in patients with or without DNMT3A(R882)

89 nd effector function in response to CD200(+) leukemic cells in vitro.

90 CMML and JMML disease-initiating and mature leukemic cells in vivo, allowing creation of genetically

91 is study, we show that autologous irradiated leukemic cells induce proliferation in CLL cells and tha

92 metabolic enzymes, and knockdown of ClpP in leukemic cells inhibited oxidative phosphorylation and m

93 , we demonstrate that expression of IL-15 in leukemic cells is associated with the activation of natu

94 Dck-defective leukemic cells may become prednisolone sensitive indicat

95 e, we show that depleting IQGAP1 in Jurkat T leukemic cells reduced CXCR4 expression, disrupted traff

96 tron retention and cassette exon skipping in leukemic cells regardless of Srsf2 genotype, the magnitu

97 f these receptors and S1P1 on the ability of leukemic cells to accumulate in SLOs.

98 High levels of FTO sensitize leukemic cells to R-2HG, whereas hyperactivation of MYC

99 Ectopic expression of lncRNA-BGL3 sensitized leukemic cells to undergo apoptosis and inhibited Bcr-Ab

100 s mimic human pathology and demonstrate that leukemic cells transit the blood-cerebrospinal fluid bar

101 lls in donor grafts, recognize and eliminate leukemic cells via graft-versus-leukemia (GVL) reactivit

102 cell activity was maintained, and all of the leukemic cells were eliminated.

103 e-specific CD4(+) T cells recognized primary leukemic cells when the mismatched HLA class II allele w

104 Strikingly, leukemic cells with Alox5 overexpression showed a signif

105 on molecules that control the interaction of leukemic cells with bone marrow and spleen microenvironm

106 Treatment of MLL-rearranged leukemic cells with dinaciclib resulted in rapidly decre

107 Human leukemic cells with EPOR rearrangements were sensitive t

108 row niche is required to regenerate HSCs and leukemic cells with functional ability to rearrange the

109 esults suggest that increasing GFI1 level in leukemic cells with low GFI1 expression level could be a

110 assays, to test the antitumoral potential on leukemic cells, and a preliminary characterization of th

111 cally, UV-HSV-1 stimulates PBMC cytolysis of leukemic cells, partly via Toll-like receptor-2/protein

112 ression data generated from JAM-C-expressing leukemic cells, we defined a single cell core gene expre

113 matin accessibility and RNA-seq data in K562 leukemic cells, we identify the cell surface marker CD24

114 imately relapse with loss of CD19 antigen on leukemic cells, which has been established as a novel me

115 e the enhanced survival and proliferation of leukemic cells, with current drug development efforts fo

116 acrophages may provide a protective niche to leukemic cells.

117 includes the PAFc, MLL1, HOXA9 and STAT5 in leukemic cells.

118 d on its ability to drive differentiation of leukemic cells.

119 uble FasL and granzyme B, and eliminated the leukemic cells.

120 m1 signaling triggers an apoptotic signal in leukemic cells.

121 or palbociclib induces apoptosis of FLT3-ITD leukemic cells.

122 5 of 6 mice after transplant of as few as 10 leukemic cells.

123 downregulated in SALL4B Tg leukemic and pre-leukemic cells.

124 te that CNS tropism is a generic property of leukemic cells.

125 rboring mRNAs, thereby promoting survival of leukemic cells.

126 this system can achieve effective killing of leukemic cells.

127 impedes the in vitro expansion of murine pre-leukemic cells.

128 importance for growth and survival of human leukemic cells.

129 on RNA interference (RNAi) screen in primary leukemic cells.

130 u (5%) and exerted killing functions against leukemic cells.

131 maintained stably ex vivo in the absence of leukemic cells.

132 effective in delivering miRNA molecules into leukemic cells.

133 in the microenvironment of hematopoietic and leukemic cells.

134 ss that is suppressed in treatment-resistant leukemic cells.

135 enter underwent gene expression profiling of leukemic cells.

136 d synergize with a cytidine analogue against leukemic cells.

137 /f)Mx1-CreCbfb(+/56M) and Mx1-CreCbfb(+/56M) leukemic cells.

138 results in a drastic reduction of Ara-CTP in leukemic cells.

139 We demonstrated that AID and RAG1-RAG2 drove leukemic clonal evolution with repeated exposure to infl

140 is presumed to be a secondary consequence of leukemic clonal expansion.

141 nosis, representing variants shared across a leukemic clonal structure, may constrain the genomic lan

142 during CLL progression and suggest that the leukemic clone can generate an autoactivation loop throu

143 f any sequenced cancer, with the predominant leukemic clone carrying a mean of 1.3 non-silent mutatio

144 nalysis of RANK/RANKL loop activation in the leukemic clone, given recent reports on its role in CLL

145 ture and increase proliferating potential of leukemic clone.

146 2-deficient mouse HSPCs and suppresses human leukemic colony formation and leukemia progression of pr

147 Our approach rationalizes leukemic complexity and constructs a platform towards ex

148 Inhibiting TIFA perturbed leukemic cytokine secretion and reduced the IC50 of chem

149 function, which facilitates MLL-AF9-mediated leukemic disease in mice.

150 reduced proliferation resulting in extended leukemic disease latency in vivo.

151 e rise to leukemia in vivo and reestablished leukemic DNA methylation/gene expression patterns, inclu

152 t they retained leukemic mutations but reset leukemic DNA methylation/gene expression patterns.

153 l circadian pathway components produces anti-leukemic effects, including impaired proliferation, enha

154 ith ATRA leads to a significant reduction in leukemic engraftment.

155 These results indicate that leukemic evasion of NK cell surveillance occurs through

156 tio [HR] = 2.69) and cumulative incidence of leukemic evolution (from 0% to 48% at 4 years, HR = 3.84

157 tly different OS and cumulative incidence of leukemic evolution.

158 -promoting BCL-2 family member, myeloid cell leukemic factor 1 (MCL-1).

159 ger marrow vessel leakiness, instigating pro-leukemic function.

160 provide mechanistic insight into which Nup98 leukemic fusion proteins promote AML.

161 hat it acts as a major regulator of the TAL1 leukemic gene expression program.

162 granulocyte-macrophage progenitors (GMP) and leukemic GMP.

163 tion of Pol I transcription reduces both the leukemic granulocyte-macrophage progenitor and leukemia-

164 We found that Runx1 deletion inhibits mouse leukemic growth in vivo and that RUNX silencing in human

165 ng the NOTCH1-ZMIZ1 interaction might combat leukemic growth while avoiding the intolerable toxicitie

166 ell surface marker CD34, resulted in reduced leukemic growth.

167 dicating a specific requirement for Hhex for leukemic growth.

168 s of AML while tracking its development (pre-leukemic haematopoietic stem cells, leukemic stem cells

169 tem cell (SC) compartment in both normal and leukemic hematopoiesis has been challenging due to the i

170 cytosolic fumarate metabolism, in normal and leukemic hematopoiesis.

171 Non-leukemic hematopoietic cells with DNMT3A(R882H) displaye

172 mutations are present and expressed within a leukemic hematopoietic stem cell has engendered some con

173 sive chromatin signatures that distinguished leukemic, host, and normal CD4(+) T cells.

174 r to exhausted T cells and that T cells from leukemic hosts become metabolically impaired.

175 regions have reduced capacity to support non-leukemic HSCs, correlating with loss of normal hematopoi

176 imab and ofatumumab depleted both normal and leukemic human CD20-expressing B cells in the mouse less

177 The ability to target the leukemic-initiating cell population is thought to be ess

178 Characterization of the leukemic initiation population in this model leads to th

179 These features are hypothesized to underlie leukemic initiation, progression, and relapse, and they

180 ted with an increased risk of extramedullary leukemic involvement.

181 sting T-lymphocytes, T-lymphoblasts, and the leukemic Jurkat T-cells all exhibit membrane rupture abo

182 A better mechanistic understanding of leukemic LGL survival will allow future consideration of

183 rleukin 15 plays a key role in activation of leukemic LGL.

184 ometric analysis of LDB1 binding partners in leukemic lines supports the notion that LMO2/LDB1 functi

185 This response drives the leukemic load below this immune window, allowing the leu

186 ults suggest that, at diagnosis, a patient's leukemic load is able to partially or fully suppress the

187 dvantage following chemotherapy and a higher leukemic long-term culture initiating cell potential, ta

188 osis have a 5 to 7 times higher frequency of leukemic long-term culture-initiating cells (L-LTC-IC) c

189 enitor cell numbers, reduced regeneration of leukemic long-term hematopoietic stem cells in secondary

190 opoietin (THPO) receptor MPL was elevated in leukemic LTHSC populations.

191 , the mechanisms underlying heterogeneity of leukemic LTHSCs are poorly understood.

192 transgenic (SALL4B Tg) mouse model with pre-leukemic MDS-like symptoms that transform to AML over ti

193 Indeed, NK cells from leukemic mice and humans with AML showed lower levels of

194 ve loss of an immature subset of NK cells in leukemic mice and in AML patients.

195 NK cells in leukemic mice displayed a marked reduction in the cytoly

196 overall survival of 73 days, while untreated leukemic mice had a median overall survival of 34 days (

197 Weekly administration of PF-06747143 to leukemic mice significantly reduced leukemia development

198 survival advantage in both p53WT and p53null leukemic mice treated with CX-5461 is associated with ac

199 Pre-leukemic mice with the Flt3(ITD) knock-in allele manifes

200 icantly prolonged the survival of t(8;21)(+) leukemic mice, whereas overexpression of activated AKT1

201 mouse model of AML, and prolongs survival of leukemic mice.

202 rsed the depletion of this NK cell subset in leukemic mice.

203 d the development of therapies targeting the leukemic microenvironment.

204 -9 on both leukemic and stromal cells in the leukemic microenvironment.

205 s another important survival signal from the leukemic microenvironment.

206 Importantly, miR-199a-3p caused AML in a pre-leukemic mouse model, supporting its role as an onco-mic

207 rearrangements and found that they retained leukemic mutations but reset leukemic DNA methylation/ge

208 btypes, one shared hallmark is the arrest of leukemic myeloblasts at an immature and self-renewing st

209 e associated with large granular lymphocytic leukemic, myelodysplastic syndrome, and aplastic anemia.

210 egulator of T-bet and EOMES, was elevated in leukemic NK cells.

211 we mutagenized a selected region within the leukemic oncogene BCR-ABL1 Using bulk competitions with

212 FTO enhances leukemic oncogene-mediated cell transformation and leuke

213 SCs in patients with AML may be derived from leukemic or apparently normal progenitors.

214 3q26.2 rearrangements emerged at different leukemic phases.

215 ibitors of this interaction that reverse the leukemic phenotype and prolong survival in murine models

216 ical blockage of fructose uptake ameliorates leukemic phenotypes and potentiates the cytotoxicity of

217 Imatinib therapy drives the leukemic population into the "immune window," allowing t

218 load below this immune window, allowing the leukemic population to partially recover until another w

219 ML-defining molecular lesions present in all leukemic populations (including subclones) has been exem

220 AML-iPSCs lacked leukemic potential, but when differentiated into hematop

221 Rapidly proliferating leukemic progenitor cells consume substantial glucose, w

222 AML patient blasts, and isolated AML patient leukemic progenitor/stem cells, with negligible effects

223 lation in AML cells and suppresses primitive leukemic progenitors from AML patients in vitro and in a

224 or IgG1 control-treated animals showed that leukemic progenitors were also targeted by PF-06747143.

225 trate the PAFc regulates Prmt5 to facilitate leukemic progression and is a potential therapeutic targ

226 herapeutic reduction of ROS may thus prevent leukemic progression and relapse in myeloid malignancies

227 tly inhibits the initiation and reverses the leukemic progression of both B cell and T cell acute lym

228 1 in MLL-AF9 leukemia: PAR-1 inhibited rapid leukemic proliferation when there were a large number of

229 Pexmetinib inhibited leukemic proliferation, prevented activation of downstre

230 Surprisingly, we find that leukemic RasGRP1-triggered Ras-Akt signals do not depend

231 (NK) cell alloreactivity in HCT can control leukemic relapse, but capturing alloreactivity in HLA-ma

232 eted T-cell immunotherapy to manage post-HCT leukemic relapse.

233 Ectopic overexpression of INPP4B conferred leukemic resistance to cytosine arabinoside (ara-C), dau

234 The term "leukemic reticuloendotheliosis" proposed a cell of origi

235 y with radial changes can be detected in pre-leukemic SALL4B Tg bone marrow (BM) cells after DNA dama

236 Leukemic samples were collected from patients with newly

237 ooperating c-Kit mutations found only in the leukemic samples.

238 e inability to separate and study normal and leukemic SCs at the single-cell level.

239 ted by beta-catenin/Hoxa9/Prmt1 in governing leukemic self-renewal.

240 ed in LSK-derived MLL-CSCs and helps sustain leukemic self-renewal.

241 nation of stem cells at both preleukemic and leukemic stages.

242 eatures (collectively) consistent with a pre-leukemic state.

243 ombination with WNT974 significantly reduced leukemic stem and progenitor cell numbers, reduced regen

244 scripts in hematopoietic and patient-derived leukemic stem and progenitor cells, and reduced progress

245 ncer, neuronal, and normal hematopoietic and leukemic stem and progenitor cells.

246 Using publicly available leukemic stem cell (LSC) gene expression profiles and ge

247 d finally, (5) how the knowledge gained into leukemic stem cell (LSC) niche dependencies might be exp

248 prognosis, and ineffective targeting of the leukemic stem cell (LSC) population remains one of sever

249 urrent models suggest transformation creates leukemic stem cell (LSC) populations arrested at a proge

250 al. (2016) reveal metabolic heterogeneity in leukemic stem cell (LSC) subpopulations and show that ch

251 emopoietic stem cell, transforming it into a leukemic stem cell (LSC) that self-renews, proliferates,

252 niche into a permissive environment favoring leukemic stem cell expansion over normal HSC maintenance

253 and mTORC2 differentially control normal and leukemic stem cell functions.

254 t yet curative, because most patients retain leukemic stem cells (LSC) and their progenitors in bone

255 of chronic myeloid leukemia do not eliminate leukemic stem cells (LSC).

256 Here, we show that a subpopulation of leukemic stem cells (LSCs) can utilize gonadal adipose t

257 Leukemic stem cells (LSCs) drive progression of chronic

258 the failure to eliminate therapy-persistent leukemic stem cells (LSCs) may result in disease relapse

259 THSCs are heterogeneous in their capacity as leukemic stem cells (LSCs).

260 g factors in realizing the goal of targeting leukemic stem cells (LSCs).

261 L) largely depends on the eradication of CML leukemic stem cells (LSCs).

262 the aberrant function of disease-initiating leukemic stem cells (LSCs).

263 et differentiated cells and do not eliminate leukemic stem cells (LSCs).

264 k for relapse remains, due to persistence of leukemic stem cells (LSCs).

265 Therapeutic targeting of pre-leukemic stem cells (pre-LSCs) may be a viable strategy

266 ent (pre-leukemic haematopoietic stem cells, leukemic stem cells [LSCs], and leukemic blasts).

267 l in mice transplanted with MLL-AF9-positive leukemic stem cells by modulating AKT and 4E-BP1 phospho

268 s between healthy hematopoietic and diseased leukemic stem cells for core circadian transcription fac

269 ddC also targeted leukemic stem cells in secondary AML xenotransplantation

270 self-renewal and promote differentiation of leukemic stem cells in the MLL-translocated molecular su

271 isoform signatures unique to patient-derived leukemic stem cells that constitute a therapeutic Achill

272 e to therapy-resistant, disease-reinitiating leukemic stem cells.

273 with their microenvironment and maintaining leukemic stem cells.

274 ibits adverse growth and partly relieves the leukemic symptoms of AEL patients.

275 JAK kinase inhibitors have depressed leukemic T cell line proliferation.

276 and Pin1 in the Notch3-overexpressing human leukemic TALL-1 cells reduces their high invasive potent

277 tibility complex class I ligand is absent on leukemic target cells can exert alloreactivity in vitro

278 dely recognized as a novel strategy for anti-leukemic therapies, it has been elusive how leukemic cel

279 genetically normal AML that contributes to a leukemic transcriptome.

280 referred option, even though their impact on leukemic transformation and survival has not been proved

281 progenitors may therefore be protected from leukemic transformation because they are not competent t

282 Hematopoietic stressors may contribute to leukemic transformation by increasing the mutation rate

283 ecent findings on the impact of autophagy on leukemic transformation of normal hematopoietic stem cel

284 interrelationship among those 3 complexes in leukemic transformation remains largely elusive.

285 No events indicative of leukemic transformation were reported.

286 een linked to genetic damage associated with leukemic transformation, including etoposide-induced chr

287 PRMT1 is necessary but not sufficient for leukemic transformation, which requires co-recruitment o

288 at certain niche alterations can even induce leukemic transformation.

289 al neutropenia syndromes with a high rate of leukemic transformation.

290 hylation is concomitant with MLL-AF9-induced leukemic transformation.

291 enhancer regions, critical for inhibition of leukemic transformation.

292 with clonal hematopoiesis in the absence of leukemic transformation.

293 s may cooperate with BRAF V600E in promoting leukemic transformation.

294 t on how these alterations may contribute to leukemic transformation.

295 3 (Y100C) completely abrogated JAK3-mediated leukemic transformation.

296 s been shown to be necessary for maintaining leukemic transformation; however, the molecular mechanis

297 sets of genes that are tightly regulated in leukemic transformations and commonly mutated in other t

298 A subset of leukemic tumors showed active BCR and NF-kappaB signalin

299 Sezary syndrome (SS) is a leukemic variant of cutaneous T-cell lymphoma (CTCL) and

300 oma variant and is closely related to a rare leukemic variant, Sezary syndrome (SS).