ライフサイエンスコーパス: leukemia

1 hematologic malignancies (e.g., CD19 CARs in leukemias).

2 k factors for outcome in acute lymphoblastic leukemia.

3 enge by clinical specialists who treat acute leukemia.

4 and a propensity to evolve to acute myeloid leukemia.

5 exclusion of any extramedullary extension of leukemia.

6 sive emergence of T cell acute lymphoblastic leukemia.

7 irement for wild-type MLL1 in MLL-rearranged leukemia.

8 nactivation is associated with acute myeloid leukemia.

9 ogical malignancies, including acute myeloid leukemia.

10 n vitro and in a disseminated mouse model of leukemia.

11 y related diagnosis atypical chronic myeloid leukemia.

12 apeutic vulnerability in this poor-prognosis leukemia.

13 a critical role in the pathogenesis of this leukemia.

14 in mice is sufficient to drive acute myeloid leukemia.

15 tural DNA alterations in acute lymphoblastic leukemia.

16 transplants, or who have acute lymphoblastic leukemia.

17 phoblastic leukemia and MLL-rearranged acute leukemia.

18 cular malignant melanoma, breast cancer, and leukemia.

19 gressive systemic mastocytosis and mast cell leukemia.

20 ay drive the transformation to acute myeloid leukemia.

21 ssion culminating in serially transplantable leukemia.

22 clonal expansion and potentially leading to leukemia.

23 and a tendency to transform to acute myeloid leukemia.

24 tive against mouse xenograft models of human leukemia.

25 l development, and its deregulation leads to leukemia.

26 es, and in a genome-scale metabolic model of leukemia.

27 patients with MDS or secondary acute myeloid leukemia.

28 ase therapy in childhood acute lymphoblastic leukemia.

29 for relapsed/refractory acute lymphoblastic leukemia.

30 tors of tyrosine kinase oncogenes in myeloid leukemias.

31 ntigen that is expressed in many cancers and leukemias.

32 th the occurrence of secondary acute myeloid leukemias.

33 therapeutic strategy to target SETD2-mutant leukemias.

34 ion of the BCL-2 family members myeloid cell leukemia 1 (MCL-1) and BCL-XL in lymphoma cells.

35 al-regulated kinase+/BCL-XL(+) /myeloid cell leukemia 1+ signature, deregulated in Alb-R26(Met) tumor

36 Mixed-lineage leukemia-1 (MLL1) has been shown to direct gene expressi

37 lasm (MPN), including chronic myelomonocytic leukemia, according to the International Prognostic Scor

38 both Hsp70 and Hsp90, exhibit enhanced anti-leukemia activity relative to the individual inhibitors.

39 as their hybrids can serve as potential anti-leukemia agents.

40 , which could drive both acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).

41 patients with pediatric acute lymphoblastic leukemia (ALL) and to identify genetic abnormalities tha

42 e Survivors of childhood acute lymphoblastic leukemia (ALL) are at risk for neurocognitive deficits t

43 eliminate CD19-positive acute lymphoblastic leukemia (ALL) blasts, was approved for use in patients

44 nthesis in ATR-inhibited acute lymphoblastic leukemia (ALL) cells reveals substantial remaining de no

45 ommon genetic feature of acute lymphoblastic leukemia (ALL) in both children and adults.

46 hromosome-like (Ph-like) acute lymphoblastic leukemia (ALL) is a high-risk subtype characterized by g

47 T-cell acute lymphoblastic leukemia (ALL) is a rare disease in adults with inferior

48 P) and risk of childhood acute lymphoblastic leukemia (ALL) were investigated using data from populat

49 samples at diagnosis of acute lymphoblastic leukemia (ALL), a uniform CSF and risk group classificat

50 hia chromosome (Ph)-like acute lymphoblastic leukemia (ALL), also referred to as BCR-ABL1-like ALL, i

51 fection in the etiology of acute lymphocytic leukemia (ALL), and the involvement of the immune system

52 In acute lymphoblastic leukemia (ALL), central nervous system (CNS) involvement

53 e B-cell precursor (BCP) acute lymphoblastic leukemia (ALL), often comprising small numbers of patien

54 Patients with acute myeloid leukemia (AML) and a FLT3 mutation have poor outcomes.

55 The heterogeneous nature of acute myeloid leukemia (AML) and its poor prognosis necessitate therap

56 otic nucleosides used to treat acute myeloid leukemia (AML) and other cancers remains a major obstacl

57 d a key therapeutic target for acute myeloid leukemia (AML) and other forms of cancer.(1-4) The natur

58 ent of primary patient-derived acute myeloid leukemia (AML) and other hematologic malignancies such a

59 m/progenitor cells (HSPCs) and acute myeloid leukemia (AML) cells carrying t(11q23), t(15;17), or t(8

60 Acute myeloid leukemia (AML) cells have increased mitochondria compare

61 Adults with acute myeloid leukemia (AML) commonly require support in the intensive

62 , most patients diagnosed with acute myeloid leukemia (AML) die of their disease.

63 Purpose Elderly patients with acute myeloid leukemia (AML) have a poor prognosis, and innovative mai

64 n during induction therapy for acute myeloid leukemia (AML) have been shown to improve remission rate

65 Previous studies in childhood acute myeloid leukemia (AML) have shown a negative correlation of IDO-

66 In this study, using acute myeloid leukemia (AML) human cell lines and a custom CRISPR/Cas9

67 Acute myeloid leukemia (AML) is a disease associated with epigenetic d

68 Acute myeloid leukemia (AML) is a major unmet medical need.

69 Childhood acute myeloid leukemia (AML) is frequently characterized by chromosoma

70 ) T cells in preclinical human acute myeloid leukemia (AML) models at the cost of severe hematologic

71 s expressed in the majority of acute myeloid leukemia (AML) patients.

72 rofiling analysis of 542 human acute myeloid leukemia (AML) samples and identified 55% with upregulat

73 s offer therapeutic targets in acute myeloid leukemia (AML) that are of great current interest.

74 mouse xenograft model of human acute myeloid leukemia (AML) that enabled chemotherapy-induced regress

75 relapsed/refractory/poor-risk acute myeloid leukemia (AML) was evaluated in 43 patients in a prospec

76 ts with relapsed or refractory acute myeloid leukemia (AML) were enrolled between January 2013 and Ju

77 Purpose Children with acute myeloid leukemia (AML) whose disease is refractory to standard i

78 ts with SCN are predisposed to acute myeloid leukemia (AML), and progression from SCN to AML is accom

79 S100A9 are highly expressed in acute myeloid leukemia (AML), and S100A8 expression has been linked to

80 FLT3-mutated acute myeloid leukemia (AML), despite not being recognized as a distin

81 T-ALL, respectively), but not acute myeloid leukemia (AML), in mouse models of these tumors.

82 iciently triggers apoptosis in acute myeloid leukemia (AML), non-Hodgkin lymphoma, and multiple myelo

83 oor prognosis in patients with acute myeloid leukemia (AML), T-cell acute lymphoblastic leukemia, and

84 Acute myeloid leukemia (AML), the most common adult acute leukemia in

85 In acute myeloid leukemia (AML), therapy resistance frequently occurs, le

86 vage chemotherapy regimens for acute myeloid leukemia (AML).

87 rate NK reactivity against acute myelogenous leukemia (AML).

88 including approximately 12% of acute myeloid leukemia (AML).

89 mphoblastic leukemia (ALL) and acute myeloid leukemia (AML).

90 ets of pediatric and adult acute myelogenous leukemia (AML).

91 lodysplastic syndrome (MDS) or acute myeloid leukemia (AML).

92 tic approach for patients with acute myeloid leukemia (AML).

93 erapy in younger patients with acute myeloid leukemia (AML).

94 blast crisis CML (BC-CML) and acute myeloid leukemias (AML) are GVL resistant.

95 s investigating primary murine acute myeloid leukemias (AMLs) generated by retroviral insertional mut

96 ile advancing maternal age increased risk of leukemia and central nervous system tumors, older patern

97 plant homeodomain finger protein 6 (PHF6) in leukemia and define its role in regulating chromatin acc

98 elow we discuss immune evasion mechanisms in leukemia and lymphoma, highlighting key differences from

99 are enriched in relapsed acute lymphoblastic leukemia and MLL-rearranged acute leukemia.

100 receptor (CD200R), is commonly increased in leukemia and other malignancies and is associated with p

101 and existence of tumor-initiating cells for leukemia and other malignancies have long been the subje

102 NK-cell reconstitution that compromise both leukemia and pathogen-specific immunity.

103 nd ATR provides therapeutic opportunities in leukemia and potentially other cancers.Leukemic cells de

104 n a model of Kras(G12D) mutant acute myeloid leukemia and propose its use as a predictive biomarker.

105 d the monitoring and in vivo imaging of both leukemia and solid tumors.

106 e of MLL2 as a drug target in MLL-rearranged leukemia and suggest its broader significance in AML.

107 p210 and p190, are associated with different leukemias and have a dramatically different signaling ne

108 As a consequence, many human leukemias and other hematologic disorders do not robustl

109 omics in myelodysplastic syndromes (MDS) and leukemias and the limitations of precision-medicine conc

110 d leukemia (AML), T-cell acute lymphoblastic leukemia, and myelodysplastic syndromes.

111 lung, kidney, and bladder cancer, lymphoma, leukemia, and unspecified metastatic cancer.

112 10, also known as common acute lymphoblastic leukemia antigen, neutral endopeptidase, or enkephalinas

113 Acute promyelocytic leukemia (APL) is commonly complicated by a complex coag

114 the immense majority of acute promyelocytic leukemia (APL) patients can be definitively cured by the

115 ewly diagnosed pediatric acute promyelocytic leukemia (APL) was a phase III historically controlled t

116 nts with newly diagnosed acute promyelocytic leukemia (APL).

117 on protein causative for acute promyelocytic leukemia (APL).

118 d immune checkpoint therapies in myelogenous leukemia are desired.

119 known oncogene in T-cell acute lymphoblastic leukemia) are present in approximately 4-13% of chronic

120 of clonal evolution in lymphoid and myeloid leukemia as a driver of tumor initiation, disease progre

121 substantially but were complicated by acute leukemia as a result of insertional mutagenesis in a hig

122 ice were investigated by ELISA, rat basophil leukemia assay, T-cell proliferation experiments using r

123 evidenced by recurrent somatic mutations in leukemia-associated genes, commonly occurs among aging h

124 iments from the paper "The common feature of leukemia-associated IDH1 and IDH2 mutations is a neomorp

125 R specific for the hematopoietic-restricted, leukemia-associated minor H antigen, HA-1; (2) a CD8 cor

126 t homology domain (RHD), a domain where most leukemia-associated point mutations cluster.

127 LARG (leukemia-associated Rho guanine nucleotide exchange fact

128 -1) is the etiological agent of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical

129 f both B cell and T cell acute lymphoblastic leukemia (B-ALL and T-ALL, respectively), but not acute

130 portant prognostic factor in B-lymphoblastic leukemia (B-ALL).

131 plasms, including B cell chronic lymphocytic leukemia (B-CLL).

132 diatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) could not be classified into any of t

133 , patient-derived B-cell acute lymphoblastic leukemia blasts compared with standard TCR transfer.

134 is curative for FA-related marrow failure or leukemia, but both radiation exposure during transplant

135 associated typically with aggressive myeloid leukemia, but is also detectable in breast carcinoma whe

136 target Bcl-2 are used in the clinic to treat leukemia, but tight and selective inhibitors are not ava

137 ociated with childhood acute B-lymphoblastic leukemia (cALL) functioning as a first-hit mutation that

138 e BCR-ABL1 in the Philadelphia chromosome of leukemia cancer cells.

139 lyzed 36 cases of -7 AML for mutations in 81 leukemia/cancer-associated genes using a customized targ

140 istinct and aggressive subset of human acute leukemia carrying chromosomal translocations of the MLL

141 Stromal coculture did not prevent leukemia cell cycle activity, but a specific sensitivity

142 to RNA-seq data of the human chronic myeloid leukemia cell line K562 in response to shRNA knockdown o

143 TOP2A cleavage genome-wide in the human K562 leukemia cell line.

144 activation effectively promotes apoptosis in leukemia cell lines and patient samples while sparing he

145 nd selectively inhibits cell growth in human leukemia cell lines harboring MLL translocations and is

146 Tested in leukemia cell lines, 35 and 39 induced apoptosis and/or

147 r activity was demonstrated in acute myeloid leukemia cell lines, where significant impairment of pro

148 encies in inhibition of cell growth in acute leukemia cell lines.

149 uman blood mononuclear cells and a subset of leukemia cell lines.

150 ntiproliferative activities in acute myeloid leukemia cell lines.

151 e novel prodrug also induced T cell mediated leukemia cell lysis.

152 geting wild-type MLL degradation impedes MLL leukemia cell proliferation, and it downregulates a spec

153 activity in vitro and in vivo by inhibiting leukemia cell proliferation/viability and by promoting c

154 , leading to synergistic inhibition of human leukemia cell viability.

155 e of VEGF produced by ALL cells in mediating leukemia-cell entry into the CNS and leptomeningeal infi

156 molecular mechanisms and pathways mediating leukemia-cell entry into the CNS need to be understood t

157 n unexpected role for MLL2 in MLL-rearranged leukemia cells and identify potential therapeutic target

158 ited the growth of acute and chronic myeloid leukemia cells and the phosphorylation and transcription

159 cellular cytotoxicity against PRAME+HLA-A2+ leukemia cells and was therapeutically effective against

160 Abl, and display lower cytotoxicity against leukemia cells compared to those of the individual const

161 itro, and primed CD56bright cells controlled leukemia cells in vivo in a murine xenograft model.

162 Inhibition of Hsp72 in acute lymphoblastic leukemia cells resulted in increased multipolar spindle

163 nd mouse mast cells, as well as rat basophil leukemia cells, and in vivo in mice.

164 cytokine production in response to CD200(+) leukemia cells, supporting clinical translation.

165 emotherapy-induced apoptosis in Jurkat human leukemia cells.

166 to kill chemotherapy-resistant acute myeloid leukemia cells.

167 of human cancers and induced cell killing in leukemia cells.

168 mia (T-ALL), a heterogenic subgroup of human leukemia characterized by a high incidence of remission

169 n approximately 4-13% of chronic lymphocytic leukemia (CLL) cases, where they are associated with dis

170 ression in patients with chronic lymphocytic leukemia (CLL) treated with ibrutinib has been attribute

171 ct of USP7 inhibition in chronic lymphocytic leukemia (CLL) where the ataxia telangiectasia mutated (

172 common genetic lesion in chronic lymphocytic leukemia (CLL), promoting overexpression of BCL2, which

173 Within chronic lymphocytic leukemia (CLL), responses to 62% of drugs were associate

174 f bulk tumors, including chronic lymphocytic leukemia (CLL).

175 cells from patients with chronic lymphocytic leukemia (CLL).

176 cupancy in patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) that was

177 logic malignancies including chronic myeloid leukemia (CML) and myelodysplastic syndromes (MDS) eithe

178 Effective treatment of chronic myelogenous leukemia (CML) largely depends on the eradication of CML

179 imal residual disease in chronic myelogenous leukemia (CML) may be relevant for long-term control or

180 population in chronic phase chronic myeloid leukemia (CML) patients at diagnosis and following conve

181 2,000 SCs from patients with chronic myeloid leukemia (CML) throughout the disease course, revealing

182 been shown to alleviate chronic myelogenous leukemia (CML) via the elimination of leukemia stem cell

183 (TKI) changed the outcome of chronic myeloid leukemia (CML), turning a life-threatening disease into

184 l hematopoiesis resembling a chronic myeloid leukemia (CML)-like disease manifesting in "lymphoid bla

185 inase-induced mouse model of chronic myeloid leukemia (CML).

186 Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic malignancy tha

187 lly penetrant, lethal chronic myelomonocytic leukemia (CMML), which was serially transplantable.

188 patients with chronic phase chronic myeloid leukemia (CP-CML) are treated with tyrosine kinase inhib

189 nt against chronic phase chronic myelogenous leukemia (CP-CML), but blast crisis CML (BC-CML) and acu

190 iving adoptive NK-92 cell therapy block anti-leukemia cytotoxicity of NK-92 cells and other NK-92 cel

191 These include new subtypes of acute myeloid leukemia defined by mutations in RUNX1 or BCR-ABL1 trans

192 Although no leukemias developed in Pml(C62A/C65A) mice, these transg

193 er patients, with 4.5% harboring presumptive leukemia driver mutations (CH-PD).

194 ations seen commonly in chronic neutrophilic leukemia (e.g., T618I), functionally defective mutations

195 ials while maintaining a robust graft-versus-leukemia effect.

196 model of aGVHD while retaining graft-versus-leukemia effects, unveiling a novel therapeutic target i

197 The inclusion of leukemia epigenomes in the healthy hematological chromat

198 e BCR-ABL1 fusion delineates chronic myeloid leukemia from classic BCR-ABL1(-) MPNs, which are largel

199 ram NK-92 cells, interfering with their anti-leukemia functions and reducing the therapeutic potentia

200 ppressive exosomes which interfere with anti-leukemia functions of activated immune cells.

201 e rearrangements involving the mixed-lineage leukemia gene (MLL) create MLL-fusion proteins, which co

202 xenografts (PDX) of pediatric mixed-lineage leukemia gene (MLL)-rearranged ALL were established in N

203 a recent large randomized trial (Cancer and Leukemia Group B/Alliance for Clinical Trials in Oncolog

204 The graft-versus-leukemia (GVL) effect in allogeneic hematopoietic stem c

205 ts GVHD while preserving strong graft-versus-leukemia (GVL) effects in allogeneic and xenogeneic muri

206 nd eliminate leukemic cells via graft-versus-leukemia (GVL) reactivity, and transfer of these cells i

207 nificant elevations in the risk of childhood leukemia have been associated with environmental exposur

208 Hairy cell leukemia (HCL) is a chronic mature B-cell neoplasm with

209 n initial diagnoses were acute lymphoblastic leukemia, Hodgkin lymphoma, and astrocytoma.

210 cooperating mutations, making MLL-FP driven leukemias ideal for animal modeling.

211 myeloma in 17 (34%), and chronic lymphocytic leukemia in 3 (6%) patients.

212 Despite nondetectable CNS leukemia in many cases, prophylactic CNS-directed conven

213 an suppress Philadelphia chromosome-positive leukemia in mice, suggesting that this therapeutic strat

214 may serve as a novel strategy to control CNS leukemia in patients, replacing conventional CNS-toxic t

215 leukemia (AML), the most common adult acute leukemia in the United States, has the poorest survival

216 ation that initiates a clinically silent pre-leukemia in utero.

217 d for the myeloid lineage, whereas the other leukemia-induced lncRNAs were dispensable in the normal

218 on protein, which causes acute promyelocytic leukemia, inhibits TNFalpha induced gene expression and

219 luding secondary glioblastoma, acute myeloid leukemia, intrahepatic cholangiocarcinoma, and chondrosa

220 for relapsed/refractory acute lymphoblastic leukemia is leading to expanded use through multicenter

221 Juvenile myelomonocytic leukemia (JMML) is a myeloproliferative disorder of chil

222 topoisomerase II, B-cell chronic lymphocytic leukemia/lymphoma 2 (BCL2), and many tyrosine kinase inh

223 on mutations have been discovered in primary leukemia/lymphoma and gastric cancer by human cancer gen

224 Purpose B-cell leukemia/lymphoma-2 (BCL-2) overexpression is common in

225 his identified several lncRNAs essential for leukemia maintenance, and found that a number act by pro

226 ced T cells efficiently lysed primary B-cell leukemia, mantle cell lymphoma, and multiple myeloma in

227 als (AML96, AML2003) from the Study Alliance Leukemia, marker chromosomes were detectable in 165/1026

228 er cell lines including, MCF-7 breast, HL-60 leukemia, MIA PaCa-2 pancreatic, DU145 prostate, HeLa ce

229 in 5 (WDR5) and block the WDR5-mixed lineage leukemia (MLL) protein-protein interaction.

230 ysine methylation, mediated by mixed-lineage leukemia (MLL) proteins, is now known to be critical in

231 Mixed lineage leukemia (MLL) represents a genetically distinct and agg

232 L2 and PTEN mRNAs in the human acute myeloid leukemia MOLM-13 cell line.

233 proved overall survival and EFS for European Leukemia Net (ELN) 2010 intermediate I prognostic risk A

234 Promyelocytic leukemia nuclear bodies (PML-NB) are sub-nuclear organel

235 the strong B-cell ALL association of MLL-AF4 leukemia observed in the clinic.

236 Patients with myeloid leukemia of Down syndrome (ML-DS) have favorable event-f

237 er demonstrated by specific reduction of CNS leukemia on in vivo VEGF capture by the anti-VEGF antibo

238 18-69 years), and 95% had acute myelogenous leukemia or high-risk myelodysplastic syndrome.

239 cell-dose-dependent role of PAR-1 in MLL-AF9 leukemia: PAR-1 inhibited rapid leukemic proliferation w

240 ing overexpression of BCL2, which factors in leukemia pathogenesis.

241 o blood basophils is largely suppressed in a leukemia patient treated with ibrutinib.

242 Primed CD56bright cells from leukemia patients demonstrated enhanced responses to aut

243 r screening of CSF3R extracellular domain in leukemia patients.

244 ies and is associated with poor prognosis in leukemia patients.

245 omosome (Ph)-like B-cell acute lymphoblastic leukemia (Ph-like ALL) is associated with activated JAK/

246 Promyelocytic Leukemia (PML) is a nuclear protein that forms sub-nucle

247 Promyelocytic leukemia (PML) is a pleiotropic tumor suppressor, but it

248 The promyelocytic leukemia (PML) protein is an essential component of PML

249 Rosa26-CreER(T2)Runx1(f/f) mice and examined leukemia progression in the presence of vehicle or tamox

250 o characterize the effects of PF-06747143 on leukemia progression, we used two different patient-deri

251 thway protein inhibitors and observed marked leukemia reduction and in vivo signaling inhibition in a

252 l killer (NK) cells can decrease the risk of leukemia relapse, we initiated a phase 1 dose-escalation

253 ime-course studies demonstrated that durable leukemia remission required CAR T-cell persistence for 4

254 on of CART123 or CART123-CD20 did not impair leukemia remission.

255 ary tumors and 20 B-cell acute lymphoblastic leukemias, respectively.

256 The chimerism or the beneficial graft-versus-leukemia response remained unaffected.

257 34), DLBCL arising from chronic lymphocytic leukemia (Richter transformation; n = 7), Waldenstrom ma

258 riants-breast cancer risk SNP rs11055880 and leukemia risk-associated SNP rs12142375-and demonstrate

259 emogenic functions and express the stem cell leukemia (SCL) gene driven by its 5' enhancer.

260 =2.6, 95% confidence interval, 2.2-3.1), and leukemia (SHR=2.5, 95% confidence interval, 1.9-3.1) wer

261 ures, and apply the methodology to the T-LGL leukemia signaling network as a case study.

262 in mice is sufficient to drive acute myeloid leukemia.Significance: This study defines a tumor suppre

263 ymphoma, non-Hodgkin lymphoma, acute myeloid leukemia, soft-tissue sarcoma, and central nervous syste

264 ce, and found that a number act by promoting leukemia stem cell signatures.

265 genous leukemia (CML) via the elimination of leukemia stem cells (LSCs) in mice.

266 m to identify potential targets expressed in leukemia stem cells, but not in normal CD34(+)CD38(-) he

267 o a cell-intrinsic role of WNT activation in leukemia stem cells, WNT activation in the BM niche is a

268 tumor samples from the California Childhood Leukemia Study.

269 These suggested criteria involved combining leukemia subtypes, excluding automobile repair facilitie

270 at H3K27me2/3 has an important and selective leukemia-suppressive activity in this genetic context.

271 T-cell acute lymphoblastic leukemia (T-ALL) is a highly proliferative hematologic m

272 ed in a subset of T-cell acute lymphoblastic leukemia (T-ALL) patients, and RUNX1 mutations are assoc

273 river of immature T-cell acute lymphoblastic leukemia (T-ALL), a heterogenic subgroup of human leukem

274 apeutic target in T-cell acute lymphoblastic leukemia (T-ALL).

275 Emu-TCL1 transgenic mouse develops a form of leukemia that is similar to the aggressive type of human

276 other hematologic malignancies, particularly leukemias, the ability to detect minimal residual diseas

277 ew will focus on the role of Runx factors in leukemias, this review will provide an overview of the n

278 , suggesting that IFN-gamma sensitizes these leukemias to T cell killing by mechanisms other than MHC

279 of CDH-implicated genes encoding pre-B cell leukemia transcription factors (Pbx) led to lethal PH in

280 98% of ex vivo primary chronic B-lymphocytic leukemia tumor cells while sparing healthy B cells.

281 cture of the BM vasculature in acute myeloid leukemia using intravital two-photon microscopy.

282 ement of the photonic inactivation of Murine Leukemia Virus (MLV) via 805 nm femtosecond pulses throu

283 that tetherin does not affect Moloney murine leukemia virus (MoMLV) spread, and only minimally affect

284 calreticulin (CALR), and myeloproliferative leukemia virus (MPL), abnormally activate the cytokine r

285 e shown to restrict the expression of murine leukemia virus genomes but not retroviral genomes of the

286 Friend leukemia virus integration 1 (FLI1), a critical transcri

287 B-cell-specific Moloney murine leukemia virus integration site 1 (BMI1) is a component

288 Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent

289 rived from three retroviruses (HIV-1, murine leukemia virus, and Mason-Pfizer monkey virus), two hepa

290 , human immunodeficiency virus, human T cell leukemia virus, human papilloma virus, hepatitis B and C

291 exposure to gammaretroviruses such as feline leukemia viruses (FeLVs) occurs worldwide, but the basis

292 or refractory B-lineage acute lymphoblastic leukemia was conducted using a CD19 CAR product of defin

293 last cells, and a diagnosis of acute myeloid leukemia was made.

294 In our studies of mouse models of acute leukemia, we used high-resolution microscopy and flow cy

295 follicular lymphoma, and chronic lymphocytic leukemia, were enrolled.

296 by immunizing mice with Jurkat acute T cell leukemia, which binds ILT3.Fc to its membrane.

297 a model) exhibited a doubling in the rate of leukemia, with a reduced latency period.

298 improves antileukemic activity in vivo in a leukemia xenograft model.

299 l proliferation both in vitro and in vivo as leukemia xenografts.

300 man NK cells in a B-cell acute lymphoblastic leukemia xenotransplants model.