ライフサイエンスコーパス: acute leukemia

1 haploidentical hematopoietic transplants for acute leukemia.

2 icantly elevated risk of developing an overt acute leukemia.

3 XA9 expression is frequently associated with acute leukemia.

4 ended due to the poor prognosis of untreated acute leukemia.

5 bling donor (n=2,656) for male patients with acute leukemia.

6 nt cause of treatment failure in adults with acute leukemia.

7 slocations, point mutations, or deletions in acute leukemia.

8 14% (N = 111) of patients had acute leukemia.

9 nslocations or partial tandem duplication in acute leukemia.

10 an increasing incidence among patients with acute leukemia.

11 erience with PM exclusively in patients with acute leukemia.

12 ajor cause of treatment failure in high-risk acute leukemia.

13 ng complications, and risk of progression to acute leukemia.

14 n and the development of MLL fusion-mediated acute leukemia.

15 ies, including one family member who died of acute leukemia.

16 r radioiodine treatment, with progression to acute leukemia.

17 Differentiation arrest is a hallmark of acute leukemia.

18 cell specification and in the development of acute leukemia.

19 oncogenes that initiate aggressive forms of acute leukemia.

20 sion to myelofibrosis, and transformation to acute leukemia.

21 nvestigate clonal diversity and evolution in acute leukemia.

22 ed in human myeloproliferative neoplasms and acute leukemia.

23 r resistance to multiple drugs used to treat acute leukemia.

24 bone marrow dysplasia, and transformation to acute leukemia.

25 nd responses to therapy or survival rates in acute leukemia.

26 of cytopenia and risk of transformation into acute leukemia.

27 ell differentiation as well as initiation of acute leukemia.

28 s, and both are frequently targeted in human acute leukemia.

29 Oncogenic gene translocations occur in acute leukemia.

30 ligand therapy (RLT) in multiple myeloma and acute leukemia.

31 ypical of a cytotoxic agent in patients with acute leukemia.

32 ng a type of rhabdomyosarcoma that resembles acute leukemia.

33 al of lenalidomide in relapsed or refractory acute leukemia.

34 n chromosomal translocations associated with acute leukemia.

35 platelet dysfunction, and predisposition to acute leukemia.

36 ent of other molecularly defined subtypes of acute leukemia.

37 yelodysplastic syndrome (SM-MDS), and 4 (3%) acute leukemia.

38 transplantation is potentially curative for acute leukemia.

39 F alterations are frequently associated with acute leukemia.

40 an half of these mice eventually progress to acute leukemia.

41 ng with several MLL fusion partners found in acute leukemia.

42 ions, and chromosome translocations in human acute leukemia.

43 gene requires cooperating mutations to cause acute leukemia.

44 ith an increased risk of transformation into acute leukemia.

45 a in a 7-year-old boy with highly-resistant, acute leukemia.

46 challenge by clinical specialists who treat acute leukemia.

47 te lymphoblastic leukemia and MLL-rearranged acute leukemia.

48 timization of 18 may yield a new therapy for acute leukemia.

49 nature of 3D chromatin architecture in human acute leukemia.

50 tic circuitry mediated by KDM4C and PRMT1 in acute leukemia.

51 3K4) and is frequently altered in aggressive acute leukemias.

52 pansion and is commonly deregulated in human acute leukemias.

53 a pivotal target of transcription factors in acute leukemias.

54 kinases and their oncogenic association with acute leukemias.

55 Cell differentiation is compromised in acute leukemias.

56 ute lymphoblastic lymphoma-like biphenotypic acute leukemias.

57 lymphoma, chronic myelogenous leukemia, and acute leukemias.

58 ge leukemia (MLL) gene are a common cause of acute leukemias.

59 These animals subsequently progress to acute leukemias.

60 ost active Ptpn11 mutation found in JMML and acute leukemias.

61 ne (FLAM) is active in adults with poor-risk acute leukemias.

62 se play a causal role in the pathogenesis of acute leukemias.

63 (mixed lineage leukemia) fusion proteins in acute leukemias.

64 ically distinctive and clinically aggressive acute leukemias.

65 d in mixed lineage leukemia (MLL)-rearranged acute leukemias.

66 proteins that are found in aggressive human acute leukemias.

67 transferases and is frequently rearranged in acute leukemias.

68 tion factors are common abnormalities in the acute leukemias.

69 correlated in hematopoietic progenitors and acute leukemias.

70 eneic hematopoietic cell transplantation for acute leukemias.

71 ms, inflammatory myofibroblastic tumors, and acute leukemias.

72 mary leukemic progenitors from patients with acute leukemias.

73 ression of FLT3, an important driver gene in acute leukemias.

74 reclinical models for these as well as other acute leukemias.

75 and has been detected in certain subtypes of acute leukemias.

76 mal developmental programs and implicated in acute leukemias.

77 ell expansion and is commonly deregulated in acute leukemias.

78 ed in a large portion of the human B-lineage acute leukemias.

79 The main underlying diseases were acute leukemia (35.7%), lymphoma (31.7%), and solid tumo

80 hin blood from patients with mixed-phenotype acute leukemia(4,5).

81 age at UCBT was 54 years, and diagnoses were acute leukemias (51%), myelodysplastic syndrome/myelopro

82 th cytogenetic abnormalities only versus MDS/acute leukemia (67% [95% CI, 52% to 81%] v 43% [95% CI,

83 bles associated with GNB were a diagnosis of acute leukemia, a transplant from a HLA-mismatched donor

84 Forty-three adults with high-risk acute leukemia (acute myeloid leukemia 33; acute lymphob

85 ion (IR) is an important form of therapy for acute leukemias administered externally or as radioimmun

86 id leukemia (AML) is the most common type of acute leukemia, affecting older individuals at a median

87 HSCT) is a suitable option for children with acute leukemia (AL) either relapsed or at high-risk of t

88 tory samples occurred more frequently in non-acute leukemia (AL) patients than in AL patients (P = .0

89 Acute leukemia (AL) patients undergoing intensive induct

90 plasms has provided a framework for defining acute leukemia (AL) subtypes, although few population-ba

91 lantation (HSCT) is potentially curative for acute leukemia (AL), but carries considerable risk.

92 ideline on the initial diagnostic work-up of acute leukemia (AL).

93 fibrosis, splenomegaly, or transformation to acute leukemia, albeit at widely varying frequencies.

94 05) of patients who received transplants for acute leukemia, all given a myeloablative conditioning r

95 resent a large clinically homogeneous group (acute leukemia), allowing all degrees of HLA matching.

96 id leukemia (AML) represents the most common acute leukemia among adults.

97 eukemia, representing 75% to 80% of cases of acute leukemia among children.

98 38% (95% CI: -11.9 to -0.9) in patients with acute leukemia and -1.0% (95% CI: -4.5 to 2.5) in patien

99 icafungin 2-3 times weekly) in patients with acute leukemia and allogeneic SCT recipients.

100 the functions of selected deubiquitinases in acute leukemia and efforts to target these enzymes with

101 MLL-AF4 leukemia is the predominant infant acute leukemia and has a poor prognosis.

102 ctive duty service member who presented with acute leukemia and inadvertent autoinoculation after sma

103 BAHCC1 is highly expressed in human acute leukemia and interacts with transcriptional corepr

104 profound immune dysfunction associated with acute leukemia and its treatment.

105 d with a comparison of different subtypes of acute leukemia and normal bone marrow samples.

106 signaling mediators in different subtypes of acute leukemia and propose that inhibition of dysregulat

107 transforms murine pro-B cells, resulting in acute leukemia and providing an experimental model for h

108 ed protein kinase (PKR) has been reported in acute leukemia and solid tumors, but the role of PKR has

109 al capability and development of ITD-Flt3(+) acute leukemia and that antagonizing Survivin may provid

110 2 were recurrent (6.2%) in 241 patients with acute leukemia and were associated with multiple major c

111 (MLL) gene occur in 60% to 80% of all infant acute leukemias and are markers of poor prognosis.

112 s potent, but it is less efficacious against acute leukemias and blast-crisis chronic myelogenous leu

113 ylic acid cycle enzyme mutated in subsets of acute leukemias and gliomas, in cancer.

114 berrantly expressed proto-oncogenes in human acute leukemias and is highly leukemogenic in experiment

115 The MYB oncogene is widely expressed in acute leukemias and is important for the continued proli

116 ncies with a high growth fraction, including acute leukemias and lymphomas, but can be encountered in

117 Other studies reveal that certain acute leukemias and small cell lung cancers, which lack

118 nscription factors are commonly activated in acute leukemias and subvert normal gene expression netwo

119 ted with the MOL4070LTR retrovirus developed acute leukemia, and ligation-mediated polymerase chain r

120 BSI patients were older, had advanced-stage acute leukemia, and received umbilical cord blood (UCB)

121 importance of MDR in cancer, with a focus on acute leukemia, and we highlight the need for rapid accu

122 (MLL) fusion proteins in the development of acute leukemias, and inhibition of the menin interaction

123 eage leukemia (MLL) plays a critical role in acute leukemias, and inhibition of this interaction repr

124 MLL1 translocations are present in acute leukemias, and mutations in several family members

125 recurrent site of genetic rearrangements in acute leukemias; and since its discovery in 1992, many a

126 noparticles (SPION) and directed against the acute leukemia antigen CD34, coupled with a "magnetic ne

127 Acute leukemias are clonal disorders of hematopoiesis wh

128 Chromosomal aberrations of MLL in acute leukemias are well documented, but the role of thi

129 age and quantify, such as ovarian cancer and acute leukemia, are discussed.

130 A number of acute leukemias arise from fusion of the mixed lineage l

131 meters substantially but were complicated by acute leukemia as a result of insertional mutagenesis in

132 myelodysplastic syndrome with progression to acute leukemia associated with acquisition of additional

133 rmation of hematopoietic cells and initiates acute leukemias at various stages of hematopoiesis.

134 emia cells from 54 infants with ALL/bilineal acute leukemia because of the role of prosurvival BCL-2

135 FLAM" in 55 adults with relapsed/refractory acute leukemias began at a total flavopiridol dose of 50

136 lism (VTE) among Californians diagnosed with acute leukemia between 1993 to 1999.

137 ic myeloid leukemia (CP-CML) evolves into an acute leukemia (blast crisis [BC]) that displays either

138 in distinct treatment-resistant subtypes of acute leukemia, but not in normal hematopoietic progenit

139 progression from blood-forming stem cells to acute leukemias by successive genetic and epigenetic eve

140 ion of miR-150, an miRNA widely repressed in acute leukemia, by blocking miR-150 precursors from bein

141 of minimal residual disease in CD34-positive acute leukemias can significantly enhance sensitivity co

142 ally distinct and aggressive subset of human acute leukemia carrying chromosomal translocations of th

143 ew therapeutic strategy for the treatment of acute leukemia carrying MLL fusion (MLL leukemia).

144 ew therapeutic strategy for the treatment of acute leukemia carrying MLL fusion (MLL leukemia).

145 proximately miR-24-2), was down-regulated in acute leukemia cell lines and primary samples compared t

146 nd selectively inhibits cell growth in human acute leukemia cell lines harboring the rearranged mixed

147 Replacement of miR-27a in acute leukemia cell lines inhibited cell growth due, at

148 Decreased miR-23a cluster expression in some acute leukemia cell lines was mediated by c-MYC.

149 ar potencies in inhibition of cell growth in acute leukemia cell lines.

150 strongly inhibit the clonogenic potential of acute leukemia cell lines.

151 proliferation and induced differentiation in acute leukemia cells and primary patient samples with ML

152 Here we show that multiple types of acute leukemia cells have an attenuated mitotic arrest w

153 illing even aggressive, treatment-refractory acute leukemia cells in vivo.

154 tributes a tumor suppressor-like activity in acute leukemia cells via regulation of apoptosis, and th

155 apidly activated in response to treatment of acute leukemia cells with As(2)O(3).

156 Acute leukemia characterized by chromosomal rearrangemen

157 c abnormalities (MDS-CA) and clinical MDS or acute leukemia ("clinical MDS/AL").

158 ariable analysis, including disease-related (acute leukemia, curative intent chemotherapy), laborator

159 nd overexpression of the oncogenes brain and acute leukemia, cytoplasmic (BAALC) and v-ets erythrobla

160 Overexpression of the brain and acute leukemia, cytoplasmic (BAALC) gene is implicated i

161 miR-3151 and the host gene BAALC (brain and acute leukemia, cytoplasmic) concomitantly affect the ou

162 97 AUC) the uric-acid signatures of gout vs. acute leukemia despite not being optimized for the task.

163 In patients with acute leukemia, detection of minimal residual disease (M

164 in the transcription factor CEBPA to promote acute leukemia development.

165 matopoietic stem/progenitor cells and induce acute leukemia development.

166 For chronic disease and acute leukemia diagnosed after the second trimester, the

167 Invariably, acute leukemia diagnosed in the first trimester necessit

168 e leading cause of death among patients with acute leukemia, due to complex disease- and treatment-de

169 ng agents commonly used for the treatment of acute leukemia (e.g., doxorubicin, vincristine, mitoxant

170 ials form the backbone for the management of acute leukemia, emergent clinical situations, predictabl

171 rovide therapeutic benefit for patients with acute leukemia expressing ITD-Flt3.

172 d transcriptional cofactor, megakaryoblastic acute leukemia factor-1 (MKL).

173 in monitoring measurable residual disease in acute leukemias following affinity enrichment of circula

174 tered in vitro growth potentials and induced acute leukemias following transplantation in immunocompr

175 patients with NPM1m who were treated in the Acute Leukemia French Association 0702 (ALFA-0702) trial

176 A review of English literature on childhood acute leukemias from the past 5 years was performed.

177 eports investigating the clonal evolution of acute leukemia genomes and discuss the implications for

178 Acute leukemia genomes commonly harbor submicroscopic ga

179 oloproliferative disorder; multiple myeloma; acute leukemia; giant cell arteritis; dialysis; esophage

180 depletion obstructs A3 T-cell lymphoblastic acute leukemia growth in vitro and in vivo, validating O

181 eraction as a novel therapeutic approach for acute leukemia harboring MLL1 fusion proteins.

182 el therapeutic strategy for the treatment of acute leukemia harboring MLL1 fusion proteins.

183 eafter referred to as TORC1/2), in models of acute leukemia harboring the Philadelphia chromosome (Ph

184 es was applied to hundreds of cells of human acute leukemia harvested from multiple patients at diagn

185 e poor prognosis of this relatively uncommon acute leukemia has led to the rapid adoption of treatmen

186 malities, myelodysplastic syndrome (MDS), or acute leukemia have not been separately analyzed.

187 ock, 7.27 (7.19-7.35); metastatic cancer and acute leukemia (Hierarchical Condition Category 8), 6.76

188 critical roles in chemotherapy responses in acute leukemias; however, the molecular mechanisms remai

189 te myeloid leukemia (AML) is the most common acute leukemia in adults and the second most common freq

190 ical exposure-benzene, a recognized cause of acute leukemia in adults-and raise the question of wheth

191 id leukemia (AML) is the most common form of acute leukemia in adults.

192 id leukemia (AML) is the most common type of acute leukemia in adults.

193 ed critical new insights into the biology of acute leukemia in children.

194 this approach has not been used to re-create acute leukemia in human cells of origin comparable to di

195 Thus, concordance of MLL-rearranged acute leukemia in infant monozygotic twins is not univer

196 Concordance of MLL-rearranged acute leukemia in infant monozygotic twins is thought to

197 egative (dn)-Survivin delayed development of acute leukemia in mice that received a transplant of Ba/

198 enhanced the oncogenicity of HOXB4, inducing acute leukemia in mice.

199 s), against Philadelphia chromosome-positive acute leukemia in murine models, including a leukemia wi

200 Y-specific CTLs prevent engraftment of human acute leukemia in nonobese diabetic/severe combined immu

201 hp2E76K-expressing HSCs yield MPD as well as acute leukemia in recipient animals.

202 l adult stem cell transplant candidates with acute leukemia in remission and MDS.

203 plantation in children and young adults with acute leukemia in remission or myelodysplasia.

204 yeloid leukemia (AML), the most common adult acute leukemia in the United States, has the poorest sur

205 fficiency cooperated with Flt3-ITD to induce acute leukemia in vivo, with potentiated Stat5 signaling

206 n FMS-like tyrosine kinase 3 (FLT3) to drive acute leukemia in vivo.

207 oid leukemia (AML) is one of the most common acute leukemias in adults and children, yet significant

208 sease that accounts for approximately 20% of acute leukemias in children and adolescents.

209 ion proteins (MLL-FPs) that cause aggressive acute leukemias in humans.

210 1 (Ptpn11) have been identified in childhood acute leukemias, in addition to juvenile myelomonocytic

211 Extramedullary (EM) manifestations of acute leukemia include a wide variety of clinically sign

212 Eight patients developed acute leukemias (including four T-cell acute lymphoblast

213 depletion of osteoblasts in mouse models of acute leukemia increased circulating blasts and tumor en

214 ted by t(1;19) chromosomal translocations in acute leukemia into the chimeric E2A-PBX1 oncoprotein.

215 Acute leukemia is a hematopoietic malignancy for which t

216 Acute leukemia is a rapidly progressing blood cancer wit

217 h FA with cytogenetic abnormalities, MDS, or acute leukemia is achievable.

218 The incidence of VTE in acute leukemia is appreciable, and is comparable with th

219 the classification of myeloid neoplasms and acute leukemia is highlighted with the aim of familiariz

220 urvival from first relapse for patients with acute leukemia is only approximately 10%.

221 hildren with JMML, because transformation to acute leukemia is rare.

222 acute lymphoblastic leukemia (T-ALL), or any acute leukemia, is poorly understood.

223 Individually, lamin B1 highlights acute leukemias, lamin A/C helps distinguish normal from

224 s associated with some myeloid neoplasms and acute leukemias, largely derived from gene expression an

225 2 are among the most common driver events in acute leukemia, leading to increased cell proliferation

226 d potent cell killing that was selective for acute leukemia lines bearing MLL translocations.

227 ograft models of SJSA-1 osteosarcoma, RS4;11 acute leukemia, LNCaP prostate cancer, and HCT-116 colon

228 nsgene, NRAS(G12V) expression contributes to acute leukemia maintenance by suppressing apoptosis and

229 The murine acute leukemia model C1498 was used to study the efficac

230 Mixed-phenotype acute leukemia (MPAL) encompasses a heterogeneous group

231 The features of 100 mixed-phenotype acute leukemias (MPALs), fulfilling WHO 2008 criteria, a

232 patients undergoing a first MAC allo-SCT for acute leukemia, myelodysplastic syndrome, or myeloprolif

233 terations define subclasses of patients with acute leukemias, myelodysplastic syndromes (MDS), myelop

234 tic abnormalities (n = 54), MDS (n = 45), or acute leukemia (n = 14) who were reported to the Center

235 d study, 90 patients with recently diagnosed acute leukemia (n = 36) or patients with malignant hemop

236 c malignancies (n = 1,700; 82.4%), including acute leukemia (n = 591; 28.7%), non-Hodgkin lymphoma (n

237 The main underlying malignancies were acute leukemia (n = 65, 48.5%), lymphoma (n = 49, 36.6%)

238 cancers including myelodysplastic syndromes, acute leukemia, non-Hodgkin lymphomas such as chronic ly

239 expression is a hallmark of most aggressive acute leukemias, notably those with KMT2A (MLL) gene rea

240 rom KRAS(G12D) or NRAS(G12D), does not cause acute leukemia on its own, and leukemia virus insertion

241 agnostic test, especially in cancers such as acute leukemia or diffuse large B-cell lymphoma that req

242 rimary vs secondary, progression of disease [acute leukemia or higher risk MDS] vs absence of hematol

243 ients (N = 7128) who underwent first HCT for acute leukemia or myelodysplastic syndrome from 2008 thr

244 fty-four patients 18 to 65 years of age with acute leukemia or myelodysplastic syndrome who underwent

245 nors of 379 HCTs performed at our center for acute leukemia or myelodysplastic syndrome.

246 ed outcomes in 582 consecutive patients with acute leukemia or the myelodysplastic syndrome who recei

247 e model of the one twenty-two-megakaryocytic acute leukemia (OTT-MAL) fusion oncogene that results fr

248 Acute leukemia patients (n = 177; 88 with acute lymphobl

249 ociated with an adverse prognosis in de novo acute leukemia patients after allo-SCT despite the imple

250 galovirus (CMV) serostatus in 16,628 de novo acute leukemia patients after allogeneic stem cell trans

251 an enhanced graft-versus-leukemia effect in acute leukemia patients after transplantation with 2 par

252 ase 1 clinical trials in relapsed refractory acute leukemia patients and is administered as a continu

253 rculating innate lymphoid cells (ILCs) in 51 acute leukemia patients.

254 sitory, we demonstrate that large studies of acute leukemia PDXs that mimic human randomized clinical

255 emia, SM-MDS, and systemic mastocytosis with-acute leukemia, rather than their broad reference as SM-

256 s exemplified with analyses from the Swedish Acute Leukemia Registry containing more than 3300 acute

257 currently the standard curative treatment of acute leukemia, relapse remains unacceptably high.

258 atment resistance remains a leading cause of acute leukemia-related deaths.

259 Mixed lineage leukemia (MLL) fusion-driven acute leukemias represent a genetically distinct subset

260 mixed lineage leukemia gene (MLL) result in acute leukemias resistant to therapy.

261 n Wnt pathway activation and asparaginase in acute leukemias resistant to this enzyme.

262 r chromosomal translocations associated with acute leukemia resulting in its fusion with a large vari

263 Sequencing translocation junctions in acute leukemias revealed that the translocations were li

264 oliferative neoplasm, but not progression to acute leukemia, suggesting that additional cooperating e

265 een linked to favorable clinical outcomes in acute leukemias, suggesting that RUNX1 may also play cri

266 8 to 45 years at diagnosis and had lymphoma, acute leukemia, testicular cancer, ovarian cancer, or fe

267 tified mutations in MPN patients who develop acute leukemia, the complement of genetic abnormalities

268 LL) family proteins has been associated with acute leukemia, the role of hSETD1A in cancer remains un

269 o form different chimeric fusion proteins in acute leukemia, the underlying molecular mechanisms and

270 lactate dehydrogenase level or stage IV) or acute leukemia to compare the addition of six doses of r

271 d from the peripheral blood of patients with acute leukemia undergoing therapy (n = 11).

272 ients with smoldering, chronic, lymphoma and acute leukemia using Affymetrix HG-U133A2.0 arrays.

273 In every case, progression to acute leukemia was defined by the persistence of an ante

274 ntaneous progression from chronic disease to acute leukemia was not observed.

275 9% in early PMF, but no transformation into acute leukemia was observed.

276 cation of lymphoid and myeloid neoplasms and acute leukemia was released in 2016.

277 In our studies of mouse models of acute leukemia, we used high-resolution microscopy and f

278 ighteen patients with relapsed or refractory acute leukemia were enrolled in the SELHEM (Selinexor Wi

279 Eight cases of acute leukemia were reported: seven in the groups receiv

280 rgone stem-cell transplantation for relapsed acute leukemia were treated with the genetically modifie

281 support double UCB unit transplantation for acute leukemia when an adequately dosed single UCB unit

282 61Y produces MPD in vivo but fails to induce acute leukemia, whereas somatic Shp2E76K produces MPD in

283 feasible option for patients with high-risk acute leukemia who do not have matched donors.

284 e of dUCB-TCF transplantation in adults with acute leukemia who may benefit from RIC transplantation

285 Included are adults with acute leukemia who received transplants with 1 (n =106)

286 s to the categories of myeloid neoplasms and acute leukemia will be published in a monograph in 2016

287 Mll(PTD/WT):Flt3(ITD/WT) mice developed acute leukemia with 100% penetrance, at a median of 49 w

288 into a Dnmt3a-deficient background produced acute leukemia with a short latency (median survival, 67

289 DOT1L has been found to be a drug target for acute leukemia with mixed lineage leukemia (MLL) gene tr

290 DOT1L has been found to be a drug target for acute leukemia with MLL (mixed lineage leukemia) gene tr

291 Acute leukemias with adverse prognostic features carry a

292 The successful treatment of acute leukemias with allogeneic hematopoietic cell trans

293 ion proteins that plays an important role in acute leukemias with MLL translocations.

294 gene define a genetically distinct subset of acute leukemias with poor prognosis.

295 e leukemia 1 (MLL1) plays a critical role in acute leukemias with translocations of the MLL1 gene or

296 ers, is a critical issue in the treatment of acute leukemia, with permeability glycoprotein (P-gp), m

297 ybrid FLAM" is active in relapsed/refractory acute leukemias, with a recommended "hybrid" dose of bol

298 spective registry study was performed by the Acute Leukemia Working Party of EBMT.

299 Using the registry data of the Acute Leukemia Working Party of the European Society for

300 ative conditioning regimen for patients with acute leukemia would result in a significant reduction i