ライフサイエンスコーパス: acute leukemia

1 challenge by clinical specialists who treat acute leukemia.

2 r radioiodine treatment, with progression to acute leukemia.

3 Differentiation arrest is a hallmark of acute leukemia.

4 oncogenes that initiate aggressive forms of acute leukemia.

5 sion to myelofibrosis, and transformation to acute leukemia.

6 nvestigate clonal diversity and evolution in acute leukemia.

7 ed in human myeloproliferative neoplasms and acute leukemia.

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

9 bone marrow dysplasia, and transformation to acute leukemia.

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

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

12 of cytopenia and risk of transformation into acute leukemia.

13 ell differentiation as well as initiation of acute leukemia.

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

15 Oncogenic gene translocations occur in acute leukemia.

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

17 ng a type of rhabdomyosarcoma that resembles acute leukemia.

18 al of lenalidomide in relapsed or refractory acute leukemia.

19 n chromosomal translocations associated with acute leukemia.

20 platelet dysfunction, and predisposition to acute leukemia.

21 ent of other molecularly defined subtypes of acute leukemia.

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

23 transplantation is potentially curative for acute leukemia.

24 F alterations are frequently associated with acute leukemia.

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

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

27 ions, and chromosome translocations in human acute leukemia.

28 gene requires cooperating mutations to cause acute leukemia.

29 events appear to be required to progress to acute leukemia.

30 ained so: GSTM1 null with bladder cancer and acute leukemia.

31 e in DNA damage and a risk of progression to acute leukemia.

32 clinical and clinical activity against human acute leukemia.

33 rate with NHD13 as the MDS transformed to an acute leukemia.

34 ia, and about two thirds progress to a fatal acute leukemia.

35 er in melanoma than in other solid tumors or acute leukemia.

36 r of Hox gene expression in the induction of acute leukemia.

37 leukostasis, a complication associated with acute leukemia.

38 l role for CDX4 expression in the genesis of acute leukemia.

39 y disrupted by chromosomal translocations in acute leukemia.

40 ivity in CML-BC and, perhaps, other types of acute leukemia.

41 h Down's syndrome have a much higher risk of acute leukemia.

42 crease the risk of vascular complications in acute leukemia.

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

44 haploidentical hematopoietic transplants for acute leukemia.

45 te lymphoblastic leukemia and MLL-rearranged acute leukemia.

46 icantly elevated risk of developing an overt acute leukemia.

47 XA9 expression is frequently associated with acute leukemia.

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

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

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

51 nslocations or partial tandem duplication in acute leukemia.

52 an increasing incidence among patients with acute leukemia.

53 erience with PM exclusively in patients with acute leukemia.

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

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

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

57 kinases and their oncogenic association with acute leukemias.

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

59 Cell differentiation is compromised in acute leukemias.

60 ute lymphoblastic lymphoma-like biphenotypic acute leukemias.

61 lymphoma, chronic myelogenous leukemia, and acute leukemias.

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

63 These animals subsequently progress to acute leukemias.

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

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

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

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

68 ically distinctive and clinically aggressive acute leukemias.

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

70 proteins that are found in aggressive human acute leukemias.

71 transferases and is frequently rearranged in acute leukemias.

72 tion factors are common abnormalities in the acute leukemias.

73 correlated in hematopoietic progenitors and acute leukemias.

74 mary leukemic progenitors from patients with acute leukemias.

75 mal developmental programs and implicated in acute leukemias.

76 ell expansion and is commonly deregulated in acute leukemias.

77 in the regulation of expression of miRNAs in acute leukemias.

78 rexpressed at the mRNA and protein levels in acute leukemias.

79 n impressive response rates in patients with acute leukemias.

80 cyclophosphamide for patients with relapsed acute leukemias.

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

82 3K4) and is frequently altered in aggressive acute leukemias.

83 pansion and is commonly deregulated in human acute leukemias.

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

85 a pivotal target of transcription factors in acute leukemias.

86 elerated the degradation of Tal1/SCL (T cell acute leukemia 1/stem cell leukemia) protein, a basic he

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

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

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

90 ers of 158 children with Down's syndrome and acute leukemia (97 acute lymphoblastic leukemia, 61 acut

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

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

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

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

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

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

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

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

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

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

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

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

103 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

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

105 gene rearrangements that are associated with acute leukemia and discuss molecular pathways leading to

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

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

108 o play a central role in the pathogenesis of acute leukemia and likely contribute to both disease ini

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

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

111 sful rational approaches to the treatment of acute leukemia and provide the promise of improved treat

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

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

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

115 2 were recurrent (6.2%) in 241 patients with acute leukemia and were associated with multiple major c

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

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

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

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

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

121 have suggested the utility of clofarabine in acute leukemias and nelarabine in T-cell diseases.

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

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

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

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

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

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

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

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

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

131 The acute leukemias are a heterogeneous and relatively uncom

132 Acute leukemias are clonal disorders of hematopoiesis wh

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

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

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

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

137 to 50% of the F(1) generation mice developed acute leukemia at a median age of 12 months.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 ipts from many cancer cell lines and primary acute leukemia cells that contain aberrant splicing at t

156 ELEX strategy in our laboratory for CCRF-CEM acute leukemia cells that, when applied in this method,

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

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

159 Acute leukemia characterized by chromosomal rearrangemen

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

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

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

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

164 97 AUC) the uric-acid signatures of gout vs. acute leukemia despite not being optimized for the task.

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

166 Acute leukemia developed in three additional patients af

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

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

169 Invariably, acute leukemia diagnosed in the first trimester necessit

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

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

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

173 th mixed-lineage leukemia (MLL) in childhood acute leukemia, encodes a putative transcriptional activ

174 on chromosomal abnormalities associated with acute leukemia, especially infant and therapy-related le

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

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

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

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

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

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

181 Acute leukemia genomes commonly harbor submicroscopic ga

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

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

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

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

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

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

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

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

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

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

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

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

194 te myeloid leukemia (AML) is the most common acute leukemia in adults.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 1 (Ptpn11) have been identified in childhood acute leukemias, in addition to juvenile myelomonocytic

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

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

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

216 Acute leukemia is a hematopoietic malignancy for which t

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

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

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

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

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

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

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

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

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

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

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

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

235 nd in tissue bank samples from children with acute leukemia not treated with temozolomide (MGMT, n =

236 coexpression of AML1-D171N and Evi1 induced acute leukemia of the same phenotype with much shorter l

237 cted serious adverse events in patients with acute leukemia on chemotherapy far exceed those in patie

238 in transplantation outcome for patients with acute leukemia or MDS, as it does in thalassemia.

239 association was restricted to patients with acute leukemia or myelodysplastic syndrome (MDS); in the

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

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

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

243 -1.77; P = 4.9 x 10(-8)), and GSTM1 null and acute leukemia (OR, 1.20; 95% CI, 1.14-1.25; P = 8.6 x 1

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

245 c lymphoid leukemias, plasma cell neoplasms, acute leukemia, paroxysmal nocturnal hemoglobinuria, mas

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

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

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

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

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

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

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

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

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

255 approval of new agents for the treatment of acute leukemia, regular and accelerated approval.

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

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

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

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

260 ther through large-scale real-time PCR on 98 acute leukemia samples covering most of the common cytog

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

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

263 evelopment of therapy-related myelodysplasia/acute leukemia (t-MDS/AML) among patients with WM treate

264 8 to 45 years at diagnosis and had lymphoma, acute leukemia, testicular cancer, ovarian cancer, or fe

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

266 he choice of end points for drug approval in acute leukemia, the Food and Drug Administration invited

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

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

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

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

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

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

273 No sign of acute leukemia was observed over the lifetime of these m

274 9% in early PMF, but no transformation into acute leukemia was observed.

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

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

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

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

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

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

281 61Y produces MPD in vivo but fails to induce acute leukemia, whereas somatic Shp2E76K produces MPD in

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

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

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

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

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

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

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

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

290 Acute leukemias with adverse prognostic features carry a

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

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

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

294 nt chromosome translocations associated with acute leukemias with poor prognosis.

295 orm into a myelodysplastic syndrome (MDS) or acute leukemia, with a cumulative rate of transformation

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 og that shows promise in adult and pediatric acute leukemias without untoward toxicity.

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

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