ライフサイエンスコーパス: blast cell

1 roduces a column of segmental founder cells (blast cells).

2 in part from one 'o' blast cell and one 'p' blast cell.

3 aracteristics of its sister cell, the hyp7/T blast cell.

4 P pattern elements arises from a single 'op' blast cell.

5 ogenitor infant acute lymphoblastic leukemia blast cells.

6 ) as the only cytogenetic abnormality in the blast cells.

7 ccumulation of increased numbers of leukemia blast cells.

8 eres, pro-teloblasts, teloblasts and primary blast cells.

9 he teloblasts are actively producing primary blast cells.

10 ene expression patterns in purified leukemic blast cells.

11 ith morphologic features of undifferentiated blast cells.

12 ty between the alternating nf and ns primary blast cells.

13 d a concomitant increase in peripheral blood blast cells.

14 had cytopenias, and 12.0% presented >/=5% BM blast cells.

15 in biochemically arrested nf and ns primary blast cells.

16 cessary for proper division of postembryonic blast cells.

17 ogy and prominent erythrophagocytosis by the blast cells.

18 G 330 targets CD33 on acute myeloid leukemia blast cells.

19 leucoerythroblastic picture without obvious blast cells.

20 AML cell lines and patient-derived leukemic blast cells.

21 iferation of primary acute myeloid leukaemia blast cells.

22 tic target for enhancing chemosensitivity in blast cells.

23 gher levels in the ns blast cells than in nf blast cells.

24 l of normal myeloid progenitors and leukemic blast cells.

25 accumulation of noncirculating hematopoietic blast cells.

26 well as on CD34(+)CD133(+) myeloid leukemic blast cells.

27 , BL-CFCs) and their differentiated progeny, Blast cells.

28 ete white blood cell count of 17000/muL (31% blast cells), a platelet count of 76000/muL, and a hemog

29 n, and were less likely to have hyperdiploid blast cells, a favorable prognostic factor in childhood

30 ralmost, primary neurogenic (N) lineage, the blast cells adopt two different fates, designated nf and

31 l-2-AS decreased Bcl-2 expression in CD34(+) blast cells after induction of apoptosis and enhancement

32 e in vitro differentiation of normal CD34(+) blast cells along the myeloid lineage.

33 peat of ectoderm arises in part from one 'o' blast cell and one 'p' blast cell.

34 ntly higher subclonal complexity compared to blast cells and contained a large number of aging-relate

35 smears demonstrated the presence of myeloid blast cells and differentiated but immature cells of bot

36 erapeutic strategy to synergistically target blast cells and drug-insensitive LSCs in patients, offer

37 with TKIs effectively targets both BCR-ABL+ blast cells and drug-insensitive LSCs, conferring a sign

38 ow-level expression of the gene in leukaemic blast cells and granulocytes does not associate with inc

39 stitutively expressed in more mature myeloid blast cells and level markedly increased with terminal m

40 eptor was greatest in fresh myeloid leukemia blast cells and myeloid leukemia cell lines.

41 s suppressed colony growth of autologous CML blast cells and myeloid progenitor cells.

42 priate deaths of many of the Pn.p hypodermal blast cells and prevent the surviving Pn.p cells from ex

43 smear revealed anemia, thrombocytopenia, and blast cells, and a diagnosis of acute myeloid leukemia w

44 e is expressed in the teloblasts and primary blast cells, and that these transcripts appear to be ass

45 n site, the very low transgene expression in blast cells, and the lack of an effect on expression of

46 d lineage, the proliferative capacity of the blast cells, and the marked asymmetry of the blast cell

47 s restricted to the dorsolateral column of p blast cells, and thus correlates with P cell fate over m

48 le deficiency, myelodysplasia with excess of blast cells, and various developmental aberrations, we i

49 royed the in vivo clonogenic fraction of ALL blast cells, and, at nontoxic dose levels, exhibited pot

50 cells, the granddaughters of the primary op blast cell are categorized into two O-type cells and two

51 robusta, pairs of adjacent 'o/p' ectodermal blast cells are known to be developmentally equipotent a

52 These two blast cells are positionally specified to distinct O and

53 symmetric divisions of the primary nf and ns blast cells are regulated by the polarized distribution

54 induces dramatic differentiation of leukemia blast cells as shown by cellular morphology and cell sur

55 Blast cells associated with TL in DS infants exhibited F

56 status) or a traumatic lumbar puncture with blast cells at diagnosis and a high level of minimal res

57 elegans larvae, including the male-specific blast cell, B, that divides asymmetrically to generate a

58 f cell fate transformations in two posterior blast cells, B and F.

59 ggest that IoNanos is involved in regulating blast cell behaviors in the 4d lineage.

60 ession of Hau-Six1/2A in the ventrolateral o blast cells by injection of an expression plasmid elicit

61 technique, we prevented the birth of primary blast cells by injection of DNase I into the teloblast,

62 that Hau-Six1/2A expression is induced in p blast cells by the interaction with the adjoining q band

63 the absence of significant BM dysplasia and blast cells can be difficult to address in FA patients,

64 Some DPhi c-kit blast cells can be salvaged to produce mature single-pos

65 Furthermore, TH1579 killed primary human AML blast cells (CD45(+)) as well as chemotherapy resistance

66 st cell laser ablations to isolate a primary blast cell clone by removal of both its anterior and its

67 t require the presence of the rest of the op blast cell clone for their normal development.

68 Each mesodermal blast cell clone goes through multiple phases of Hau-Pax

69 ntal repeat in the leech embryo, the primary blast cell clone, can develop normally in the apparent a

70 of normal segmental organization within the blast cell clone.

71 ned the mechanism by which the leech primary blast cell clones acquire segment polarity - i.e. a fixe

72 r potential interactions between neighboring blast cell clones along the anterior-posterior axis.

73 r-posterior axis between neighboring primary blast cell clones are not required for development of no

74 m, we ablated single cells from both o and p blast cell clones at stages when the clone was two to fo

75 The nf and ns blast cell clones exhibit strikingly different cell divi

76 Hau-Pax3/7A expression causes the mesodermal blast cell clones to undergo irregular patterns of morph

77 morpholino oligomer (AS MO), to label single blast cell clones.

78 ther more anterior or more posterior primary blast cell clones.

79 s that cki-1 is developmentally regulated in blast cells coincident with G1, and in differentiating c

80 dentify comparable progenitors that can form blast cell colonies (displaying haematopoietic and vascu

81 Blast cell colonies contain higher numbers and a broader

82 e previously described hemangioblast-derived blast cell colonies in that they typically lacked Brachy

83 in populations that contain BL-CFCs, and in blast cell colonies, the progeny of the BL-CFCs.

84 SIRT1(-/-) ESCs formed fewer mature blast cell colonies.

85 ression of Numb in the hemangioblast-derived blast cell colonies.

86 In fact, on replating, the blast-cell colonies cultured from the Rho-dull populatio

87 Furthermore, while the same numbers of blast-cell colonies were detected in culture of Rho-brig

88 with IL-3 alone or in combination with SCF, blast-cell colonies were generated in cultures of Rho-du

89 ents a stage of development earlier than the blast cell colony and one that uniquely defines the requ

90 this study, a primitive progenitor cell, the blast-cell colony-forming cell (BC-CFC), which is though

91 d nf and ns, in exact alternation within the blast cell column; this is termed a grandparental stem c

92 y of Bruton's tyrosine-kinase (BTK) in their blast cells compared with normal haemopoietic cells, ren

93 long-term repopulating LSCs and infiltrating blast cells, conferring a survival advantage in preclini

94 is of peripheral-blood samples revealed that blast cells contained a BB305 lentiviral vector insertio

95 alternate segmental founder cells (nf and ns blast cells) contribute distinct sets of progeny to the

96 patient each: myalgia (one [2%]), increased blast cell count (one [2%]), and general physical health

97 und in 10 RAEB, 12 AML cases with low marrow blast cell count, and 25 other AML cases.

98 RAEB) patients, 29 AML cases with low marrow blast cell count, and 325 other AML patients and determi

99 ver to imatinib]; imatinib group, n=1 [1%]), blast cell crisis (nilotinib group, n=1 [1%]; imatinib g

100 teloblast gives rise to a column of primary blast cell daughters, and the blast cells generate desce

101 In leukemic cells, the CD34+ blast cells demonstrated significantly greater conversio

102 ifferentiation and growth inhibition of NB-4 blast cells, demonstrating that its function is required

103 we used a similar approach to determine f in blast cells derived from 19 individuals with acute lymph

104 es were observed, together with induction of blast cell differentiation, in particular, in patients w

105 t to the inability to regulate the extent of blast cell division in lin-23 mutants, the timing of ini

106 rturbed the normal patterns of teloblast and blast cell divisions and disrupted gangliogenesis.

107 blast cells, and the marked asymmetry of the blast cell divisions.

108 ntamination of CSF with circulating leukemic blast cells during diagnostic lumbar puncture can advers

109 ML-DS blast cells ex vivo have increased sensitivity to cytara

110 Transcriptome profiles of the blast cells exhibited significant inter-patient heteroge

111 the normal percentage and suppress leukemic blast cell expansion.

112 The latter blast cell expansions occurred over a 3- to 6-week perio

113 patients with acute myeloid leukaemia whose blast cells express CD117 should be considered for forth

114 Leukemic blast cells express the CD33 antigen in most patients wi

115 Blast cells expressed gene signatures characteristic of

116 nalysis identified an enriched population of blast cells expressing ICAM1/lymphocyte function associa

117 Even though blast cell expression of myeloid-associated antigen expr

118 Blast cell expression of the NG2 molecule was strongly a

119 Mesenchymal and thymic blast cell expression patterns of LMO4 and LMO2 are cons

120 ry and sufficient to promote a proliferating blast cell fate, the sex myoblast fate, over a different

121 Inhibition occurred at the level of blast-cell formation through a mechanism or mechanisms i

122 cells were identified within the lymphocyte/blast-cell fraction in 58 (94%) of these specimens.

123 lecule NG2, was used to screen prospectively blast cells from 104 consecutive children at initial pre

124 We studied blast cells from 21 acute leukemia patients (20 acute my

125 We obtained acute myeloid leukaemia blast cells from 29 patients.

126 Activation of C/EBPalpha in blast cells from 4 patients with CML-BC, including one r

127 ic finding was absence of myeloperoxidase in blast cells from 5 patients.

128 age, but was increased up to 90% of total in blast cells from a significant proportion of patients wi

129 33 is expressed on acute myelocytic leukemic blast cells from about 90% of patients, normal hematopoi

130 We isolated primary acute myeloid leukaemia blast cells from heparinised blood and human peripheral

131 ral infection or interferon treatment and in blast cells from patients with acute promyelocytic leuke

132 se observations in model systems, we studied blast cells from patients with Philadelphia chromosome-p

133 ble-negative T cells (DNTs) effectively kill blast cells from the majority of AML patients and are no

134 We obtained acute myeloid leukaemia blast cells from unselected patients attending our UK ho

135 umn of primary blast cell daughters, and the blast cells generate descendant clones that serve as the

136 TC) through 3 serial culture rounds-that is, blast cells generated in unicellular ELTC were reseeded

137 Each blast cell generates a lineage-specific clone via a ster

138 rocess and the degree of incongruity between blast cell genotype and phenotype in different clinical

139 GFL7 in vitro leads to increases in leukemic blast cell growth and levels of phosphorylated AKT.

140 nts with bone marrow disease with peripheral blast cells) had lymphopenia, and 178 (48%) of 368 had h

141 Our data suggest that hES-derived blast cells (hES-BCs) could be important in vascular rep

142 -3 counterparts in other organisms determine blast cell identity and for this reason may lead to cell

143 d for subgroups defined by treatment era and blast-cell immunophenotype.

144 rable efficacy to standard therapies against blast cells in 63 primary leukemias.

145 molecular and morphologic differentiation of blast cells in acute myeloid leukemia (AML) patients har

146 ith the discovery of drug-resistant leukemic blast cells in AML patients, have made resistance to FLT

147 or more leukocytes/microL with identifiable blast cells in an atraumatic sample or the presence of c

148 ) cells were frequently observed in leukemic blast cells in both pretherapy and relapsed samples, con

149 The 64 patients (39%) who had 1 or more blast cells in cytocentrifuged preparations of cerebrosp

150 Residual blast cells in MRD+ EOI samples exhibited significant up

151 pS6), and Stat5 (pStat5) in CD34(+)/CD117(+) blast cells in normal bone marrow from 9 healthy adult d

152 er, the discovery of drug-resistant leukemic blast cells in PKC412-treated patients with AML has prom

153 the accumulation of primitive hematopoietic blast cells in the blood and bone marrow.

154 Isolated del(5q) and less than 5% of blast cells in the bone marrow were the most relevant la

155 G6 significantly decreased the percentage of blast cells in the peripheral blood, reduced splenomegal

156 ce and highly effectively depleted the T-ALL blast cells in the peripheral blood, spleen, liver, bone

157 s is the case for of a pair of postembryonic blast cells in the tail.

158 ug resistance, determined either on leukemic blast cells in vitro or by studies of MRD, is being look

159 e proteins in KCL22 chronic myeloid leukemia blast cells including Cbl, Bcr-Abl, Erk1/2, and CrkL.

160 and effectively target BM-resident malignant blast cells, including CD33-low/negative leukemia stem a

161 TET2 deficiency in AML blast cells increases expression of Tetraspanin 13 (TSPA

162 nted with a pro-B phenotype ALL and moderate blast cell infiltration.

163 ith Alox5 overexpression in MLL-AF9-leukemic blast cells; inhibition of the above signaling pathways

164 the hierarchical differentiation of immature blast cells into mature, functional cell types and linea

165 nd phenotypic heterogeneity between leukemic blast cells is a well-recognized phenomenon, there remai

166 s, the timing of initial cell cycle entry of blast cells is not affected.

167 tivity of mebendazole using primary leukemia blast cells isolated from human acute myeloid leukemia (

168 alue of cytogenetics in childhood T-ALL, the blast cell karyotypes of 343 cases of pediatric T-ALL, t

169 vival differences associated with some T-ALL blast cell karyotypes.

170 in massive mitotic DNA re-replication in the blast cells, largely due to failed degradation of the DN

171 Using double blast cell laser ablations to isolate a primary blast ce

172 hat may result from infiltration of leukemic blast cells (LBCs) into lung parenchyma and interstitium

173 specifically localized in the mesendodermal blast cell lineage derived from the strongly conserved 4

174 During animal development, blast cell lineages are generated by repeated divisions

175 enzyme switched off in normal diploid fibro-blasts-cells lose telomeric DNA at each cell division.

176 ng the early lineages; in contrast, a single blast cell (M) is responsible for all nongonadal mesoder

177 portance of TET2 in leukemogenesis, leukemic blast cell migration/homing, and LSC self-renewal as an

178 After marked decrease of AML blast cells, myeloproliferative disease (MPD)-like AML r

179 EBPdelta, myeloid differentiation of the CML blast cells occurred as shown by morphologic changes and

180 le neutrophilic differentiation of the KCL22 blast cells occurred as shown by morphologic changes, in

181 Sphingosine kinase activity in the CD34+ blast cells of 3 patients with acute myeloid leukemia wa

182 d and partially purified telomerase from the blast cells of a patient with acute myelogenous leukemia

183 yte colony-stimulating factor (G-CSF) in the blast cells of two out of 555 AML patients examined.

184 emi-ganglia, while ablation of an ns primary blast cell often caused a 'slippage' of blast cells post

185 h both LMO2 and LMO4 are activated in thymic blast cells, only LMO4 is expressed in mature T cells.

186 cytosis and a high percentage of bone marrow blast cells (P <.001 for both).

187 iferation of primary acute myeloid leukaemia blast cells (p=0.028).

188 ted with childhood AML with a differentiated blast cell phenotype and the presence of a del(5q).

189 -CSF were similar to each other with half of blast cells phosphorylating Stat5 and 15% to 20% respond

190 e count, sex, era of treatment, and leukemia blast cell ploidy, we found that AA children had a 42% e

191 tations, maintaining a rapidly proliferating blast cell population with fatal consequences for the pa

192 l blood (PB), cord blood (CB), and adult AML blast cell populations.

193 mary blast cell often caused a 'slippage' of blast cells posterior to the lesion.

194 to the teloblast, thereby depriving the last blast cell produced before the ablation of its normal po

195 n of zygotic transcription restricted to the blast cell progeny of the mesodermal M teloblasts.

196 ments in which we specifically ablated those blast cell progeny that are known to express the engrail

197 g that PTEN acts non-autonomously to control blast cell quiescence may be relevant to its function as

198 We also examined the possibility that blast cells receive redundant signals from both anterior

199 show rapid and significant peripheral blood blast cell reduction, however a marginal decrease in bon

200 ults show that the asymmetric divisions of n blast cells result from a posterior shift of both the sp

201 In this study, blast cell samples from relapsed AML patients eligible f

202 eages, the earliest divisions of the primary blast cell segregate anterior and posterior cell fates a

203 , we show that the decision of somatic gonad blast cells (SGBs) and germline stem cells (GSCs) to be

204 extensive DNA rereplication in postembryonic BLAST cells, similar to what is observed in cul-4(RNAi)

205 ze by different proportions, with hypodermal blast cell size most closely proportional to body size.

206 Specifically, ablation of an nf primary blast cell sometimes resulted in the fusion of ipsilater

207 ignificantly reduced white blood cell count, blast cells, splenomegaly, lactate dehydrogenase levels,

208 Blast cell structure and immunophenotype are similar in

209 Thus, blast cell surface expression of NG2 is useful for ident

210 myeloid leukemia plays an important role in blast cell survival and resistance to chemotherapy.

211 yrosine kinase (SYK)-dependent antiapoptotic blast cell survival machinery with a unique nanoscale ph

212 A thymic blast cell system was developed and used to demonstrate

213 induced apoptosis in primary B-precursor ALL blast cells taken directly from patients as well as in v

214 hich is expressed at higher levels in the ns blast cells than in nf blast cells.

215 d to maintain the developmental potential of blast cells that are generated in the embryo but divide

216 e of myeloid differentiation, similar to the blast cells that are the hallmark of human acute myeloid

217 he o and p bandlets, two parallel columns of blast cells that collectively constitute the O/P equival

218 es, but readily killed MHC class-I-deficient blast cells that express only low levels of Clr-b.

219 enerate through aberrant differentiation the blast cells that make up the bulk of the malignant clone

220 The other patient had a relapse, with blast cells that no longer expressed CD19, approximately

221 The rare DPhic-Kit- blast cells that thus are salvaged for positive selectio

222 The majority of cases (91%) had blasts cells that simultaneously expressed either T-line

223 ves rise to segmental founder cells (primary blast cells) that contribute iterated sets of definitive

224 ins of segment founder cells (called primary blast cells) that divide in a stereotypical manner to pr

225 Upon treatment of primary AML patient blast cells, the dual inhibition of FLT3 and c-KIT was s

226 imens often ablate actively cycling leukemic blast cells, the primitive LSC population is likely to b

227 ge is necessary and sufficient to induce o/p blast cells to assume the P fate.

228 CD117-mediated adhesion of CD117-expressing blast cells to bone-marrow stromal cells was significant

229 In primary human AML, exposure of fresh blast cells to daunorubicin activated the stress-respons

230 sult from the inability of the postembryonic blast cells to escape G(1) cell cycle arrest.

231 erized by the accumulation of clonal myeloid blast cells unable to differentiate into mature leukocyt

232 In lin-23 null mutants, all postembryonic blast cells undergo extra divisions, creating supernumer

233 Ks within 3 weeks or expansion to 200-10,000 blast cells, up to 25% of which expressed CD34.

234 n primary chronic lymphocytic leukemia (CLL) blasts; cell viability effects in diffuse large B-cell l

235 molecules of chronic myeloid leukemia (CML) blast cells was performed to characterize the antigen pr

236 ospinal fluid (CSF) sample contaminated with blast cells was worse than that for patients with no con

237 cs in the asymmetric divisions of individual blast cells, we have injected teloblasts with mRNA encod

238 terior neuroblast daughter of the ABpl/rpppa blast cell were frequently duplicated, while non-neurona

239 Relapse blast cells were shown to express the common ALL antigen

240 Blast cells were tested for ETV6 and MLL rearrangement u

241 mia (with CD22 expression on at least 70% of blast cells) were enrolled at six centres in France.

242 andlets) of segmental founder cells (primary blast cells), which in turn generate segmentally iterate

243 ts in the accumulation of CALR(low) leukemic blast cells, which are now protected against phagocytosi

244 ansitions in the temporal fates of epidermal blast cells, which are programmed by genes in the hetero

245 etric cell fates in the descendants of the T blast cell, whose polarity is controlled by Wnt signalin

246 he fates of the descendants of the TL and TR blast cells, whose polarity is regulated by lin-44/Wnt a

247 We also ablated single blast cells with a laser microbeam, which allowed us to

248 This enabled categorization into leukemic blast cells with MDR activity (MDR(+)) and leukemic blas

249 that is comprised of primitive hematopoietic blast cells with ongoing, mainly myeloid, differentiatio

250 ia (AML) is a malignancy of immature myeloid blast cells with stem-like and chemoresistant cells bein

251 logies were observed: expansion of up to 200 blast cells with subsequent differentiation to large ref

252 dly effective against a panel of primary AML blast cells, with low nanomolar IC(50)s and, based on co

253 stembryonic development of the male-specific blast cells within the hindgut, the hindgut morphology i

254 Individual blast cells within this equivalence group become committ

255 anglionic precursor cells (nf and ns primary blast cells) within the N lineage.

256 ells with MDR activity (MDR(+)) and leukemic blast cells without MDR activity (MDR(-ve)).