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 d a concomitant increase in peripheral blood blast cells.

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

7 he teloblasts are actively producing primary blast cells.

8 ith morphologic features of undifferentiated blast cells.

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

10 iferation of primary acute myeloid leukaemia blast cells.

11 tic target for enhancing chemosensitivity in blast cells.

12 in biochemically arrested nf and ns primary blast cells.

13 cessary for proper division of postembryonic blast cells.

14 ogy and prominent erythrophagocytosis by the blast cells.

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

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

17 l of normal myeloid progenitors and leukemic blast cells.

18 accumulation of noncirculating hematopoietic blast cells.

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

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

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

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

23 ccumulation of increased numbers of leukemia blast cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 Blast cells associated with TL in DS infants exhibited F

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

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

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

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

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

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

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

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

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

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

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

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

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

60 of normal segmental organization within the blast cell clone.

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

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

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

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

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

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

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

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

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

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

71 Blast cell colonies contain higher numbers and a broader

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 the normal percentage and suppress leukemic blast cell expansion.

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

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

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

100 Blast cells expressed gene signatures characteristic of

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

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

103 Blast cell expression of the NG2 molecule was strongly a

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

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

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

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

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

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

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

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

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

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

114 33 is expressed on acute myelocytic leukemic blast cells from about 90% of patients, normal hematopoi

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

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

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

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

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

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

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

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

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

124 -3 counterparts in other organisms determine blast cell identity and for this reason may lead to cell

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 Blast cell structure and immunophenotype are similar in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

203 Blast cells were tested for ETV6 and MLL rearrangement u

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

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

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

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

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

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

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

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

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

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

214 Individual blast cells within this equivalence group become committ

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

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