戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ations of white blood cells, both normal and leukaemic.
2  is feasible, safe, and mediates potent anti-leukaemic activity in children and young adults with che
3 ectively inhibits Mediator kinases, has anti-leukaemic activity in vitro and in vivo, and disproporti
4 oxyprogesterone acetate (BaP) has shown anti-leukaemic activity in vitro and in vivo.
5 onditioning is well tolerated and shows anti-leukaemic activity, although without durability outside
6 cell products, as well as their in vivo anti-leukaemic activity, were comparable to those of T cells
7 ferentiation and the associated loss of anti-leukaemic activity.
8 these SE-associated genes, yet also has anti-leukaemic activity.
9 xokinase 2 (HK2) localizes to the nucleus in leukaemic and normal haematopoietic stem cells.
10           Mitochondrial metabolites regulate leukaemic and normal stem cells by affecting epigenetic
11 be the case, then the cell type that becomes leukaemic and the chromosomal/molecular changes that occ
12  the haematopoietic stem cell lineage causes leukaemic and tumoural diseases but not neurodegenerativ
13 how that low-level expression of the gene in leukaemic blast cells and granulocytes does not associat
14    Apaf-1 protein deficiency occurs in human leukaemic blasts and confers resistance to cytochrome-c-
15 ne in c-Kit(mid)CD3(+)Lin(-) LSCs and CD3(+) leukaemic blasts, recapitulating a subset of human T-ALL
16  myelopoiesis and myeloid differentiation of leukaemic blasts, which protects mice from death related
17 t correlate with Apaf-1 mRNA levels in human leukaemic blasts.
18 n occur within the Apaf-1 promoter region in leukaemic blasts.
19 diated resistance to cytochrome c in primary leukaemic blasts.
20 this balance in mice, resulting in decreased leukaemic burden and increased survival in vivo.
21  of drug resistance and the minimal residual leukaemic burden providing effective strategies for futu
22 kinase (BTK) blocks AML blast proliferation, leukaemic cell adhesion to bone marrow stromal cells as
23 meter flowcytometry capable of detecting one leukaemic cell among 10,000 normal cells.
24  of actionable molecular targets by studying leukaemic cell and host genetics, precise risk stratific
25        Genome-wide profiling of germline and leukaemic cell DNA has identified novel submicroscopic s
26  of a microbial metabolite that promotes pre-leukaemic cell expansion.
27  of B cells (NF-kappaB) and is essential for leukaemic cell function.
28       Little is known about the mechanism of leukaemic cell infiltration of the CNS, despite its clin
29 als in human erythroleukaemia (HEL) cells, a leukaemic cell line of platelet-megakaryocyte lineage.
30 za2dc) increased the sensitivity of the K562 leukaemic cell line to UV light-induced apoptosis in ass
31 n global gene expression in t(8;21)-positive leukaemic cell lines and in primary AML blasts using cDN
32 efficacy against human and murine MLL-fusion leukaemic cell lines, through the induction of early cel
33 mature (MT) Smac genes into the K562 and CEM leukaemic cell lines.
34  to determine optimal assay conditions using leukaemic cell lines.
35                                              Leukaemic cell populations showed clonal rearrangements
36 xpression of miR-22 significantly suppresses leukaemic cell viability and growth in vitro, and substa
37    A higher degree of marrow infiltration by leukaemic cells (> or = 0.1%) in week 14 samples identif
38 ed standard was tested using ex vivo patient leukaemic cells (n=5).
39                                              Leukaemic cells also show an elevated percentage of Ras
40 lts in cell cycle arrest, differentiation of leukaemic cells and failure to establish leukaemia in im
41 n TET2-deficient mouse embryonic stem cells, leukaemic cells and haematopoietic stem and progenitor c
42 tively blocking proliferation of TET2-mutant leukaemic cells and largely reversing the haematopoiesis
43 at was based on genetic abnormalities of the leukaemic cells and measurements of minimal residual dis
44 isk stratification by biological features of leukaemic cells and response to treatment, treatment mod
45     However, failure to completely eradicate leukaemic cells and the escape of these cells from previ
46          Immunological detection of residual leukaemic cells at any point in the treatment course is
47            Molecular cytogenetic analysis of leukaemic cells by banded karyotype and FISH revealed a
48    Further studies revealed that circulating leukaemic cells can engraft around these vessels, sugges
49 phocytic leukaemia, and studies suggest that leukaemic cells carrying ABL-class fusions can be target
50 pecifically targeting the genetic defects of leukaemic cells could revolutionise management of this d
51         Inhibition of JAK2 activity in human leukaemic cells decreases both the expression of the hae
52                  The presence of AML1-ETO in leukaemic cells does not prevent this disassembly.
53                                         Some leukaemic cells expressed high levels of Apaf-1 mRNA but
54                                    Resistant leukaemic cells expressed high levels of Bruton's tyrosi
55                                   In t(8;21) leukaemic cells expressing the aberrant fusion protein A
56                                              Leukaemic cells from 239 patients with T-ALL enrolled at
57 ions, we performed a genome-wide analysis of leukaemic cells from 242 paediatric ALL patients using h
58                    Here we show that primary leukaemic cells from children with NF1 show a selective
59 cal significance of submicroscopic levels of leukaemic cells in bone-marrow aspirates from children w
60                  Fusions are not observed in leukaemic cells in these patients.
61 therapeutic effects against murine and human leukaemic cells in vitro and in vivo.
62 cleared by NK cells, whereas NKG2DL-negative leukaemic cells isolated from the same individual escape
63 te relapses might represent new mutations in leukaemic cells not eliminated by conventional therapy.
64 slocation, t(8;21)(q22;q22), observed in the leukaemic cells of approximately 40% of patients with th
65 a fusion oncogene in hard to transfect human leukaemic cells raising the possibility of targeting mal
66 rentially expressed genes were identified in leukaemic cells that were secondarily resistant to STI57
67 unresponsiveness of PLZF-RARalpha-expressing leukaemic cells to RA.
68 sion could be used to predict sensitivity of leukaemic cells to STI571.
69 c transfectants increased the sensitivity of leukaemic cells to UV light-induced apoptosis and the ac
70 ming for effective metastatic dissemination, leukaemic cells uniquely possess the innate ability for
71   The proportion of patients with detectable leukaemic cells was 23% at remission induction and 17% a
72 ing and NF-kappaB activation that endows pre-leukaemic cells with a competitive advantage due to exce
73 ing ADC enables the selective eradication of leukaemic cells with preserved haematopoiesis.
74                             The treatment of leukaemic cells with SAHM1 results in genome-wide suppre
75                  Here we show that, in human leukaemic cells, AML1-ETO resides in and functions throu
76 over, Lmo2 knock-down impaired the growth of leukaemic cells, and high LMO2 expression at diagnosis c
77 nhibitor of the production of differentiated leukaemic cells, but does not deplete leukaemic stem cel
78                                   We studied leukaemic cells, collected at diagnosis, to identify cas
79 one marrow in vivo in the proximity of other leukaemic cells, differentiate upon exposure to blue lig
80 y, treatment based on biological features of leukaemic cells, host genetics, and the amount of residu
81 ink between ageing and expansion of rare pre-leukaemic cells, suggesting that the ADP-heptose-ALPK1 a
82 presents the turnover rate of differentiated leukaemic cells, while the second slope of 0.008 per day
83 ucture of the human c-FMS gene in normal and leukaemic cells.
84 ced colony formation and Ki-67 expression in leukaemic cells.
85 ur understanding of their role in normal and leukaemic cells.
86 on the LSC surface but not on healthy or pre-leukaemic cells.
87 and immunophenotypic and genetic features of leukaemic cells.
88 individuals and favours the expansion of pre-leukaemic cells.
89 library was used to transduce human Jurkat T-leukaemic cells.
90 ear clonal relationship between parental and leukaemic cells.
91 d co-expressed with HOXA9, in MLL-rearranged leukaemic cells.
92 y leads to a biphasic exponential decline of leukaemic cells.
93 tosis and suppressing proliferation in human leukaemic cells.
94 togenetic clones and without any evidence of leukaemic change.
95  specific DPB1 alleles and two groups of non-leukaemic children, one consisting of children with soli
96 ining self-renewal of HSCs and promoting pre-leukaemic clonal dominance.
97  normal lymphocyte development, facilitating leukaemic clonal expansion.
98 yrosine kinase resistance in CML, leading to leukaemic clone escape and disease propagation.
99 ired driver mutations, showing that advanced leukaemic clones can originate from a different cell typ
100           This study was to isolate the anti-leukaemic component from edible mushroom Hypsizygus marm
101  Osteoblasts were recently implicated in pre-leukaemic conditions in mice.
102 n-leukaemic microenvironmental cells and the leukaemic counterpart, and the primary drivers of their
103   Our results, obtained using TALL-104 human leukaemic CTLs as a model system, are consistent with th
104                       We used TALL-104 human leukaemic cytotoxic T cells as a model system, and stimu
105 eukemia initiating cells (LICs) comprise pre-leukaemic, differentiation inhibited thymocytes allowing
106 R-Cas9-mediated depletion of ENL led to anti-leukaemic effects, including increased terminal myeloid
107 ity of a number of oncogenic drivers and pre-leukaemic events, adding further layers of context and g
108 us T-cell lymphoma, and predominantly in its leukaemic form, Sezary syndrome.
109              Inhibition of IRAK4-L abrogates leukaemic growth, particularly in AML cells with higher
110 eader domain was essential for ENL-dependent leukaemic growth.
111 involves the gradual expansion of mutant pre-leukaemic haematopoietic cells, which increases with age
112 c and epigenetic changes accumulating in pre-leukaemic HSCs prior to the emergence of leukaemic stem
113 -activated CAR T cells exhibited higher anti-leukaemic in vivo activity per cell than the correspondi
114 aemic subtypes, the clinical significance of leukaemic invasion into specific tissues and the current
115 th cDNAs representing the RNAs of normal and leukaemic leucocyte populations were sufficiently differ
116                      30 patients (12.6%) had leukaemic lymphoblasts with an ETP-related gene-expressi
117 carcinomatosis', neoplastic meningitis' and 'leukaemic/lymphomatous meningitis', arises secondary to
118 e expression of the CD2-myc transgene in pre-leukaemic mice.
119            The relationships between the non-leukaemic microenvironmental cells and the leukaemic cou
120                                         In a leukaemic mouse model, type 2(high) CAR T cell products
121 ned as clonal haematopoiesis driven by a pre-leukaemic mutation in at least 2% of sequenced alleles,
122 Flt3 internal tandem duplication (Flt3(ITD)) leukaemic mutations to accelerate leukaemogenesis, throu
123                                         'Pre-leukaemic' mutations are thought to promote clonal expan
124 (GMP) behaviour in mice during emergency and leukaemic myelopoiesis.
125 ntonic regulatory element) during normal and leukaemic myelopoiesis.
126 ant cell populations and remotely modulating leukaemic niches.
127 the expression of important mediators of the leukaemic phenotype such as HHEX/PRH.
128 ssion of miR-196b results in more aggressive leukaemic phenotypes and causes much faster leukemogenes
129 )c chromosome with gene dosage optimized for leukaemic potential, showing constrained copy-number lev
130 Granulocytic differentiation from normal and leukaemic precursors is accompanied by loss of transcrip
131 ronic phase of CML the primitive multipotent leukaemic progenitor cells remain growth factor dependen
132 .008 per day represents the turnover rate of leukaemic progenitors.
133 potential therapeutic target for controlling leukaemic progression in Noonan syndrome and for improvi
134 culated that DNA damage might also constrain leukaemic self-renewal and malignant haematopoiesis.
135 way that is necessary for maintenance of the leukaemic state and identify this enzyme as a potential
136 L3 and is implicated in the maintenance of a leukaemic state.
137      Overexpression of nuclear HK2 increases leukaemic stem cell properties and decreases differentia
138 ess, increasing chromatin accessibilities at leukaemic stem cell-positive signature and DNA-repair si
139               Deficiency of CaSR reduces AML leukaemic stem cells (LSC) 6.5-fold.
140 ive way to functionally impair the quiescent leukaemic stem cells (LSC) that persist as residual dise
141 pre-leukaemic HSCs prior to the emergence of leukaemic stem cells (LSCs) and the development of acute
142 (1) that is driven by chemotherapy-resistant leukaemic stem cells (LSCs)(2,3).
143 expressed on healthy HSCs and upregulated on leukaemic stem cells (LSCs), where it serves as a qualit
144 d disease management, but fails to eradicate leukaemic stem cells (LSCs), which maintain CML.
145 metabolism is upregulated in patient-derived leukaemic stem cells (LSCs).
146 ed genetic deletion in bone-marrow-engrafted leukaemic stem cells and leukaemia cells.
147 ich may contribute to the mechanism by which leukaemic stem cells resist DNA-damaging agents.
148 marrow, including healthy and diseased HSCs, leukaemic stem cells, B cells, T cells, macrophages and
149 t the rare and notoriously therapy-resistant leukaemic stem cells, which represent the roots of myelo
150 loid regulator expressed on immune cells and leukaemic stem cells.
151 tiated leukaemic cells, but does not deplete leukaemic stem cells.
152  leukaemogenesis and sustain self-renewal of leukaemic stem cells/leukaemia-initiating cells through
153                       Can imatinib eradicate leukaemic stem cells?
154 , and we detail our current understanding of leukaemic 'stemness' regulation.
155 s that facilitate metastasis in a variety of leukaemic subtypes, the clinical significance of leukaem
156                              In human Jurkat leukaemic T cells expressing an ER-targeted Ca(2+) indic
157 show here, that expression of TCL1 occurs in leukaemic T cells from A-T patients with chromosome 14 r
158 , these results show that PTEN expression in leukaemic T cells leads to reduced proliferation via an
159 PMCA in shaping Ca2+ signals in Jurkat human leukaemic T cells using single-cell voltage-clamp and ca
160 dhesion signal required for the targeting of leukaemic T-cells into the CNS.
161     hDOT1L contributes to CALM-AF10-mediated leukaemic transformation by preventing nuclear export of
162                Although the absolute risk of leukaemic transformation in individuals with CHIP is ver
163 2;p13) chromosomal translocation, drives the leukaemic transformation of early B-cell precursors, but
164  p16(INK4A), increases the susceptibility to leukaemic transformation of haematopoietic progenitor ce
165 endogenous and environmental changes, drives leukaemic transformation.
166 on (LLPS) puncta of chimera and for inducing leukaemic transformation.
167 nction of PAX5 and IKZF1 and readily enabled leukaemic transformation.
168 phenomenon is connected to susceptibility to leukaemic transformation.
169 hat abrogated H3K4me3 binding also abolished leukaemic transformation.
170  fusion is both necessary and sufficient for leukaemic transformation.
171 lation of c-FMS expression may contribute to leukaemic transformation.
172 opoiesis, and an important fusion partner in leukaemic translocations.
173 erted high growth inhibitory effect on human leukaemic U937 cells and sufficient toxicological safety

 
Page Top