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1 d differentiation in vivo in TM and were not leukemogenic.
2 tion appear to support the notion that it is leukemogenic.
3  ETO in hematopoietic cells is not by itself leukemogenic.
4 ntrast, HTLV-2, which expresses Tax2, is non-leukemogenic.
5 us the inhibitory K413 acetylation optimizes leukemogenic ability of mIDH2 in AML cells by both produ
6 l expansion of hematopoietic stem cells with leukemogenic acquired genetic variants, is associated wi
7 though murine models have demonstrated their leukemogenic activities, the steps from a normal human c
8 at CD105(+) blasts are endowed with superior leukemogenic activity compared with the CD105(-) populat
9 epressor recruitment by ETO and clues to the leukemogenic activity of AML1-ETO.
10 iferation, clonogenic potential, and in vivo leukemogenic activity of BCR/ABL-expressing myeloid 32Dc
11                  The effectors mediating the leukemogenic activity of CDX2 and the mechanism underlyi
12                                          The leukemogenic activity of MLL fusion proteins is dependen
13 sential oncogenic co-factor required for the leukemogenic activity of MLL fusion proteins.
14     Disruption of this pathway abrogates the leukemogenic activity of MLL fusions.
15 m in a lineage-dependent manner, showing the leukemogenic activity of MLL-Af4 was interlinked with ly
16 rthenolide (PTL) can impair the survival and leukemogenic activity of primary human acute myeloid leu
17  protein stabilization may contribute to the leukemogenic activity of the fusion protein.
18 focus-forming (MCF) viruses and the enhanced leukemogenic activity of the latter, we tested XMRV for
19 vitro transformation properties, and in vivo leukemogenic activity of the P190, P210, and P230 forms
20 naling to Abl interactor proteins affect its leukemogenic activity.
21 suggesting the three proteins have different leukemogenic activity.
22 mology domain of Runx2 are essential for its leukemogenic activity.
23 which is consistently impaired or deleted in leukemogenic AF10 translocations, plays a critical role
24    Dosing per cycle and cumulative dosing of leukemogenic agents peaked with N6, which included four
25 idence that alkylating agents, certain other leukemogenic agents, and total-body irradiation (TBI) ca
26 n interactions advances the understanding of leukemogenic AGO2 functions and underlines the role of a
27 alfold higher than that of the LTR of weakly leukemogenic Akv virus.
28                  ETO family proteins and the leukemogenic AML1-ETO fusion protein are corepressors of
29                       Both viruses were less leukemogenic and had a longer mean latency period than M
30 is expressed by this translocation is poorly leukemogenic and requires additional mutations for trans
31 of high-dose chemotherapy might be minimally leukemogenic, and (2) it contrasts strikingly with the p
32 controls hematopoiesis, its dysregulation is leukemogenic, and its influence on GATA factor function
33  constitutive v-Rel expression appears to be leukemogenic at earlier stages of T-cell development.
34 eted agents able to restore the aberrant and leukemogenic "block" in normal differentiation.
35             This combination can be potently leukemogenic, but the particular manner in which these t
36 a factor-dependent cell line FDC.P1 was made leukemogenic by transfection with the human BCR/ABL gene
37 corporation of functional AF10(PZP) into the leukemogenic CALM-AF10 fusion prevents the transforming
38 n in response to THPO in vitro and increased leukemogenic capacity in vivo.
39 tem cells) may be particularly vulnerable to leukemogenic changes induced by carcinogens.
40          Here, we investigate NUP98-PHF23, a leukemogenic chimera of the disordered phenylalanine-and
41                            To understand the leukemogenic chromatin signature, we analyzed acute prom
42 predicting therapy response and BC, tracking leukemogenic clones longitudinally, targeting TKI-insens
43                  This study reveals that the leukemogenic CM fusion protein disrupts adult erythropoi
44                                     With the leukemogenic concerns of viral gene therapy there is a n
45 nses and the mechanisms of the hemotoxic and leukemogenic consequences of radiation exposure.
46             We provide key insights into the leukemogenic determinants of MLL-AF4+ infant B-ALL.
47                In contrast, clones harboring leukemogenic DNMT3A R882 mutations increase upon stimula
48 S transcription factors, targeting important leukemogenic driver genes.
49 expansion of hematopoietic stem cells due to leukemogenic driver mutations, increases risk for both h
50 f the FLT3 and PIM1 genes, another important leukemogenic driver.
51  may contribute an essential function to the leukemogenic effect of DEK-CAN and SET-CAN.
52                                    Thus, the leukemogenic effect of MN1-TEL in our knock-in mice is p
53 hat BHLHB1, similar to SCL/TAL1, may exert a leukemogenic effect through a functional inactivation of
54  that MN1-TEL exerts its nonlineage-specific leukemogenic effects by promoting the growth of primitiv
55  susceptibility of myeloid stem cells to the leukemogenic effects of etoposide have not been elucidat
56               These results suggest that the leukemogenic effects of HRX fusion proteins may be relat
57                  The molecular basis for the leukemogenic effects of these fusion proteins is incompl
58 ced insulation at TAD borders, with putative leukemogenic effects.
59 with topoisomerase-II inhibitors is strongly leukemogenic, even with modest cumulative doses of each
60 f the GATA1 mutation suggests it is an early leukemogenic event.
61                                  Cooperating leukemogenic events in MLL-rearranged (MLL-r) infant acu
62 ogenic levels of Notch1 can complement other leukemogenic events, such as activation of K-ras.
63 naling induces Meis1, recapitulating several leukemogenic features of Hoxa9/Meis1-driven leukemia.
64 roperty appears to be specific to exogenous, leukemogenic FeLVs.
65 ls expressing PKC412-sensitive or -resistant leukemogenic FLT3 mutants.
66  expansion and sensitizes progenitors to the leukemogenic FLT3(ITD) mutation.
67 ntaining HOX gene dysregulation as a driving leukemogenic force.
68 oproteolytic domain, frequently missing from leukemogenic forms of the protein, in complex with the N
69 n the myeloid compartment, and modulates the leukemogenic function of Cbfbeta-SMMHC in mouse leukemia
70 L-AF6 fusion gene represents the most common leukemogenic fusion of mixed lineage leukemia (MLL) to a
71                                MOZ-TIF2 is a leukemogenic fusion oncoprotein that confers self-renewa
72 the MLL repression domain is retained in the leukemogenic fusion protein and is required for transfor
73                                The resulting leukemogenic fusion proteins are transcriptional repress
74 d with an inability to target the removal of leukemogenic fusion proteins, aberrant epigenetic regula
75                          Here we show that 3 leukemogenic fusion proteins, BCR-ABL, CBFB-MYH11, and R
76 atic RUNX1 alteration was found in AMLs with leukemogenic fusion proteins, such as core-binding facto
77  human cord blood cells and those expressing leukemogenic fusion proteins, we discovered a dual role
78 c malignancies are typically associated with leukemogenic fusion proteins, which are required to main
79 ation by an MLL fusion protein but not other leukemogenic fusion proteins.
80 promising therapeutic strategy for AMLs with leukemogenic fusion proteins.
81                    As many genes involved in leukemogenic fusions play a role in normal hematopoiesis
82 ons reduce H3K27me3 levels, which results in leukemogenic gene expression and the development of myel
83  NUP98-IDR fusions convergently drive a core leukemogenic gene expression program in donor-derived hu
84  MLL fusion proteins that bind DNA and drive leukemogenic gene expression.
85 ssing TCF3 but lacking PBX1, upregulated the leukemogenic genes BLK and NOTCH3, arguing that function
86  stem cells can acquire somatic mutations in leukemogenic genes that confer a proliferative advantage
87 ematopoietic cells with somatic mutations in leukemogenic genes was associated with age and correlate
88 H3K79 methylation and aberrant expression of leukemogenic genes.
89 r with E47, to activate aberrantly a set of "leukemogenic" genes in T cells.
90 o smoke exposure influences the formation of leukemogenic genomic deletions.
91                                          The leukemogenic GMP displayed higher levels of beta-catenin
92 ncy may have contributed to the formation of leukemogenic GMP, restoration of E2A-function did not re
93 ptors, these Lckpr-hTCL1Atg T cells gained a leukemogenic growth advantage in scenarios of receptor s
94 ress only non-DNA binding dominant-negative "leukemogenic" Ikaros isoforms lacking critical N-termina
95 genes in human acute leukemias and is highly leukemogenic in experimental models.
96                  Whether this gene, which is leukemogenic in mice, also plays a leukemogenic role in
97     Conversely, enforced HOXA9 expression is leukemogenic in mice, and HOXA9 is frequently activated
98 iferation and survival, has been shown to be leukemogenic in mice, is detected in LSCs of more than 5
99 R/ABL-BaF3 cells, a murine cell line that is leukemogenic in mice, SCH66336 potently inhibited soft a
100 3 and NHR4 domains of AML1-ETO and is highly leukemogenic in the mouse model.
101 one marrow failure and that loss of Trp53 is leukemogenic in this model.
102 th acute lymphoblastic leukemia (ALL) can be leukemogenic in vivo when expressed in normal hematopoie
103 sed levels of the shorter, dominant negative leukemogenic isoform (p30) of CCAAT enhancer-binding pro
104 arness, rather than inhibit, the activity of leukemogenic kinases to kill transformed cells, this app
105                      Here we report that the leukemogenic kinases, Bcr-Abl, FLT3/D835Y, and Tel-PDGFR
106 l hematopoiesis (such as Tet2 deletion), the leukemogenic KrasG12D mutation dramatically accelerated
107 n accessibility at putative enhancers of key leukemogenic loci.
108 emic disease and indicates a cell autonomous leukemogenic mechanism.
109                             In this article, leukemogenic mechanisms have been identified in a number
110  leukemia (CML) and may help elucidate basic leukemogenic mechanisms in CML stem cells during disease
111 scovery of novel, therapeutically targetable leukemogenic mechanisms.
112 or down-regulating high endogenous levels of leukemogenic microRNAs by antisense oligonucleotides (an
113 7-W) of the murine leukemia virus MCF 247, a leukemogenic mink cell focus-inducing (MCF) virus, the U
114 n1 excision also suppresses proliferation of leukemogenic mixed lineage leukemia-AF9 fusion-protein-t
115                                A subgroup of leukemogenic mixed-lineage leukemia (MLL) fusion protein
116                       When transduced with a leukemogenic MLL fusion gene, prospectively isolated ste
117                                            A leukemogenic MLL fusion protein that activates Hox expre
118                                              Leukemogenic MLL fusion proteins cause overexpression of
119                                              Leukemogenic MLL fusion proteins delete the MLL SET doma
120 ssed increased levels of MEIS1, an important leukemogenic MLL target gene that plays a role in regula
121 ed the MLL CXXC domain in the context of the leukemogenic MLL-AF9 fusion with CXXC domains from DNMT1
122 om stem cells or conferred on progenitors by leukemogenic molecules remains unknown.
123                         Interactions between leukemogenic mutations and normal developmental switches
124                    Hematopoietic clones with leukemogenic mutations arise in healthy people as they a
125 iggers and is exploited in malignancy, where leukemogenic mutations epigenetically increase MCT4.
126 the age-related acquisition and expansion of leukemogenic mutations in hematopoietic stem cells (HSCs
127 elated expansion of hematopoietic cells with leukemogenic mutations without detectable malignancy, is
128  by expansion of hematopoietic cells bearing leukemogenic mutations, predisposes both hematologic mal
129 cells are sustained in distinct fractions by leukemogenic mutations.
130 studies show that (1) mice vaccinated with a leukemogenic number of AML cells engineered to express B
131                                        These leukemogenic NUP98 fusion proteins interacted with CRM1,
132 y was undertaken to determine the effects of leukemogenic NUP98 fusion proteins on CRM1-mediated nucl
133        Using dCas9 fused to the paradigmatic leukemogenic NUP98 IDR, we also demonstrate that IDRs ca
134 d in response to some oncogenes, such as the leukemogenic oncogene BCR-ABL, which is created by a rec
135 hat is transformed into a significantly more leukemogenic oncoprotein.
136  that result in defective splicing are a new leukemogenic pathway.
137 ever, BCR-ABL-independent factors, including leukemogenic pathways involving kinases other than BCR-A
138 nd the development of new agents targeted to leukemogenic pathways promise to further improve outcome
139  of E2A-corepressor interactions in distinct leukemogenic pathways.
140 F10 translocated leukemias that share common leukemogenic pathways.
141 demonstrate a highly penetrant mutagenic and leukemogenic phenotype associated with ATC.
142                             Induction of the leukemogenic phenotype is generally associated with inap
143 terleukin 3 dependence and produced a highly leukemogenic phenotype.
144 vertheless abrogated during progression to a leukemogenic phenotype.
145 hout undergoing apoptosis and retained their leukemogenic phenotype.
146 ociated with a facilitated diminution of the leukemogenic PML-RARalpha protein and retained DeltaPML-
147  mutation analyses among individuals without leukemogenic point mutations (LPM), which we term CH-LPM
148 ons that confer a fitness advantage, such as leukemogenic point mutations or mosaic chromosomal alter
149 lentiviral vectors can effectively alter the leukemogenic potency when the degree of suppression of e
150 cellular checkpoints, resulting in increased leukemogenic potential (heterozygous TP53 inactivation).
151 lmitoylation in AML could interfere with the leukemogenic potential and block MDSC accumulation to im
152 tly, inhibition of FOXM1 markedly suppresses leukemogenic potential and induces apoptosis of primary
153  apoptotic program where translocations with leukemogenic potential are created within cells that hav
154 f activating c-KIT mutations differ in their leukemogenic potential in association with RUNX1-ETO, we
155 dent cell cycle progression, and rescued the leukemogenic potential in mice.
156 liferation of these cells, but reduced their leukemogenic potential in vivo, possibly by recruitment
157 tivity of Bcr-Abl/p210 was essential for its leukemogenic potential in vivo.
158 ematopoietic cells but is essential for full leukemogenic potential in vivo.
159                                          The leukemogenic potential is cause for concern and preclude
160 n a more physiological system, we tested the leukemogenic potential of a clone of K562 cells (K6 K562
161               In this study, we compared the leukemogenic potential of activated NRAS, KRAS, and HRAS
162 I1 oncogenic components are required for the leukemogenic potential of AME and for the cooperation of
163 for determining which factors compromise the leukemogenic potential of AML1-ETO.
164                                          The leukemogenic potential of BCR/ABL oncoproteins depends o
165  of some RNA binding proteins suppresses the leukemogenic potential of BCR/ABL-expressing cells.
166 e of Vav by viral proteins may relate to the leukemogenic potential of certain HTLV-I-infected cells.
167 kemia (AML, n = 81), and directly tested the leukemogenic potential of constitutive expression of SAL
168          In parallel, we studied the in vivo leukemogenic potential of dominant negative (DN) and tru
169              In this study, we evaluated the leukemogenic potential of EVI1-, MDS1/EVI1- and AML1-rel
170 A mutations on this process, we assessed the leukemogenic potential of hematopoietic progenitor cells
171  hematopoiesis and demonstrate the conserved leukemogenic potential of human IDH1 mutations in zebraf
172  to increase the risk of transformation, the leukemogenic potential of hydroxyurea (HU) continues to
173 role in APL pathogenesis by facilitating the leukemogenic potential of PML-RARalpha.
174 isease background may be a crucial factor in leukemogenic potential of retroviral gene therapy and un
175                        Here, we assessed the leukemogenic potential of SET-CAN in the hematopoietic s
176 cription and ultimately the cell tropism and leukemogenic potential of the virus.
177 th factor-independent proliferation, and the leukemogenic potential of these cells.
178                                To define the leukemogenic potential of V72M NE, a tumor watch was est
179  for BCR/ABL clonogenic activity and in vivo leukemogenic potential.
180 ions, and outline putative mechanisms of its leukemogenic potential.
181 range of chimeric transcription factors with leukemogenic potential.
182 rest and apoptosis prior to fulfilling their leukemogenic potential.
183  reduced THPO-induced JAK/STAT signaling and leukemogenic potential.
184 cells expressing only p185DeltaBCR showed no leukemogenic potential.
185 osine kinase that possesses sarcomagenic and leukemogenic potential.
186 leukemia (AML) activated AMPK and maintained leukemogenic potential.
187 endent or newly emerging clones of uncertain leukemogenic potential.
188 nus have been shown to have greatly enhanced leukemogenic potential.
189  cytokine receptor common gamma-chain yields leukemogenic pre-B cells that exhibit greater sensitivit
190       Our findings provide insights into the leukemogenic process and may be clinically important in
191 on, and for the use of in vivo models of the leukemogenic process in preclinical or diagnostic studie
192 haracterize the role of the ALL1 gene in the leukemogenic process, and possibly in solid malignancies
193 leukemias and MDS and may play a role in the leukemogenic process.
194 egulated Notch target gene activation in the leukemogenic process.
195 ruption of TNTs significantly inhibits these leukemogenic processes and resensitizes B-cell precursor
196                    PML-RARalpha protein, the leukemogenic product of t(15,17) in acute promyelocytic
197  the PI3K-AKT pathway as key elements of the leukemogenic program activated by NOTCH1 and provide the
198 hancer plays a causal role in the onset of a leukemogenic program.
199  protein-1 (XBP1) mediated repression of pro-leukemogenic programs exemplified by the Wnt-beta-cateni
200 grity of the blood system by restricting pro-leukemogenic programs in HSPCs.
201 LSCs depend on not only active expression of leukemogenic programs, but also DNA methylation-mediated
202  acute promyelocytic leukemia (APL) carrying leukemogenic promyelocytic leukemia-retinoic acid recept
203          These results show that Tel-Abl has leukemogenic properties from distinct from those of Bcr-
204                             In addition, the leukemogenic properties of BCR/ABL in a murine model sys
205 ooperating events that may contribute to its leukemogenic properties, are discussed.
206 nts remain unknown, as do the basis of their leukemogenic properties, impact on steady-state hematopo
207 e-differentiate and reacquire clonogenic and leukemogenic properties.
208 ) translocation and target PML-RARalpha, the leukemogenic protein, by different pathways suggesting a
209 ing domain transforms AML1-ETO into a potent leukemogenic protein.
210  more than one signaling pathway required by leukemogenic PTKs may improve the treatment of primary a
211    Thus, we reveal an entirely novel type of leukemogenic Ras signals that is based on a RasGRP1-driv
212 ation of a histone methyltransferase and its leukemogenic rearrangement that regulates expression of
213 vidence that this constitutive activation is leukemogenic renders this receptor a potential target fo
214  which is leukemogenic in mice, also plays a leukemogenic role in humans will require further study.
215 mic p27 induces apoptosis, consistent with a leukemogenic role of cytoplasmic p27.
216         Therefore, the current study shows a leukemogenic scenario of human ALL in which programs of
217  contend with a spectrum of patient-specific leukemogenic scenarios.
218 g-receptor editing and after germinal-center leukemogenic selection.
219 tential (CHIP), defined as clonally expanded leukemogenic sequence variations (particularly in DNMT3A
220 positions PA2G4 at the crosstalk of the EVI1 leukemogenic signal for developing new therapeutics and
221 pregulation of HGF expression in maintaining leukemogenic signaling by this receptor.
222 otch1 in T-cell progenitors and suggest that leukemogenic signaling involves recruitment of transcrip
223  the FTK protein network and transduction of leukemogenic signaling.
224 l expansion of hematopoietic cells driven by leukemogenic somatic mutations yet without hematologic m
225 SRS 19-6 MuLV genome contribute to its broad leukemogenic spectrum.
226  induce myeloid leukemias, yet have distinct leukemogenic strengths and phenotypes.
227 lex, a master regulator of hematopoiesis and leukemogenic target.
228 id malignancy (secondary AML [s-AML]), after leukemogenic therapy (therapy-related AML [t-AML]), or w
229 c treatment for neuroblastoma or to truncate leukemogenic therapy, eg, by exploiting molecular techni
230 enous leukemia stems from events invoked for leukemogenic topo II cleavable complex-stabilizing antit
231 ich revealed distinct genomic landscapes and leukemogenic trajectories.
232 r CBP, as well as core components of a major leukemogenic transcriptional complex that contains RUNX1
233 + cells, unlike HSCs, are more accessible to leukemogenic transformation after the loss of p18.
234        Point mutations within IBM2 abolished leukemogenic transformation by MLL-AF9, validating that
235 Fas may act as a tumor suppressor to control leukemogenic transformation in myeloid progenitor cells.
236 is a hematopoietic disorder initiated by the leukemogenic transformation of myeloid cells into leukem
237 ns and Kras G12D contribute cooperatively to leukemogenic transformation of normal T-cells.
238 ansplanted cells drives clonal expansion and leukemogenic transformation of preexisting premalignant
239 ivated Akt and growth-factor independence in leukemogenic transformation, and demonstrate the potenti
240 or epigenetic defects are necessary for full leukemogenic transformation.
241 e chimeric fusion protein resulting from the leukemogenic translocation t(17;19), appears to employ e
242 the spleen and bone marrow and was part of a leukemogenic translocation, its role in hematopoiesis ha
243 r failed decatenation, it is surprising that leukemogenic translocations do not occur more frequently
244  yielded new insights into the mechanisms of leukemogenic translocations.
245         Efforts to devise effective but less leukemogenic treatment for neuroblastoma or to truncate
246 ation for apoptosome inhibition by activated leukemogenic tyrosine kinases and suggest that alteratio
247 rse leukemia cell lines expressing different leukemogenic tyrosine kinases, including BCR-ABL and FMS
248 P2/p27 conduit may be a universal target for leukemogenic tyrosine kinases.
249 e potential (CHIP), the expansion of somatic leukemogenic variations in hematopoietic stem cells, has
250                        The retrovirus type B leukemogenic virus (TBLV) causes T-cell lymphomas in mic
251                                       Type B leukemogenic virus (TBLV) induces rapidly appearing T-ce
252                                       Type B leukemogenic virus (TBLV) induces rapidly appearing T-ce
253                                       Type B leukemogenic virus (TBLV) is a variant of mouse mammary
254                                       Type B leukemogenic virus (TBLV) is highly related to mouse mam
255                                       Type B leukemogenic virus (TBLV), a mouse mammary tumor virus (
256                                       Type B leukemogenic virus is a variant of mouse mammary tumor v
257 85 delta BCR/Bcl-2 double transfectants were leukemogenic when injected into immunodeficient mice, bu
258 riant of M-MuLV, Mo+PyF101 M-MuLV, is poorly leukemogenic when used to inoculate mice s.c., but not w
259 p185DeltaBCR/M-Raf double transfectants were leukemogenic, whereas cells expressing only p185DeltaBCR

 
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