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1 rosine kinase inhibitor approved for chronic myelogenous leukemia.
2 lance and result in the development of acute myelogenous leukemia.
3 ces similar survival for patients with acute myelogenous leukemia.
4 milar survival times for patients with acute myelogenous leukemia.
5 in patients with imatinib-resistant chronic myelogenous leukemia.
6 transform to myelodysplastic syndrome/acute myelogenous leukemia.
7 re implicated in leukemias, especially acute myelogenous leukemia.
8 n a syndrome highly similar to human chronic myelogenous leukemia.
9 inib for the first-line treatment of chronic myelogenous leukemia.
10 eukemic progenitors from patients with acute myelogenous leukemia.
11 some hematopoietic cancers, such as chronic myelogenous leukemia.
12 ainst a mouse model of chronic-phase chronic myelogenous leukemia.
13 a substrate of the BCR-ABL kinase in chronic myelogenous leukemia.
14 nificant activity in patients with MDS/acute myelogenous leukemia.
15 the current role of the procedure in chronic myelogenous leukemia.
16 arnib exhibits modest activity against acute myelogenous leukemia.
17 antation into congenic WT mice, led to acute myelogenous leukemia.
18 titutively active kinase that causes chronic myelogenous leukemia.
19 incidence of myelodysplastic syndrome/acute myelogenous leukemia.
20 in the development of both acute and chronic myelogenous leukemia.
21 n 6 years after HCT for treatment of chronic myelogenous leukemia.
22 hematopoietic cell transplantation for acute myelogenous leukemia.
23 n chromosome translocations that cause acute myelogenous leukemia.
24 nic fusion protein characteristic of chronic myelogenous leukemia.
25 xtended life to the degree seen with chronic myelogenous leukemia.
26 both acute lymphoblastic leukemia and acute myelogenous leukemia achieve remission with upfront chem
27 one marrow or peripheral blood HCT for acute myelogenous leukemia, acute lymphoblastic leukemia, chro
29 re previously avoided in patients with acute myelogenous leukemia aged more than 55 years because of
30 level of 27 C&Ckines in serum from 176 acute myelogenous leukemia (AML) and 114 myelodysplastic syndr
31 tein levels were robustly expressed in acute myelogenous leukemia (AML) and acute lymphoblastic leuke
32 hosphatase, is overexpressed in 50% of acute myelogenous leukemia (AML) and associated with poor surv
33 potent in vivo anticancer activity in acute myelogenous leukemia (AML) and endemic Burkitt lymphoma
34 by platelet defects, predisposition to acute myelogenous leukemia (AML) and germ-line heterozygous RU
35 ) expression is frequently observed in acute myelogenous leukemia (AML) and has been implicated in le
38 are important for the pathogenesis of acute myelogenous leukemia (AML) and represent a reservoir of
41 a well-defined cohort of patients with acute myelogenous leukemia (AML) at diagnosis and relapse to a
42 ion factor family member, is linked to acute myelogenous leukemia (AML) by chromosomal events at the
43 xpression of IGF1R and IR isoform A in acute myelogenous leukemia (AML) cell lines as well as in >80%
44 ntly, AEG-1 markedly protected HCC and acute myelogenous leukemia (AML) cells from retinoid- and rexi
45 strategies to eradicate primary human acute myelogenous leukemia (AML) cells is a major challenge to
46 eraction between the integrin VLA-4 on acute myelogenous leukemia (AML) cells with stromal fibronecti
48 naling cues in the microenvironment of acute myelogenous leukemia (AML) contribute to disease progres
50 he chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion tra
51 stic syndrome (MDS) that progresses to acute myelogenous leukemia (AML) in association with overexpre
52 (Trib2) is a pseudokinase that induces acute myelogenous leukemia (AML) in mice and is highly express
53 We studied LSCs in mouse models of acute myelogenous leukemia (AML) induced either by coexpressio
58 d implement therapeutic approaches for acute myelogenous leukemia (AML) originated primarily from adu
62 were also screened against M9-ENL1 and acute myelogenous leukemia (AML) primary cell lines and exhibi
63 The survival of most patients with acute myelogenous leukemia (AML) remains poor, and novel thera
65 d next-generation sequencing to assess acute myelogenous leukemia (AML) response to induction chemoth
68 ver, the interactions and influence of acute myelogenous leukemia (AML) stem cells with the microenvi
71 a panel of cell lines representing all acute myelogenous leukemia (AML) subtypes using selective, rev
72 nding protein 2 (SSBP2) is a candidate acute myelogenous leukemia (AML) suppressor gene located at ch
73 9 presented by cell lines, and primary acute myelogenous leukemia (AML) targets that endogenously exp
74 o further accrual after three cases of acute myelogenous leukemia (AML) were reported of a total of 4
75 stic syndrome (MDS) transforms into an acute myelogenous leukemia (AML) with associated increased bon
76 ssion of the MLL-AF9 fusion results in acute myelogenous leukemia (AML) with different behaviors depe
77 topoietic progenitor cells and induces acute myelogenous leukemia (AML) with long latency in bone mar
79 or acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), and chronic myelogenous leuk
80 and clinical outcome of patients with acute myelogenous leukemia (AML), and conventional karyotype-b
81 been implicated in the pathogenesis of acute myelogenous leukemia (AML), but the functional significa
82 kinase commonly found in patients with acute myelogenous leukemia (AML), led to the down-regulation o
84 ssful use of cytotoxic chemotherapy in acute myelogenous leukemia (AML), the biological basis for its
86 understanding of the genetic basis of acute myelogenous leukemia (AML), we determined the coding exo
87 lt3, an additional important target in acute myelogenous leukemia (AML), with pharmacologically usefu
108 rs from 1409 unrelated transplants for acute myelogenous leukemia (AML; n = 1086) and acute lymphobla
110 Here, we identify two patients with acute myelogenous leukemia and B-cell acute lymphoblastic leuk
111 s the history of transplantation for chronic myelogenous leukemia and defines the new natural history
112 The trail blazed by imatinib for chronic myelogenous leukemia and GIST has become a desired route
113 increasing the time to progression to acute myelogenous leukemia and improving overall response rate
114 of inactivating mutations of DNMT3A in acute myelogenous leukemia and myelodysplastic syndrome, our r
115 erapeutic response for patients with chronic myelogenous leukemia and Philadelphia chromosome-positiv
116 ioned drug candidates against breast cancer, myelogenous leukemia and prostate cancer by looking for
117 94 and 88 candidate drugs for breast cancer, myelogenous leukemia and prostate cancer, 32%, 13% and 1
118 ndous impact on clinical outcomes in chronic myelogenous leukemia and revolutionized the field of tar
119 xpressed in breast cancer), BCR-ABL (chronic myelogenous leukemia and some cases of acute lymphoblast
120 ole caregiver for her husband, who has acute myelogenous leukemia and was undergoing allogeneic hemat
121 on kinase is the driving mutation of chronic myelogenous leukemias and is also expressed in a subset
122 emotherapy in patients with refractory acute myelogenous leukemia (and other hematologic malignancies
124 kemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, and myelodysplastic syndrome betwe
125 kemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, and myelodysplastic syndrome enrol
128 ified as chromosomal translocations in acute myelogenous leukemia, are transcriptional corepressors t
131 This procedure remains an option in chronic myelogenous leukemia but its use will become more sparin
132 mic blasts isolated from patients with acute myelogenous leukemia but was relatively sparing of norma
133 condary glioblastomas, and a subset of acute myelogenous leukemias but have not been detected in othe
134 the clinical outcome for patients with acute myelogenous leukemia by reducing the incidence of leukem
135 nd broad H3K4me3 domains in the K562 chronic myelogenous leukemia cell line as well as the MCF-7 brea
136 Ectopic expression of PTPROt in the chronic myelogenous leukemia cell line K562 indeed resulted in h
138 ere cellular membrane fragments of a chronic myelogenous leukemia cell line, KU-812, were immobilized
140 s Crk was robustly phosphorylated in chronic myelogenous leukemia cell lines and in A431 and MDA-MB-4
142 eration of the effects of As(2)O(3) on acute myelogenous leukemia cells and raise the potential of mo
145 e that Id genes are expressed in human acute myelogenous leukemia cells, and that knock down of Id1 e
149 mg twice daily in chronic-phase (CP) chronic myelogenous leukemia (CML) after imatinib treatment fail
150 parts, leukemia stem cells (LSCs) in chronic myelogenous leukemia (CML) and acute myeloid leukemia (A
152 elf-renewal in p210(BCR-ABL)-induced chronic myelogenous leukemia (CML) and exhibits synergistic effe
153 Cancer stem cells lie at the root of chronic myelogenous leukemia (CML) and mediate its continued gro
154 rine fashion, their possible role in chronic myelogenous leukemia (CML) and resistance to imatinib me
157 repressed in 32D-BCR/ABL, K562, and chronic myelogenous leukemia (CML) blast crisis (BC) primary cel
158 effective therapy for patients with chronic myelogenous leukemia (CML) but is now mostly indicated f
159 mical DNA biosensor for detection of chronic myelogenous leukemia (CML) by covalently immobilizing th
160 mical DNA biosensor for detection of chronic myelogenous leukemia (CML) by immobilizing amine termina
163 ighly active against primary CD34(+) chronic myelogenous leukemia (CML) cells and Ba/F3 cells bearing
165 ere assessed in cell-free medium and chronic myelogenous leukemia (CML) cells overexpressing BCR-Abl
166 regulator of imatinib sensitivity in chronic myelogenous leukemia (CML) cells through an unknown mech
176 chromosomal abnormalities (ACAs) in chronic myelogenous leukemia (CML) is generally associated with
179 lance of minimal residual disease in chronic myelogenous leukemia (CML) may be relevant for long-term
180 donor lymphocyte infusion (DLI) for chronic myelogenous leukemia (CML) may result from immunologic a
182 effective in inducing remissions in chronic myelogenous leukemia (CML) patients but do not eliminate
183 We previously demonstrated that chronic myelogenous leukemia (CML) patients treated with DLI dev
189 bility to chromosomal aberrations in chronic myelogenous leukemia (CML) progenitors after exposure to
192 ely active mutant of Abl that causes chronic myelogenous leukemia (CML) stimulated the expression and
194 ia stem cells (LSC) in chronic phase chronic myelogenous leukemia (CML) using a transgenic mouse mode
195 selenium has been shown to alleviate chronic myelogenous leukemia (CML) via the elimination of leukem
196 in Philadelphia chromosome-positive chronic myelogenous leukemia (CML) where all available kinase in
197 e in CLL, GRN was not upregulated in chronic myelogenous leukemia (CML) where miR-107 paralogs are no
198 ction (QPCR) levels in patients with chronic myelogenous leukemia (CML) who are in complete cytogenet
201 imatinib is remarkably effective in chronic myelogenous leukemia (CML), although drug resistance is
202 complete remissions in patients with chronic myelogenous leukemia (CML), and evidence supports an imm
203 a major role in the pathogenesis of chronic myelogenous leukemia (CML), and is the target of the bre
204 highly effective in the treatment of chronic myelogenous leukemia (CML), but primary and acquired res
205 hibitors are effective therapies for chronic myelogenous leukemia (CML), but these inhibitors target
206 se inhibitors (TKIs), a treatment of chronic myelogenous leukemia (CML), has largely replaced curativ
207 eted therapies, such as imatinib for chronic myelogenous leukemia (CML), represent the first agents t
208 b at inhibiting Bcr-Abl and treating chronic myelogenous leukemia (CML), resistance to the therapy oc
209 ncogene homolog 1 (BCR-ABL1)-induced chronic myelogenous leukemia (CML)-like myeloproliferative neopl
229 ors (TKI) have improved treatment of chronic myelogenous leukemia (CML); however, most patients are n
230 and revolutionized the treatment of chronic myelogenous leukemia (CML); in 2006 and 2007, approval o
231 e long-term response in blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia chromosom
232 ss of miR-328 occurs in blast crisis chronic myelogenous leukemia (CML-BC) in a BCR/ABL dose- and kin
233 t myeloid leukemia blasts (including chronic myelogenous leukemia [CML]-blast crisis cells) rely on c
234 s with acute lymphoblastic leukemia or acute myelogenous leukemia compared with normal bone marrow.
235 VI1 and EVI1, previously implicated in acute myelogenous leukemia, contribute to the pathophysiology
236 Leukemic stem cells in chronic phase chronic myelogenous leukemia (CP-CML) are responsible for diseas
237 half of patients with chronic-phase chronic myelogenous leukemia (CP-CML) in complete molecular resp
238 leukemia (GVL) against chronic-phase chronic myelogenous leukemia (CP-CML) is potent, but it is less
239 SCT) is potent against chronic phase chronic myelogenous leukemia (CP-CML), but blast crisis CML (BC-
240 IDH1), frequently found in gliomas and acute myelogenous leukemia, creates a neoenzyme that produces
241 atment in HL-60 cells, a cell model of acute myelogenous leukemia, decreased miR181b expression and i
243 cell transplantation was the goal in chronic myelogenous leukemia for over 20 years and remains an op
244 n patients developed myelodysplasia or acute myelogenous leukemia, four of those being the rare but u
246 R-ABL inhibitor for the treatment of chronic myelogenous leukemia, has created a great impetus for th
249 lated tyrosine kinase BCR-ABL causes chronic myelogenous leukemia in humans and forms a large multipr
251 ntiation of quiescent drug-resistant chronic myelogenous leukemia-initiating cells (CML LICs), thereb
252 eased risk of development of secondary acute myelogenous leukemia involving the mixed-lineage leukemi
256 well-known therapeutic agent against chronic myelogenous leukemia, is an effective inhibitor of Abl t
257 of human tumor cell lines and clinical acute myelogenous leukemia isolates, which express abundant PK
259 used the experimental data from immortalised myelogenous leukemia (K562) and healthy lymphoblastoid (
260 amster Ovary (CHO) cells, Human Immortalized Myelogenous Leukemia (K562) cells and hematopoietic stem
262 l lines isolated from a patient with chronic myelogenous leukemia (KBM7 and HAP1), as well as haploid
263 m a very early age a more aggressive chronic myelogenous leukemia-like disease than mice deficient in
264 mples from 15 myelodysplastic syndrome/acute myelogenous leukemia (MDS/AML) patients undergoing decit
265 as the cause of some familial cases of acute myelogenous leukemia/myelodysplastic syndrome and in Mon
266 ukemia virus or those expressing the chronic myelogenous leukemia oncoprotein BCR-ABL in the hematopo
267 ary blasts isolated from patients with acute myelogenous leukemia or acute lymphocytic leukemia.
268 ears (range, 18-69 years), and 95% had acute myelogenous leukemia or high-risk myelodysplastic syndro
270 kemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, or myelodysplastic syndrome; 98% r
272 ne kinase FLT3 are frequently found in acute myelogenous leukemia patients and confer poor clinical p
273 acinus are overexpressed in some human acute myelogenous leukemia patients and correlate with elevate
274 ue, we analyzed outcomes of 2223 adult acute myelogenous leukemia patients who underwent allogeneic H
277 he BCR-Abl translocation involved in chronic myelogenous leukemia, reportedly produces alopecia accor
278 cute myelogenous leukemia (AML), and chronic myelogenous leukemia (RR = 26.9, 66.5, and 93.1, respect
279 tive neoplasms (MDS/MPN), or secondary acute myelogenous leukemia (sAML) and may point toward genes h
280 oth leukemic cell lines and in primary acute myelogenous leukemia samples that was not abrogated by M
281 cluding therapy-refractory B-ALL and chronic myelogenous leukemia samples, and inhibits growth of hum
282 ma, colorectal and prostate cancers, chronic myelogenous leukemia, small cell lung cancer, and medull
284 -related myelodysplastic syndromes and acute myelogenous leukemia (t-MDS/AML) comprise an increasingl
285 Therapy-related myelodysplasia or acute myelogenous leukemia (t-MDS/AML) is a lethal complicatio
286 corepressors originally identified in acute myelogenous leukemia that have recently been linked to e
288 orrelates with sensitivity of clinical acute myelogenous leukemia to chemotherapy, whereas low BAK le
289 -Abl tyrosine kinase associated with chronic myelogenous leukemia to small molecule inhibitors that t
291 e been reported in patients who have chronic myelogenous leukemia treated with the tyrosine kinase in
294 (-/-) mouse model of engrafted human chronic myelogenous leukemia, we now demonstrate the complete el
296 1 case in which neoplastic cells of chronic myelogenous leukemia were intermingled with the cells of
297 ed by the Philadelphia chromosome in chronic myelogenous leukemia were unraveled, and these have led
298 optosis of CSC derived from chronic or acute myelogenous leukemias when administered at supraphysiolo
299 he BCR-ABL oncogene in patients with chronic myelogenous leukemia who evolve resistance to ABL kinase
300 ders, 7 nonresponders) with relapsed chronic myelogenous leukemia who received CD4(+) DLI in the pre-
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