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1 xtended life to the degree seen with chronic myelogenous leukemia.
2 rosine kinase inhibitor approved for chronic myelogenous leukemia.
3 lance and result in the development of acute myelogenous leukemia.
4 ces similar survival for patients with acute myelogenous leukemia.
5 milar survival times for patients with acute myelogenous leukemia.
6 in patients with imatinib-resistant chronic myelogenous leukemia.
7 transform to myelodysplastic syndrome/acute myelogenous leukemia.
8 re implicated in leukemias, especially acute myelogenous leukemia.
9 n a syndrome highly similar to human chronic myelogenous leukemia.
10 inib for the first-line treatment of chronic myelogenous leukemia.
11 eukemic progenitors from patients with acute myelogenous leukemia.
12 some hematopoietic cancers, such as chronic myelogenous leukemia.
13 ainst a mouse model of chronic-phase chronic myelogenous leukemia.
14 a substrate of the BCR-ABL kinase in chronic myelogenous leukemia.
15 nificant activity in patients with MDS/acute myelogenous leukemia.
16 the current role of the procedure in chronic myelogenous leukemia.
17 arnib exhibits modest activity against acute myelogenous leukemia.
18 antation into congenic WT mice, led to acute myelogenous leukemia.
19 titutively active kinase that causes chronic myelogenous leukemia.
20 to myelodysplastic syndrome (MDS) and acute myelogenous leukemia.
21 incidence of myelodysplastic syndrome/acute myelogenous leukemia.
22 in the development of both acute and chronic myelogenous leukemia.
23 n 6 years after HCT for treatment of chronic myelogenous leukemia.
24 hematopoietic cell transplantation for acute myelogenous leukemia.
25 n chromosome translocations that cause acute myelogenous leukemia.
26 may be a potent candidate for treating acute myelogenous leukemia.
27 nic fusion protein characteristic of chronic myelogenous leukemia.
28 both acute lymphoblastic leukemia and acute myelogenous leukemia achieve remission with upfront chem
29 one marrow or peripheral blood HCT for acute myelogenous leukemia, acute lymphoblastic leukemia, chro
31 re previously avoided in patients with acute myelogenous leukemia aged more than 55 years because of
32 level of 27 C&Ckines in serum from 176 acute myelogenous leukemia (AML) and 114 myelodysplastic syndr
33 tein levels were robustly expressed in acute myelogenous leukemia (AML) and acute lymphoblastic leuke
34 hosphatase, is overexpressed in 50% of acute myelogenous leukemia (AML) and associated with poor surv
35 potent in vivo anticancer activity in acute myelogenous leukemia (AML) and endemic Burkitt lymphoma
36 by platelet defects, predisposition to acute myelogenous leukemia (AML) and germ-line heterozygous RU
37 ) expression is frequently observed in acute myelogenous leukemia (AML) and has been implicated in le
40 are important for the pathogenesis of acute myelogenous leukemia (AML) and represent a reservoir of
43 a well-defined cohort of patients with acute myelogenous leukemia (AML) at diagnosis and relapse to a
44 ion factor family member, is linked to acute myelogenous leukemia (AML) by chromosomal events at the
45 xpression of IGF1R and IR isoform A in acute myelogenous leukemia (AML) cell lines as well as in >80%
46 ntly, AEG-1 markedly protected HCC and acute myelogenous leukemia (AML) cells from retinoid- and rexi
47 strategies to eradicate primary human acute myelogenous leukemia (AML) cells is a major challenge to
48 eraction between the integrin VLA-4 on acute myelogenous leukemia (AML) cells with stromal fibronecti
50 naling cues in the microenvironment of acute myelogenous leukemia (AML) contribute to disease progres
52 he chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion tra
53 stic syndrome (MDS) that progresses to acute myelogenous leukemia (AML) in association with overexpre
54 (Trib2) is a pseudokinase that induces acute myelogenous leukemia (AML) in mice and is highly express
55 We studied LSCs in mouse models of acute myelogenous leukemia (AML) induced either by coexpressio
56 nthracyclines used in the treatment of acute myelogenous leukemia (AML) inhibit the activity of the m
61 d implement therapeutic approaches for acute myelogenous leukemia (AML) originated primarily from adu
66 were also screened against M9-ENL1 and acute myelogenous leukemia (AML) primary cell lines and exhibi
67 The survival of most patients with acute myelogenous leukemia (AML) remains poor, and novel thera
69 d next-generation sequencing to assess acute myelogenous leukemia (AML) response to induction chemoth
72 ver, the interactions and influence of acute myelogenous leukemia (AML) stem cells with the microenvi
75 a panel of cell lines representing all acute myelogenous leukemia (AML) subtypes using selective, rev
76 nding protein 2 (SSBP2) is a candidate acute myelogenous leukemia (AML) suppressor gene located at ch
77 9 presented by cell lines, and primary acute myelogenous leukemia (AML) targets that endogenously exp
78 o further accrual after three cases of acute myelogenous leukemia (AML) were reported of a total of 4
79 stic syndrome (MDS) transforms into an acute myelogenous leukemia (AML) with associated increased bon
80 ssion of the MLL-AF9 fusion results in acute myelogenous leukemia (AML) with different behaviors depe
81 topoietic progenitor cells and induces acute myelogenous leukemia (AML) with long latency in bone mar
83 or acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), and chronic myelogenous leuk
84 and clinical outcome of patients with acute myelogenous leukemia (AML), and conventional karyotype-b
85 been implicated in the pathogenesis of acute myelogenous leukemia (AML), but the functional significa
87 ssful use of cytotoxic chemotherapy in acute myelogenous leukemia (AML), the biological basis for its
89 understanding of the genetic basis of acute myelogenous leukemia (AML), we determined the coding exo
90 lt3, an additional important target in acute myelogenous leukemia (AML), with pharmacologically usefu
110 rs from 1409 unrelated transplants for acute myelogenous leukemia (AML; n = 1086) and acute lymphobla
112 Here, we identify two patients with acute myelogenous leukemia and B-cell acute lymphoblastic leuk
114 s the history of transplantation for chronic myelogenous leukemia and defines the new natural history
115 The trail blazed by imatinib for chronic myelogenous leukemia and GIST has become a desired route
116 increasing the time to progression to acute myelogenous leukemia and improving overall response rate
117 of inactivating mutations of DNMT3A in acute myelogenous leukemia and myelodysplastic syndrome, our r
118 erapeutic response for patients with chronic myelogenous leukemia and Philadelphia chromosome-positiv
119 ioned drug candidates against breast cancer, myelogenous leukemia and prostate cancer by looking for
120 94 and 88 candidate drugs for breast cancer, myelogenous leukemia and prostate cancer, 32%, 13% and 1
121 ndous impact on clinical outcomes in chronic myelogenous leukemia and revolutionized the field of tar
122 xpressed in breast cancer), BCR-ABL (chronic myelogenous leukemia and some cases of acute lymphoblast
123 ole caregiver for her husband, who has acute myelogenous leukemia and was undergoing allogeneic hemat
124 on kinase is the driving mutation of chronic myelogenous leukemias and is also expressed in a subset
125 emotherapy in patients with refractory acute myelogenous leukemia (and other hematologic malignancies
127 kemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, and myelodysplastic syndrome betwe
128 kemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, and myelodysplastic syndrome enrol
131 ified as chromosomal translocations in acute myelogenous leukemia, are transcriptional corepressors t
134 This procedure remains an option in chronic myelogenous leukemia but its use will become more sparin
135 mic blasts isolated from patients with acute myelogenous leukemia but was relatively sparing of norma
136 condary glioblastomas, and a subset of acute myelogenous leukemias but have not been detected in othe
137 the clinical outcome for patients with acute myelogenous leukemia by reducing the incidence of leukem
138 nd broad H3K4me3 domains in the K562 chronic myelogenous leukemia cell line as well as the MCF-7 brea
139 Ectopic expression of PTPROt in the chronic myelogenous leukemia cell line K562 indeed resulted in h
141 ere cellular membrane fragments of a chronic myelogenous leukemia cell line, KU-812, were immobilized
143 s Crk was robustly phosphorylated in chronic myelogenous leukemia cell lines and in A431 and MDA-MB-4
145 eration of the effects of As(2)O(3) on acute myelogenous leukemia cells and raise the potential of mo
147 It is also used to sort K562 human chronic myelogenous leukemia cells that have either been treated
149 e that Id genes are expressed in human acute myelogenous leukemia cells, and that knock down of Id1 e
152 mg twice daily in chronic-phase (CP) chronic myelogenous leukemia (CML) after imatinib treatment fail
153 parts, leukemia stem cells (LSCs) in chronic myelogenous leukemia (CML) and acute myeloid leukemia (A
155 elf-renewal in p210(BCR-ABL)-induced chronic myelogenous leukemia (CML) and exhibits synergistic effe
156 Cancer stem cells lie at the root of chronic myelogenous leukemia (CML) and mediate its continued gro
157 rine fashion, their possible role in chronic myelogenous leukemia (CML) and resistance to imatinib me
160 repressed in 32D-BCR/ABL, K562, and chronic myelogenous leukemia (CML) blast crisis (BC) primary cel
161 effective therapy for patients with chronic myelogenous leukemia (CML) but is now mostly indicated f
162 mical DNA biosensor for detection of chronic myelogenous leukemia (CML) by covalently immobilizing th
163 mical DNA biosensor for detection of chronic myelogenous leukemia (CML) by immobilizing amine termina
166 ighly active against primary CD34(+) chronic myelogenous leukemia (CML) cells and Ba/F3 cells bearing
168 ere assessed in cell-free medium and chronic myelogenous leukemia (CML) cells overexpressing BCR-Abl
169 regulator of imatinib sensitivity in chronic myelogenous leukemia (CML) cells through an unknown mech
177 chromosomal abnormalities (ACAs) in chronic myelogenous leukemia (CML) is generally associated with
180 lance of minimal residual disease in chronic myelogenous leukemia (CML) may be relevant for long-term
181 donor lymphocyte infusion (DLI) for chronic myelogenous leukemia (CML) may result from immunologic a
183 effective in inducing remissions in chronic myelogenous leukemia (CML) patients but do not eliminate
184 We previously demonstrated that chronic myelogenous leukemia (CML) patients treated with DLI dev
190 bility to chromosomal aberrations in chronic myelogenous leukemia (CML) progenitors after exposure to
193 ely active mutant of Abl that causes chronic myelogenous leukemia (CML) stimulated the expression and
195 ia stem cells (LSC) in chronic phase chronic myelogenous leukemia (CML) using a transgenic mouse mode
196 selenium has been shown to alleviate chronic myelogenous leukemia (CML) via the elimination of leukem
197 in Philadelphia chromosome-positive chronic myelogenous leukemia (CML) where all available kinase in
198 e in CLL, GRN was not upregulated in chronic myelogenous leukemia (CML) where miR-107 paralogs are no
199 ction (QPCR) levels in patients with chronic myelogenous leukemia (CML) who are in complete cytogenet
202 imatinib is remarkably effective in chronic myelogenous leukemia (CML), although drug resistance is
203 complete remissions in patients with chronic myelogenous leukemia (CML), and evidence supports an imm
204 a major role in the pathogenesis of chronic myelogenous leukemia (CML), and is the target of the bre
205 highly effective in the treatment of chronic myelogenous leukemia (CML), but primary and acquired res
206 ion in the majority of patients with chronic myelogenous leukemia (CML), but the persistence of CML s
207 hibitors are effective therapies for chronic myelogenous leukemia (CML), but these inhibitors target
208 se inhibitors (TKIs), a treatment of chronic myelogenous leukemia (CML), has largely replaced curativ
209 eted therapies, such as imatinib for chronic myelogenous leukemia (CML), represent the first agents t
210 b at inhibiting Bcr-Abl and treating chronic myelogenous leukemia (CML), resistance to the therapy oc
211 ncogene homolog 1 (BCR-ABL1)-induced chronic myelogenous leukemia (CML)-like myeloproliferative neopl
231 ors (TKI) have improved treatment of chronic myelogenous leukemia (CML); however, most patients are n
232 and revolutionized the treatment of chronic myelogenous leukemia (CML); in 2006 and 2007, approval o
233 e long-term response in blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia chromosom
234 ss of miR-328 occurs in blast crisis chronic myelogenous leukemia (CML-BC) in a BCR/ABL dose- and kin
235 t myeloid leukemia blasts (including chronic myelogenous leukemia [CML]-blast crisis cells) rely on c
236 s with acute lymphoblastic leukemia or acute myelogenous leukemia compared with normal bone marrow.
237 Leukemic stem cells in chronic phase chronic myelogenous leukemia (CP-CML) are responsible for diseas
238 half of patients with chronic-phase chronic myelogenous leukemia (CP-CML) in complete molecular resp
239 leukemia (GVL) against chronic-phase chronic myelogenous leukemia (CP-CML) is potent, but it is less
240 SCT) is potent against chronic phase chronic myelogenous leukemia (CP-CML), but blast crisis CML (BC-
241 IDH1), frequently found in gliomas and acute myelogenous leukemia, creates a neoenzyme that produces
242 atment in HL-60 cells, a cell model of acute myelogenous leukemia, decreased miR181b expression and i
244 cell transplantation was the goal in chronic myelogenous leukemia for over 20 years and remains an op
245 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
247 n patients with autoimmune diseases or acute myelogenous leukemia illustrate the potential use of the
250 lated tyrosine kinase BCR-ABL causes chronic myelogenous leukemia in humans and forms a large multipr
252 ntiation of quiescent drug-resistant chronic myelogenous leukemia-initiating cells (CML LICs), thereb
253 eased risk of development of secondary acute myelogenous leukemia involving the mixed-lineage leukemi
257 well-known therapeutic agent against chronic myelogenous leukemia, is an effective inhibitor of Abl t
258 of human tumor cell lines and clinical acute myelogenous leukemia isolates, which express abundant PK
260 used the experimental data from immortalised myelogenous leukemia (K562) and healthy lymphoblastoid (
261 amster Ovary (CHO) cells, Human Immortalized Myelogenous Leukemia (K562) cells and hematopoietic stem
263 l lines isolated from a patient with chronic myelogenous leukemia (KBM7 and HAP1), as well as haploid
264 m a very early age a more aggressive chronic myelogenous leukemia-like disease than mice deficient in
265 mples from 15 myelodysplastic syndrome/acute myelogenous leukemia (MDS/AML) patients undergoing decit
266 as the cause of some familial cases of acute myelogenous leukemia/myelodysplastic syndrome and in Mon
267 ukemia virus or those expressing the chronic myelogenous leukemia oncoprotein BCR-ABL in the hematopo
268 ary blasts isolated from patients with acute myelogenous leukemia or acute lymphocytic leukemia.
269 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 could act as prognostic biomarkers of acute myelogenous leukemia though influencing cancer-related b
289 orrelates with sensitivity of clinical acute myelogenous leukemia to chemotherapy, whereas low BAK le
290 -Abl tyrosine kinase associated with chronic myelogenous leukemia to small molecule inhibitors that t
292 e been reported in patients who have chronic myelogenous leukemia treated with the tyrosine kinase in
295 (-/-) mouse model of engrafted human chronic myelogenous leukemia, we now demonstrate the complete el
297 1 case in which neoplastic cells of chronic myelogenous leukemia were intermingled with the cells of
298 ed by the Philadelphia chromosome in chronic myelogenous leukemia were unraveled, and these have led
299 optosis of CSC derived from chronic or acute myelogenous leukemias when administered at supraphysiolo
300 ders, 7 nonresponders) with relapsed chronic myelogenous leukemia who received CD4(+) DLI in the pre-