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1 alpha fusion proteins have been described in acute promyelocytic leukemia.
2 ions in patients with relapsed or refractory acute promyelocytic leukemia.
3 ic by its dramatic clinical efficacy against acute promyelocytic leukemia.
4 mplified by the prototypical RA treatment of acute promyelocytic leukemia.
5 ioxide (As2O3), a highly effective agent for acute promyelocytic leukemia.
6 nd likely responsible for the development of acute promyelocytic leukemia.
7 interacts with the PLZF protein of t(11;17) acute promyelocytic leukemia.
8 ently disrupted by t(15;17) in patients with acute promyelocytic leukemia.
9 lpha (RARalpha), causes a refractory form of acute promyelocytic leukemia.
10 nes and clinical remissions in patients with acute promyelocytic leukemia.
11 its efficacy as a chemotherapeutic agent for acute promyelocytic leukemia.
12 cription factor that is fused to RARalpha in acute promyelocytic leukemia.
13 (15;17), a consistent cytogenetic feature of acute promyelocytic leukemia.
14 hus contribute to its therapeutic effects on acute promyelocytic leukemia.
15 tations can contribute to the development of acute promyelocytic leukemia.
16 Arsenic is effective in the treatment of acute promyelocytic leukemia.
17 treatment of relapsed and resistant cases of acute promyelocytic leukemia.
18 are commonly associated with development of acute promyelocytic leukemia.
19 d in several pathogenic conditions including acute promyelocytic leukemia.
20 n patients with t(11;17)(q23;q21)-associated acute promyelocytic leukemia.
21 l function of PML and in the pathogenesis of acute promyelocytic leukemia.
22 e high-level expression of cyclin A1 seen in acute promyelocytic leukemia.
23 ohort comprising 280 adults with primary non-acute promyelocytic leukemia.
24 the continuing problem with early deaths in acute promyelocytic leukemia.
25 de (ATO, As2 O3 ) is currently used to treat acute promyelocytic leukemia.
26 l counts after chemotherapy in patients with acute promyelocytic leukemia.
27 for acute myeloid leukemia (AML), excluding acute promyelocytic leukemia.
28 emotherapeutic drug used in the treatment of acute promyelocytic leukemia.
29 that is disrupted during the pathogenesis of acute promyelocytic leukemia, a disease characterized by
30 eukemogenic chromatin signature, we analyzed acute promyelocytic leukemia, a subtype of leukemia char
31 cedent chemotherapy were varied and included acute promyelocytic leukemia, acute myeloid leukemia wit
32 (As(2)O(3)) induces remission of refractory acute promyelocytic leukemia and apoptosis of cell lines
33 wth which is characteristically disrupted in acute promyelocytic leukemia and by a variety of viruses
34 (2)O(3)) is an effective therapeutic against acute promyelocytic leukemia and certain solid tumors.
35 he authors summarize current mouse models of acute promyelocytic leukemia and describe current knowle
36 y been used successfully in the treatment of acute promyelocytic leukemia and has been shown to induc
37 a tumor suppressor originally identified in acute promyelocytic leukemia and implicated in tumorigen
38 mmunomodulatory effects and is used to treat acute promyelocytic leukemia and inflammatory disorders
39 As(2)O(3)) causes remission in patients with acute promyelocytic leukemia and multiple myeloma withou
40 useful adjuvant with ATRA for patients with acute promyelocytic leukemia and possibly retinoid-resis
41 tential contributions to the pathogenesis of acute promyelocytic leukemia and variety of viral infect
42 ed in a variety of human disorders including acute promyelocytic leukemia and viral infections, sugge
43 ic lymphocytic leukemia, arsenic trioxide in acute promyelocytic leukemia, and the BH3-mimetic ABT199
44 rative syndrome, but only 15% to 20% develop acute promyelocytic leukemia (APL) after a latent period
46 been successfully used for the treatment of acute promyelocytic leukemia (APL) and has activity in m
48 plays a critical role in the pathogenesis of acute promyelocytic leukemia (APL) and non-Hodgkin's lym
49 sociated with increased penetrance of murine acute promyelocytic leukemia (APL) and the frequent acqu
50 , we elucidated the DNA methylome in primary acute promyelocytic leukemia (APL) and the role of promy
51 minimal residual disease (MRD) monitoring in acute promyelocytic leukemia (APL) are available only in
53 rans-retinoic acid (ATRA) -based therapy for acute promyelocytic leukemia (APL) averages 70% at 5 yea
54 this study, we investigated the dynamics of acute promyelocytic leukemia (APL) before and during the
55 e the gap in quality of care and outcomes in acute promyelocytic leukemia (APL) between developed and
56 on of p70 S6 kinase was inducible in primary acute promyelocytic leukemia (APL) blasts and RA-sensiti
57 rentiation of normal hematopoietic cells and acute promyelocytic leukemia (APL) blasts by transcripti
58 ed fibrinolysis is an important component of acute promyelocytic leukemia (APL) bleeding diathesis.
59 ide (AS) has excellent cytotoxic activity in acute promyelocytic leukemia (APL) but its activity in s
60 ously generated a transgenic mouse model for acute promyelocytic leukemia (APL) by expressing the pro
61 We previously developed a murine model of acute promyelocytic leukemia (APL) by using human cathep
62 clinical remission in patients with t(15;17) acute promyelocytic leukemia (APL) carrying leukemogenic
64 ic acid (RA) treatment induces remissions in acute promyelocytic leukemia (APL) cases expressing the
67 on induced monocytic differentiation of NB-4 acute promyelocytic leukemia (APL) cells and HL-60 AML c
68 n to induce differentiation and apoptosis in acute promyelocytic leukemia (APL) cells concomitant wit
76 r, HK3 expression was significantly lower in acute promyelocytic leukemia (APL) compared with non-APL
77 promyelocytic leukemia protein (PML) gene of acute promyelocytic leukemia (APL) encodes a cell growth
80 as been successfully used as a treatment for acute promyelocytic leukemia (APL) for more than a decad
82 The t(15;17) chromosomal translocation in acute promyelocytic leukemia (APL) generates the PML-RAR
84 all-trans retinoic acid (ATRA) treatment in acute promyelocytic leukemia (APL) has been the paradigm
85 sive promyelocytic leukemia (PML) protein of acute promyelocytic leukemia (APL) has served as one of
86 pha (PR) and RARalpha-PML frequently develop acute promyelocytic leukemia (APL) in association with a
87 ents with the microgranular variant (M3V) of acute promyelocytic leukemia (APL) in the all-trans reti
97 ptor (RAR) activity that characterizes human acute promyelocytic leukemia (APL) is associated with a
115 yelocytic leukemia (PML) tumor suppressor of acute promyelocytic leukemia (APL) is essential for a nu
117 th all-trans retinoic acid and chemotherapy, acute promyelocytic leukemia (APL) is now the most curab
118 cid receptor alpha (PML-RARalpha) protein of acute promyelocytic leukemia (APL) is oncogenic in vivo.
120 lpha (RARalpha) gene in the vast majority of acute promyelocytic leukemia (APL) patients as a consequ
121 ve demonstrated that the immense majority of acute promyelocytic leukemia (APL) patients can be defin
126 large population of unselected patients with acute promyelocytic leukemia (APL) remains unknown becau
127 transplantation advantage and development of acute promyelocytic leukemia (APL) required DNMT3A.
128 ll-trans retinoic acid (ATRA)--a therapy for acute promyelocytic leukemia (APL) that is considered th
129 ent anti-leukemic chemotherapeutic agent for acute promyelocytic leukemia (APL) that results from a t
131 the outcome of patients with newly diagnosed acute promyelocytic leukemia (APL) treated with all-tran
132 AAML0631 trial for newly diagnosed pediatric acute promyelocytic leukemia (APL) was a phase III histo
135 is an effective treatment for patients with acute promyelocytic leukemia (APL) who have relapsed fro
136 mples from 406 patients with newly diagnosed acute promyelocytic leukemia (APL) who were receiving al
137 protein PML-RARalpha in 5 of 8 patients with acute promyelocytic leukemia (APL) with 2 or more relaps
138 (As2O3) has been shown to effectively treat acute promyelocytic leukemia (APL) with greater than 80%
144 protein is the initiating genetic event for acute promyelocytic leukemia (APL), but the molecular me
145 by the chromosomal translocation t(15;17) in acute promyelocytic leukemia (APL), encodes a multifunct
146 in the t(15;17) chromosomal translocation of acute promyelocytic leukemia (APL), encodes a protein wh
147 signaling in leukemogenesis, particularly in acute promyelocytic leukemia (APL), has started to emerg
148 17)(q22;q11.2) translocation associated with acute promyelocytic leukemia (APL), initiates APL when e
149 ith a retinoic acid (RA)-insensitive form of acute promyelocytic leukemia (APL), involving the produc
150 d in approximately 8% of adult patients with acute promyelocytic leukemia (APL), is defined molecular
151 PML) gene, a tumor suppressor inactivated in acute promyelocytic leukemia (APL), regulates apoptosis
153 ith chemotherapy is the standard of care for acute promyelocytic leukemia (APL), resulting in cure ra
155 The most common chromosomal translocation in acute promyelocytic leukemia (APL), t15;17(q22;q21), cre
156 c acid (RA)-based differentiation therapy in acute promyelocytic leukemia (APL), the broad promise of
159 e commonly dysregulated in a murine model of acute promyelocytic leukemia (APL), we first defined gen
160 e has been shown to be effective in treating acute promyelocytic leukemia (APL), with minimal overall
161 psy was performed, yielding the diagnosis of acute promyelocytic leukemia (APL), with t(15;17)(q23;q2
162 is of chronic myelogenous leukemia (CML)- or acute promyelocytic leukemia (APL)-derived cell lines.
163 We found PMLRARalpha interaction with Fas in acute promyelocytic leukemia (APL)-derived cells and APL
205 cid (ATRA) was evaluated in 69 patients with acute promyelocytic leukemia (APL): 32 new diagnoses, 35
206 (ATO), a curative agent in clinical use for acute promyelocytic leukemia (APL); in our studies, ATO
207 fective treatment for patients with relapsed acute promyelocytic leukemia (APL); its role as consolid
210 leukemias (MLL-AF9;Nras(G12D); PML-RARalpha acute promyelocytic leukemia [APL] cells) and Emicro-Myc
212 in blast-phase chronic myeloid leukemia and acute promyelocytic leukemia arguing against this strate
213 aired for corepressor release and operate in acute promyelocytic leukemia as dominant-negative inhibi
214 tor fused to retinoic acid receptor alpha in acute promyelocytic leukemia associated with the (11;17)
216 MRP8 promoter recapitulated the phenotype of acute promyelocytic leukemia but had the unexpected resu
217 zumab ozogamicin is efficacious not only for acute promyelocytic leukemia but, in combination with co
218 for the treatment of relapsed and refractory acute promyelocytic leukemia by induction of partial dif
219 ccessful strategy to treat AML, as proved in acute promyelocytic leukemia by treatment with all-trans
220 the dominant molecular signatures of murine acute promyelocytic leukemia can be influenced by severa
223 myl-transpeptidase (gamma-GT) protects human acute promyelocytic leukemia cells (NB4) from Dar, but n
224 phosphorylation was also observed in primary acute promyelocytic leukemia cells and resulted in activ
225 proliferation and induces differentiation of acute promyelocytic leukemia cells in vitro and in vivo.
227 suggesting that the expression signature of acute promyelocytic leukemia cells reflects the genetic
228 ccumulation of oxidized proteins, we exposed acute promyelocytic leukemia cells to arsenic trioxide (
229 es including NCI-H929 myeloma cells and NB-4 acute promyelocytic leukemia cells, whereas normal lymph
231 d in the passive selection of ATRA-resistant acute promyelocytic leukemia clones leading to disease r
234 have been shown to be capable of initiating acute promyelocytic leukemia development, and dictate th
235 reciprocal translocation fusion proteins on acute promyelocytic leukemia development, and have demon
236 is, cytarabine-induced cellebellar toxicity, acute promyelocytic leukemia differentiation syndrome, t
238 3)) is highly effective for the treatment of acute promyelocytic leukemia, even in patients who are u
239 e then focus on a discussion of RARalpha and acute promyelocytic leukemia followed by a discussion of
240 with acute myeloid leukemia (AML; excluding acute promyelocytic leukemia) from 1990 to 2006 who rece
243 cess of arsenic trioxide in the treatment of acute promyelocytic leukemia has renewed interest in the
244 senic trioxide is an effective treatment for acute promyelocytic leukemia has renewed interest in the
245 ties of our method not only by screening two acute promyelocytic leukemia human cells lines (NB4 and
248 lishments of the International Consortium on Acute Promyelocytic Leukemia (IC-APL), an initiative of
249 ts), and 2% for SPT (one patient), which was acute promyelocytic leukemia (ie, not of the upper aerod
250 associated with remissions in patients with acute promyelocytic leukemia, implying that G0S2 may pos
254 , 282 were excluded, including patients with acute promyelocytic leukemia, incorrect diagnosis, or no
255 that arsenic trioxide, a frontline agent for acute promyelocytic leukemia, inhibits DeltaNp63 but not
256 de, a drug FDA approved for the treatment of acute promyelocytic leukemia, inhibits the growth of Ewi
257 L-RARalpha) oncofusion protein, which causes acute promyelocytic leukemia, inhibits TNFalpha induced
262 ein, the leukemogenic product of t(15,17) in acute promyelocytic leukemia, is cleaved into a truncate
263 Arsenic trioxide, a drug for patients with acute promyelocytic leukemia, is found to target and deg
264 antineoplastic compound for the treatment of acute promyelocytic leukemia, is proarrhythmic via two s
265 ion syndrome, thrombohemorrhagic syndrome in acute promyelocytic leukemia, L-asparaginase-associated
266 man subjects, overexpression of annexin 2 in acute promyelocytic leukemia leads to a bleeding diathes
267 ofiles of fully transformed cells from three acute promyelocytic leukemia model systems were all diff
268 biomarkers of differentiation therapy in an acute promyelocytic leukemia model treated with all-tran
269 14e were further tested in vivo in a murine acute promyelocytic leukemia model, resulting 14d the mo
270 sion events, we compared two high-penetrance acute promyelocytic leukemia models that both commonly a
274 on in NB4 cells, a cell line derived from an acute promyelocytic leukemia patient with t(15;17) trans
275 Here, we report the expression of miRNAs in acute promyelocytic leukemia patients and cell lines dur
276 been found to be an effective treatment for acute promyelocytic leukemia patients and is being teste
277 sseminated intravascular coagulation scores, acute promyelocytic leukemia patients had higher fibrino
279 eported that As(2)O(3), a drug used to treat acute promyelocytic leukemia (PML), stimulates HIV-1 rep
283 However, with notable exceptions such as acute promyelocytic leukemia, significant improvements i
284 e chromatin marks generated by the aberrant, acute promyelocytic leukemia specific promyelocytic locu
286 fied 2 additional cases of t(15;17)-negative acute promyelocytic leukemia that had cytogenetically in
287 from arsenic poisoning and in patients with acute promyelocytic leukemia that have been treated with
288 ly severe complication seen in patients with acute promyelocytic leukemia treated with all-trans reti
289 atus in 1333 young adult patients, excluding acute promyelocytic leukemia, treated in the United King
290 427 young adult patients with AML, excluding acute promyelocytic leukemia, using denaturing high-perf
291 tPCR]) measurements of PML-RAR alpha mRNA in acute promyelocytic leukemia was retrospectively assesse
295 uding those with core binding factor AML and acute promyelocytic leukemia, were randomly assigned to
296 including subclones) has been exemplified by acute promyelocytic leukemia, where successful targeting
297 rentiation therapy has been the treatment of acute promyelocytic leukemia with all-trans retinoic aci
298 were referred a difficult diagnostic case of acute promyelocytic leukemia with no pathogenic X-RARA f
299 complete clinical remission in patients with acute promyelocytic leukemia with t(15;17) translocation
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