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1 focusing on recent advances in treatment of Philadelphia chromosome positive acute lymphoblastic leu
2 h tyrosine kinase inhibitors (TKIs), against Philadelphia chromosome-positive acute leukemia in murin
3 s, we studied blast cells from patients with Philadelphia chromosome-positive acute leukemic transfor
4 and cytogenetic remissions in patients with Philadelphia chromosome-positive acute lymphoblastic leu
7 remissions in patients with newly diagnosed Philadelphia chromosome-positive acute lymphoblastic leu
8 hemotherapy with ponatinib for patients with Philadelphia chromosome-positive acute lymphoblastic leu
10 e inhibitor is effective in the treatment of Philadelphia chromosome-positive acute lymphoblastic leu
11 al, adult patients with previously untreated Philadelphia chromosome-positive acute lymphoblastic leu
13 ients with chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leu
14 1 to 2011, 122 patients with newly diagnosed Philadelphia chromosome-positive acute lymphoblastic leu
15 tinib-resistant chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leu
16 ents with chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leu
18 tients with chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphoblastic leu
19 ly known curative modality for patients with Philadelphia chromosome-positive acute lymphoblastic leu
20 reatment of chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphoblastic leu
21 val for high-risk groups, such as those with Philadelphia chromosome-positive acute lymphoblastic leu
22 inib mesylate into the treatment regimen for Philadelphia chromosome-positive acute lymphoblastic leu
23 have previously developed a murine model of Philadelphia chromosome-positive acute lymphoblastic leu
24 ctly causes chronic myelogenous leukemia and Philadelphia-chromosome positive acute lymphoblastic leu
25 h an expression signature resembling that of Philadelphia chromosome-positive ALL and poor prognosis
27 es is uncommon in ALL, with the exception of Philadelphia chromosome-positive ALL, where the t(9,22)(
28 ) therapy allows a much higher proportion of Philadelphia-chromosome-positive ALL patients to attain
30 table population of quiescent (G0) leukemic (Philadelphia chromosome-positive and BCR-ABL-positive [B
32 rs of age, within 6 months of diagnosis, and Philadelphia chromosome-positive by cytogenetic assessme
33 particularly challenging example is found in Philadelphia chromosome-positive chronic myelogenous leu
34 mesylate has been useful in the treatment of Philadelphia chromosome-positive chronic myelogenous leu
35 on (CE) is a known poor prognostic factor in Philadelphia chromosome-positive chronic myelogenous leu
36 an imatinib in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukaem
37 le patients were aged 18 years or older with Philadelphia chromosome-positive chronic myeloid leukaem
38 ay 1985 and December 1994, 196 patients with Philadelphia chromosome-positive chronic myeloid leukemi
39 they had been diagnosed with chronic phase, Philadelphia chromosome-positive CML within the previous
40 of more than 30 x 10(9)/L was found in 26%, Philadelphia chromosome-positive disease in 16% (20% of
42 ALL.Significance: MYB blockade can suppress Philadelphia chromosome-positive leukemia in mice, sugge
43 TEN functions as a tumor suppressor in human Philadelphia chromosome-positive leukemia that includes
44 ractory solid tumors or imatinib-refractory, Philadelphia chromosome-positive leukemia was performed.
45 ylate (Gleevec) is effective therapy against Philadelphia chromosome-positive leukemia, but resistanc
54 s been effectively used for the treatment of Philadelphia chromosome-positive leukemias and gastroint
57 tyrosine kinase activity of abl oncogene in Philadelphia chromosome positive-leukemic cells leads to
59 rrangement, yet demonstrated from 12% to 20% Philadelphia chromosome-positive metaphase cells in the
62 3 studies including 2962 patients, excluding Philadelphia chromosome-positive patients, showed a surv
64 romising agent for the treatment of advanced Philadelphia chromosome positive (Ph(+)) acute lymphobla
65 al blood and 55 bone marrow samples with 127 Philadelphia chromosome positive (Ph+) and 6 Ph-/BCR-ABL
66 25 metaphases for monitoring the presence of Philadelphia chromosome positive (Ph+) cells in chronic
67 tients with acute lymphoblastic leukemia are Philadelphia chromosome positive (Ph-positive acute lymp
69 is chronic myelogenous leukemia (CML-BC) and Philadelphia chromosome-positive (Ph(+)) acute lymphobla
70 b has improved the outcome for patients with Philadelphia chromosome-positive (Ph(+)) acute lymphobla
71 etic stem cell transplantation (alloHSCT) in Philadelphia chromosome-positive (Ph(+)) acute lymphobla
72 development testing in patients with CML and Philadelphia chromosome-positive (Ph(+)) acute lymphobla
73 tyrosine kinase inhibitors are effective in Philadelphia chromosome-positive (Ph(+)) acute lymphobla
74 udy, we identified a unique subpopulation of Philadelphia chromosome-positive (Ph(+)) acute lymphobla
75 hieving complete molecular response (CMR) in Philadelphia chromosome-positive (Ph(+)) acute lymphobla
78 utic options are available for patients with Philadelphia chromosome-positive (Ph(+)) B-precursor acu
79 Whereas all patients were approximately 100% Philadelphia chromosome-positive (Ph(+)) before transpla
81 ht overcome drug resistance in patients with Philadelphia chromosome-positive (Ph(+)) chronic myeloge
82 ated with the development and progression of Philadelphia chromosome-positive (Ph(+)) chronic myeloge
84 ered orally twice daily to 280 patients with Philadelphia chromosome-positive (Ph(+)) chronic myeloid
85 atinib is highly effective at treating human Philadelphia chromosome-positive (Ph(+)) chronic myeloid
86 inib mesylate is the preferred treatment for Philadelphia chromosome-positive (Ph(+)) chronic myeloid
87 at suppresses all BCR-ABL1 single mutants in Philadelphia chromosome-positive (Ph(+)) leukemia, inclu
90 disorders can be broadly characterized into Philadelphia chromosome-positive (Ph(+)) or negative (Ph
92 B) in 268 adults (median age, 47 years) with Philadelphia chromosome-positive (Ph+) acute lymphoblast
93 prevention of resistance in a mouse model of Philadelphia chromosome-positive (Ph+) acute lymphoblast
94 imatinib, for patients with newly diagnosed Philadelphia chromosome-positive (Ph+) acute lymphoblast
97 A2 induced alpha5Beta1-dependent adhesion of Philadelphia chromosome-positive (Ph+) CD34+/HLA-DR+ cel
98 en a remarkable success for the treatment of Philadelphia chromosome-positive (Ph+) chronic myelogeno
99 ls, derived from a patient with blast crisis Philadelphia chromosome-positive (Ph+) chronic myelogeno
100 he outcomes for patients with every stage of Philadelphia chromosome-positive (Ph+) chronic myeloid l
101 nd dasatinib are the preferred treatment for Philadelphia chromosome-positive (Ph+) leukemias, and th
102 ne kinase inhibitor imatinib is effective in Philadelphia chromosome-positive (Ph-positive) leukemias
103 a promising agent for treatment of advanced Philadelphia-chromosome-positive (Ph+) acute lymphoblast
104 ard define optimal response, whereas no CyR (Philadelphia chromosome-positive [Ph+] >95%) at 3 months
106 hronic myeloid leukemia (CML-BC) and against Philadelphia chromosome-positive (Ph1) acute lymphoblast
107 ted donors was investigated in patients with Philadelphia chromosome-positive (Ph1+) acute lymphoblas
108 is chronic myelogenous leukemia (CML-BC) and Philadelphia chromosome-positive (Ph1-positive) acute ly
110 arry the oncogenic BCR-ABL1 tyrosine kinase (Philadelphia chromosome positive), which mimics constitu
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