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1  intensification 3 (high-dose cytarabine and l-asparaginase).
2 ase (ASNS) was not predictive of response to l-asparaginase.
3 n pattern was associated with sensitivity to l-asparaginase.
4 xpectedly high rate of allergic reactions to L-asparaginase.
5 a continuous infusion of high-dose ara-C and L-asparaginase.
6 poside, but not to a non-DNA damaging agent, l-asparaginase.
7 n regimen of vincristine, dexamethasone, and l-asparaginase.
8 th a regimen of prednisone, vincristine, and L-asparaginase.
9  present in lymphoblasts are able to degrade l-asparaginase.
10 duction and then high-dose methotrexate with l-asparaginase.
11  almost identical to that observed for other L-asparaginases.
12 ent regions found in other type-II bacterial L-asparaginases.
13 th the structures of other type-II bacterial L-asparaginases.
14 cement rather than a ping-pong mechanism for l-asparaginases.
15                  Because gpASNase1 and human L-asparaginase 1 (hASNase1) share 70% amino-acid identit
16 biochemically characterized the enzyme human L-asparaginase 3 (hASNase3), which possesses L-asparagin
17                            After exposure to l-asparaginase, 5 cell lines and 10 clinical samples exh
18 L-asparaginase 3 (hASNase3), which possesses L-asparaginase activity and belongs to the N-terminal nu
19 ty than WoA-P121, yet both showed comparable L-asparaginase activity.
20 th non-reducing alternatives, application of L-asparaginase, addition of divalent cations which affec
21 vation therapy using the clinical stage drug L-asparaginase after frontline treatment with docetaxel.
22 e regimen of vincristine, dexamethasone, and L-asparaginase against Ph-like ALL xenografts, offering
23                         Current FDA-approved l-asparaginases also possess significant l-glutaminase a
24  in combination with chemotherapy containing L-asparaginase, an enzyme that uncovers the glutamine de
25               Over the past several decades, L-asparaginase, an important component of therapy for ac
26                          Regimens containing l-asparaginase and drugs unaffected by P-glycoprotein ar
27 types exhibiting the greatest sensitivity to L-asparaginase and glucocorticoids.
28 ication courses (high-dose methotrexate plus L-asparaginase and hyper-CVAD plus ofatumumab on courses
29 n the amino acid sequence of W. succinogenes L-asparaginase and that of related enzymes are discussed
30 emotherapeutic agents including doxorubicin, l-asparaginase, and dexamethasone.
31                     Since currently approved L-asparaginases are of bacterial origin, immunogenicity
32                                              L-Asparaginases are used to treat acute lymphoblastic le
33                  Coupled with the success of L-asparaginase as a therapy for childhood leukemia, the
34 illing factor was shown to be an enzyme with L-asparaginase (ASNase) activity.
35                                              l-asparaginase (ASNase) is a first-line therapy for ALL
36     Depletion of circulating asparagine with l-asparaginase (ASNase) is a mainstay of leukemia treatm
37 ric biotherapeutic enzyme (anticancer agent) l-asparaginase (ASNase) were studied.
38 rian cancer cell response to the enzyme-drug L-asparaginase (ASNase).
39                                              L-Asparaginases (ASNases) have been used as first line d
40 ic syndrome in acute promyelocytic leukemia, L-asparaginase-associated thrombosis, leukemic meningiti
41 is recognized as a prognostic biomarker, and l-asparaginase-based treatments (e.g., Asparlas) are fre
42 thylene glycol conjugate of Escherichia coli L-asparaginase, by intravenous infusion in children with
43                                              L-Asparaginase CLEAs were prepared utilizing sodium trip
44 sted of five drugs (vincristine, prednisone, l-asparaginase, daunorubicin, and cyclophosphamide).
45 ion current treatment of ALL using different l-asparaginase delivery and encapsulation methods as wel
46  or treatment with the glutaminolytic enzyme l-asparaginase depleted the cell contents of Gln, glutam
47 e structural and functional integrity of the L-asparaginase domain and provide a direct comparison of
48 nd a novel dosing method of Escherichia coli L-asparaginase (EC-Asnase) in children and adolescents w
49 published previously for complexes of type I L-asparaginase (EcAI) from E. coli.
50                                    Bacterial L-asparaginases, enzymes that catalyze the hydrolysis of
51 ribed structures of the Erwinia chrysanthemi l-asparaginase (ErA) to inform the design of mutants wit
52 res of the complexes of Erwinia chrysanthemi L-asparaginase (ErA) with the products of such reactions
53 s for the clinical agents 5-fluorouracil and L-asparaginase exemplify how variations in the transcrip
54  samples, increased expression of ASNS after l-asparaginase exposure was not associated with in vitro
55 f an evolutionary conserved motif among this L-asparaginase family.
56  orange-emitting CDs (O-CDs), and the enzyme L-asparaginase for ratiometric detection of L-asparagine
57 hanism of hydrolysis of L-Asn by the type II L-asparaginase from E. coli (EcAII), but that work was l
58                                A recombinant L-asparaginase from Geobacillus kaustophilus was immobil
59 report, we postulate that all homotetrameric L-asparaginases from mesophilic bacteria utilize a commo
60              We are exploring the guinea pig L-asparaginase (gpASNase1) as a potential replacement of
61 We recently identified the low KM guinea pig L-asparaginase (gpASNase1).
62  Our long-term goal is the design of a human l-asparaginase (hASNase3) variant, suitable for use in c
63 ic use, we determined the structure of human l-asparaginase (hASNase3).
64    Many side effects of current FDA-approved L-asparaginases have been related to their secondary L-g
65                           However, all human L-asparaginases have millimolar KM for asparagine.
66 respondingly, pharmacologic profiling showed L-asparaginase hypersensitivity in the siTop1 cells.
67 del of infection, S Typhimurium lacking both l-asparaginase I and II genes competes poorly with wild-
68 rily to the periplasm and acts together with l-asparaginase I to provide S Typhimurium the ability to
69  L-asparaginase structural homology isozymes L-asparaginases I (AnsA) and II (AnsB), which are shown
70 citrate anion to the active sites of E. coli L-asparaginases I and II, even in the presence of the na
71 rapy with a glucocorticoid, vincristine, and L-asparaginase if the patient responds poorly.
72                             Escherichia coli L-asparaginase II (EcAII), the only nonhuman enzyme appr
73                                              l-asparaginase II (MW 135 kDa) from E. coli is an FDA-ap
74 , we have studied the catalytic mechanism of L-asparaginase II computationally.
75                   S. Typhimurium lacking the L-Asparaginase II gene (STM3106) are unable to inhibit T
76                                              L-Asparaginase II is necessary and sufficient to suppres
77                  Furthermore, we report that l-asparaginase II localizes primarily to the periplasm a
78 aragine deprivation such as that mediated by l-asparaginase II of S Typhimurium causes suppression of
79                    We previously showed that l-asparaginase II produced by Salmonella enterica serova
80  (dsbA) of Escherichia coli, is required for l-asparaginase II stability and function.
81  homogeneity determined that the periplasmic l-asparaginase II, AnsB (EC 3.5.1.1), co-purified with A
82 murium inhibit T cell responses by producing L-Asparaginase II, which catalyzes the hydrolysis of L-a
83                                              L-Asparaginase-II from Escherichia coli (EcA) is a centr
84 h at baseline and after in vitro exposure to l-asparaginase in cell lines and pediatric ALL samples.
85 n cooperates with chemotherapy, particularly L-asparaginase, in reducing live KMT2A-AFF1 infant ALL c
86 s not associated with in vitro resistance to l-asparaginase, indicating that ASNS-independent mechani
87  but not in normal lymphocytes, ABT-737 plus L-asparaginase induced greater mitochondrial depolarizat
88 orated cyclophosphamide and the early use of L-asparaginase into the backbone of daunorubicin, vincri
89                                              L-asparaginase is a chemotherapy drug used to treat acut
90                                              l-Asparaginase is a key therapeutic agent for treatment
91                                              l-asparaginase is a universal component of treatment for
92 istration of the asparagine depletion enzyme l-asparaginase is an important therapy option.
93  of the two Bacillus subtilis genes encoding L-asparaginase is controlled by independent regulatory f
94 kemic protein macromolecule Escherichia coli L-asparaginase is degraded by leukemic lysosomal cystein
95                                              L-asparaginase is important in the induction regimen for
96 e main prerequisite for clinical efficacy of L-asparaginases is micromolar KM for asparagine to allow
97                                              l-asparaginase (l-ase) is an anticancer agent also harbo
98                                   The enzyme L-asparaginase (L-ASNase) is used in the treatment of Ac
99                                              L-Asparaginase (L-ASP) is a key component of therapy for
100                Allergies to Escherichia coli L-asparaginase (L-ASP) occurred in 35% of patients.
101 for thrombosis, caused in part by the use of l-asparaginase (L-ASP).
102                            Type II bacterial L-asparaginases (L-ASP) have played an important therape
103 Upon enzymatic hydrolysis of L-asparagine by L-asparaginase, liberated ammonia induced a pH increase
104 y, we also show that these highly human-like L-asparaginases maintain their in vitro ALL killing pote
105 les, including corticosteroids, vincristine, L-asparaginase, methotrexate, and 6-mercaptopurine.
106 s, we successfully predicted the more active L-asparaginase mutants N24T and N24A.
107                 To investigate the effect of l-asparaginase on acute lymphoblastic leukemia (ALL), we
108                                              l-asparaginase, one of the primary drugs used in treatme
109 served in all 7 cell lines with ABT-737 plus L-asparaginase or vincristine, and in 5 of 7 cell lines
110 -glutaminase activity of these highly active l-asparaginases, our engineered ErA variants hold promis
111 tigate if an intensive exposure to pegylated L-asparaginase (PEG-ASNASE, 2,500 IU/sqm once a week x 4
112                                    Bacterial L-asparaginases play an important role in the treatment
113   The mechanisms of therapeutic failure with l-asparaginase remain speculative.
114              This bacterial-type cytoplasmic L-asparaginase resides in the N-terminal subdomain of an
115 that ASNS-independent mechanisms of in vitro l-asparaginase resistance are common in ALL.
116 LL cells may provide a novel way to overcome l-asparaginase resistance.
117 seline gene expression pattern distinguished l-asparaginase sensitivity from resistance.
118 ructure of ErA with those of other bacterial L-asparaginases shows that the presence of two active-si
119 itor and depletion of extracellular Asn with L-asparaginase significantly reduced Asn production and
120 he characterization of water dynamics on the L-asparaginase structural homology isozymes L-asparagina
121 sed on the characterization of another human L-asparaginase, termed hASNase1.
122  understanding of the catalytic mechanism of L-asparaginases that is in agreement with the available
123 y mutational analysis to encode a functional L-asparaginase, the expression of which is activated dur
124         The addition of dexamethasone and/or L-asparaginase to reduced-intensity dasatinib therapy im
125 he present study, we successfully engineered L-asparaginase to resist proteolytic cleavage and at the
126                  The exact mechanism used by L-asparaginases to catalyze the hydrolysis of asparagine
127           ASNS expression can counterbalance l-asparaginase treatment by mitigating nutrient stress.
128  explain why ALL cells are most sensitive to l-asparaginase treatment compared with other cancers.
129 e to Asn restriction by knockdown of ASNS or L-asparaginase treatment to deplete the intracellular an
130 ination with vincristine, dexamethasone, and L-asparaginase (VXL) in 7 ALL cell lines.
131 e the MTD in combination with cytarabine and l-asparaginase was 2 mg/m(2).
132 n of the ansA gene, which encodes the second L-asparaginase, was found to be induced by asparagine.
133 he N24A and N24A R195S mutations to the drug L-asparaginase, we are a step closer to individualized d
134 tertiary structure of Wolinella succinogenes L-asparaginase were determined, and were compared with t
135 esult of this observation, several bacterial L-asparaginases were developed and are currently approve
136  notable examples of a therapeutic enzyme is L-asparaginase, which has been established as an antileu
137 S-PEG), a pegylated form of Escherichia coli L-asparaginase with a succinimidyl succinate (SS) linker
138  our engineered ErA variants hold promise as l-asparaginases with fewer side effects.
139                                   Therefore, l-asparaginases with reduced l-glutaminase activity are
140                   The Wolinella succinogenes L-asparaginase (WoA) has been reported to be L-glutamina

 
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