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1 eukemia (ALL) includes prednisone and oral 6-mercaptopurine.
2 dose, and all patients received daily oral 6-mercaptopurine.
3 mined the efficacy of dexamethasone and IV 6-mercaptopurine.
4 ectiveness of the immuno-suppressive agent 6-mercaptopurine.
5 S-methylation of thiopurine drugs such as 6-mercaptopurine.
6 rove on azathioprine but responded well to 6-mercaptopurine.
7 ed notable sensitivities to asparaginase and mercaptopurine.
8 ristine, L-asparaginase, methotrexate, and 6-mercaptopurine.
9 1.27 (95% CI, 0.48-3.39) for azathioprine/6-mercaptopurine.
10 treated with the thiopurines azathioprine or mercaptopurine.
11 ntenance with ATRA, oral methotrexate, and 6-mercaptopurine.
12 rapy comprising ATRA, oral methotrexate, and mercaptopurine.
13 lone or in combination with methotrexate and mercaptopurine.
14 ys 1 to 5, and a regimen of methotrexate and mercaptopurine.
15 ts a decreased V max and increased K m for 6-mercaptopurine.
16 sms in TPMT, can cause severe toxicity after mercaptopurine.
17 travenous methotrexate (1 g/m(2)) with daily mercaptopurine.
18 e mice were pretreated with leflunomide or 6-mercaptopurine.
19 , 11), whereas 6-thio NHD(+) (nicotinamide 6-mercaptopurine 5'-dinucleotide, 17) generates a cyclic d
21 iving in extreme poverty were nonadherent to mercaptopurine (57.1% vs 40.9%); however, poor adherence
24 he aim of the current trial was to compare 6-mercaptopurine (6-MP) and mesalamine with placebo for th
28 kemia (ALL) are generally instructed to take mercaptopurine (6-MP) in the evening and without food or
31 ted AICAR production, or administration of 6-mercaptopurine (6-MP), a clinically approved inhibitor o
34 f immunomodulators [azathioprine (AZA), or 6-mercaptopurine (6-MP)] and newer biologic agents (inflix
35 lassified into a high DI phenotype (either 6-mercaptopurine [6-MP] or methotrexate [MTX] DI >=110% du
37 ed for the simultaneously determination of 6-mercaptopurine, 6-thioguanine and dasatinib for the firs
38 for the selective and precise analysis of 6-mercaptopurine, 6-thioguanine and dasatinib in pharmaceu
39 ata revealed that the electro-oxidation of 6-mercaptopurine, 6-thioguanine and dasatinib is facilitat
40 at pH 8.0, the oxidation peak currents for 6-mercaptopurine, 6-thioguanine and dasatinib were found t
42 bolites of three clinically useful agents (6-mercaptopurine, 6-thioguanine, and Abacavir) can inhibit
47 ned either 6-thioguanine (750 patients) or 6-mercaptopurine (748 patients) during interim maintenance
48 ntenance therapy regimen included daily oral mercaptopurine (75 mg/m2) and weekly oral methotrexate (
49 lecular mechanism(s) of cellular response to mercaptopurine, a widely used antileukemic agent, we ass
50 azathioprine were superior to azathioprine/6-mercaptopurine: adalimumab (OR, 2.9; 95% CrI, 1.6-5.1),
51 In contrast, pretreatment of mice with 6-mercaptopurine, an inhibitor of de novo purine synthesis
53 conferred resistance to chemotherapy with 6-mercaptopurine and 6-thioguanine when expressed in ALL l
54 he MRP4 drug resistance profile extends to 6-mercaptopurine and 6-thioguanine, two anticancer purine
56 an syndrome, the activator of the prodrugs 6-mercaptopurine and allopurinol, and a target for antipar
57 -TP) medications, including 6-thioguanine, 6-mercaptopurine and azathioprine, commonly used for immun
58 he immunosuppressive agents, azathioprine, 6-mercaptopurine and cyclosporine A, are compatible with p
59 lguanine, 8-azaguanine, 6-thioguanine, and 6-mercaptopurine and do not recognize any of the PurP liga
61 -year treatment period with the following: 6-mercaptopurine and metronidazole [6MP/met] (comparator),
62 te the extensive clinical use and study of 6-mercaptopurine and other purine analogues, the cellular
64 g some of the antiproliferative effects of 6-mercaptopurine and potentially implicate Nurr1 as a mole
65 on of MSH6 was associated with resistance to mercaptopurine and prednisone, thereby providing a plaus
68 armacokinetic and pharmacodynamic studies of mercaptopurine and thioguanine were done in Tpmt(-/-), T
70 of TPMT on activation versus inactivation of mercaptopurine and thioguanine, we used a retroviral gen
73 etabolites revealed elevated 6-MMP (6-methyl mercaptopurine) and low 6-TGN (6-thioguanine nucleotide)
74 andard dose of thiopurine (azathioprine or 6-mercaptopurine), and patients homozygous for a variant r
75 vement of guanylate kinase in 6-thioguanine, mercaptopurine, and abasic guanosine analog (e.g., ganci
76 hiopurines including 6-thioguanine ((S)G), 6-mercaptopurine, and azathioprine are effective anticance
77 ine drugs, including 6-thioguanine ((S)G), 6-mercaptopurine, and azathioprine, are widely employed an
78 ptions for 5-aminosalicylates azathioprine/6-mercaptopurine, and corticosteroids were extracted from
79 sessed the pharmacokinetics of methotrexate, mercaptopurine, and erythrocyte thioguanine nucleotide l
80 ians in optimizing therapeutic response to 6-mercaptopurine, and in identifying individuals at increa
81 % CI, 1.3-1.9]), and exposure to platinum, 6-mercaptopurine, and intrathecal chemotherapy, and a lowe
82 erapy followed by prednisone, vincristine, 6-mercaptopurine, and methotrexate (POMP) maintenance chem
84 city during consolidation therapy containing mercaptopurine, and remained significant in a multivaria
87 th doxorubicin, vincristine, corticosteroid, mercaptopurine, and weekly high-dose asparaginase; and c
88 tarabine/etoposide; high-dose methotrexate/6-mercaptopurine; and daunorubicin, vincristine, prednison
91 nd Arg221, the only polar amino acids near 6-mercaptopurine, are highlighted as possible participants
92 ceptor Nurr1, interestingly, we identified 6-mercaptopurine as a specific activator of this receptor.
93 d following treatment with 10 daily doses of mercaptopurine at 100 mg/kg/d (0%, 68%, and 100% 50-day
94 resolution and the chemotherapeutic agent 6-mercaptopurine at 2.6 A resolution have been determined,
95 web-based randomisation system to oral daily mercaptopurine at a dose of 1 mg/kg bodyweight rounded t
96 of asparagine synthetase or treatment with 6-mercaptopurine attenuated the increased function of GLAS
97 ictor of outcome, but a direct comparison of mercaptopurine AUC in the remission and relapsed patient
99 Thiopurine drugs (i.e., thioguanine [TG], mercaptopurine, azathioprine) are commonly used for the
100 the S-methylation (that is, inactivation) of mercaptopurine, azathioprine, and thioguanine and exhibi
102 ntial 6-methylmercaptopurine production on 6-mercaptopurine/azathioprine (odds ratio, 3.0; 95% CI, 1.
104 rticosteroids alone, 52 patients receiving 6-mercaptopurine/azathioprine alone or with corticosteroid
105 who were receiving corticosteroids and/or 6-mercaptopurine/azathioprine before surgery compared with
106 bowel disease receive corticosteroids and 6-mercaptopurine/azathioprine during elective bowel surger
107 adjusted odds ratio for patients receiving 6-mercaptopurine/azathioprine for any and major infectious
108 ine/azathioprine alone and the addition of 6-mercaptopurine/azathioprine for patients receiving corti
112 acid decreases V max and increases K m for 6-mercaptopurine but not K m for S-adenosyl- l-methionine.
113 xic effects of thiopurine prodrugs such as 6-mercaptopurine by methylating them in a reaction using S
117 Seven ALL drugs (asparaginase, prednisolone, mercaptopurine, dasatinib, nelarabine, daunorubicin, and
118 regimens containing either oral (PO) MTX, PO mercaptopurine, dexamethasone, and vincristine or IV MTX
121 undred ninety-one methotrexate doses and 190 mercaptopurine doses were monitored in 89 patients.
125 teroids and/or cyclosporine, azathioprine, 6-mercaptopurine, FK-506, methotrexate) were identified an
128 p analysis, three (10%) of 29 smokers in the mercaptopurine group and 12 (46%) of 26 in the placebo g
129 pared with 13 (13%) of 99 non-smokers in the mercaptopurine group and 14 (16%) of 86 in the placebo g
131 treatment in 39 (30%) of 128 patients in the mercaptopurine group versus 41 (37%) of 112 in the place
132 topurine; however, patients assigned to IV 6-mercaptopurine had decreased survival after relapse.
136 nferred comparable levels of resistance to 6-mercaptopurine in B-ALL cells both in vitro and in vivo.
138 eport our experience with azathioprine and 6-mercaptopurine in patients with microscopic colitis.
139 potential benefit from the earlier use of 6-mercaptopurine in T-ALL therapy or the development of ad
140 = 39) comparing methotrexate, azathioprine/6-mercaptopurine, infliximab, adalimumab, certolizumab, ve
143 oietic toxicity in vivo after treatment with mercaptopurine is attenuated but not abolished by MSH2 d
145 es of the human polymorphism; indicates that mercaptopurine is more affected by the TPMT polymorphism
147 nosuppressant thiopurines, azathioprine or 6-mercaptopurine, is associated with acute skin sensitivit
148 (TPMT) are known to have a marked effect on mercaptopurine metabolism and toxicity; however, some pa
149 rine methyl transferase and measurement of 6-mercaptopurine metabolites appear to be valuable for man
151 95% CI, 1.17-2.58; P = .006), azathioprine/6-mercaptopurine monotherapy (OR, 1.84; 95% CI, 1.30-2.61;
152 py, methotrexate monotherapy, azathioprine/6-mercaptopurine monotherapy, and Janus kinase (Jak) inhib
153 f vincristine, adriamycin, prednisone, and 6-mercaptopurine (MP) and after continuous infusion of hig
154 ubstitution of oral 6-thioguanine (TG) for 6-mercaptopurine (MP) and triple intrathecal therapy (ITT)
156 uorouracil, cytosine arabinoside (araC), and mercaptopurine (MP) demonstrated that Hmgb1(-/-) mouse e
157 (IBD), who have failed azathioprine (AZA) or mercaptopurine (MP) due to adverse events or suboptimal
160 widely used antileukemic agent, we assessed mercaptopurine (MP) sensitivity in mismatch repair (MMR)
165 -cell ALL included 2 years of treatment with mercaptopurine, MTX, vincristine, and prednisone (POMP).
168 ower risk of isolated CNS relapse than did 6-mercaptopurine (odds ratio [OR] 0.53, 95% CI 0.30-0.92,
170 s in the azathioprine group were switched to mercaptopurine or methotrexate therapy because of intole
171 rexate sodium (OR, 0.60; 95% CI, 0.29-1.22), mercaptopurine (OR, 0.62; 95% CI, 0.15-2.53), and mycoph
172 s (OR, 3.4; 95% CI, 1.8-6.2), azathioprine/6-mercaptopurine (OR, 3.1; 95% CI, 1.7-5.5), and inflixima
173 rd, second-line (mycophenolate mofetil and 6-mercaptopurine) or third-line (tacrolimus or cyclosporin
174 xposed to 5-aminosalicylates, azathioprine/6-mercaptopurine, or corticosteroids during their first tr
175 iffered among genotypes after treatment with mercaptopurine (P < 0.0001 and P = 0.044, respectively)
178 rine regulation of Nurr1 demonstrates that 6-mercaptopurine regulates Nurr1 through a region in the a
183 (p < 0.05) increased the S6-(4-nitrobenzyl)-mercaptopurine riboside (NBMPR) IC50 values by approxima
184 th trisomy of chromosomes 16 and 17, whereas mercaptopurine sensitivity was linked to gains of chromo
187 contrast, TPMT+ cells were more sensitive to mercaptopurine than MOCK cells (IC(50) = 0.52 +/- 0.20 m
188 inhibitor in combination with azathioprine/6-mercaptopurine therapy (odds ratio [OR], 1.74; 95% CI, 1
189 bo-controlled trial reported the efficacy of mercaptopurine therapy for children newly diagnosed with
190 nhibitors in combination with azathioprine/6-mercaptopurine therapy, methotrexate monotherapy, azathi
194 adenosyl- l-homocysteine and the substrate 6-mercaptopurine, to 1.8 and 2.0 A resolution, respectivel
195 identify additional genetic determinants of mercaptopurine toxicity, a genome-wide analysis was perf
196 with wild-type TPMT develop toxicity during mercaptopurine treatment for reasons that are not well u
197 econd DI; however, replacement of PO MTX, PO mercaptopurine, vincristine, and dexamethasone during IM
198 ved 30 courses of maintenance therapy with 6-mercaptopurine, vincristine, methotrexate, and prednison
199 ars post-CR date, alternated three cycles of mercaptopurine, vincristine, methotrexate, and prednison
200 lternating blocks of three cycles of POMP (6-mercaptopurine, vincristine, methotrexate, and prednison
201 aintenance therapy with dose-reduced POMP (6-mercaptopurine, vincristine, methotrexate, and prednison
202 The higher sensitivity of TPMT+ cells to mercaptopurine was associated with higher concentrations
204 used antileukemic agents (eg, methotrexate, mercaptopurine), we determined the rate of DNPS and the
205 that 6-thioguanine is more effective than 6-mercaptopurine, we compared the efficacy and toxicity of
206 xhibited a haploinsufficient phenotype after mercaptopurine, whereas haploinsufficiency was less prom
209 particular sensitivities to asparaginase and mercaptopurine, with chromosome-specific associations.
210 ient response to the chemotherapeutic drug 6-mercaptopurine, with some model parameters being patient
211 with NT5C2 mutations are chemoresistant to 6-mercaptopurine yet show impaired proliferation and self-