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1 ts (25%) had toxicity requiring them to stop pentostatin.
2 (MMF), denileukin diftitox (denileukin), or pentostatin.
3 steroid taper was begun after three doses of pentostatin.
4 ine, 3 underwent splenectomy, and 1 received pentostatin.
5 ntial for inappropriate immunosuppression by pentostatin.
6 r were decreased in septic mice treated with pentostatin.
7 ly improved at 48 hours in mice treated with pentostatin.
8 ly attenuated in septic animals treated with pentostatin (0.42 +/- 0.05 versus 0.21 +/- 0.04; p < 0.0
9 re treated with six cycles of induction with pentostatin (2 mg/m(2) on day 1), cyclophosphamide (600
10 emia (CLL), we initiated a trial of combined pentostatin (2 mg/m2), cyclophosphamide (600 mg/m2), and
20 e agent (5) or combined with: rituximab (2), pentostatin (6), fludarabine, cyclophosphamide, and ritu
21 10(-13) M) (8R)-hydroxyl-2'-deoxycoformycin (pentostatin), a transition state analogue, and (6S)-hydr
24 ic inhibition of AMP-metabolizing pathway by Pentostatin activates muscle AMPK, confers resistance to
25 nt 24 hrs in advance of the inciting insult, pentostatin also has the unique potential for use as a t
26 potential usefulness of 2'-deoxycoformycin (pentostatin), an inhibitor of adenosine deaminase, as a
28 Eight dogs were conditioned with 6x4 mg/m pentostatin and 100 cGy TBI, whereas two dogs received 3
29 t introduction of purine nucleoside analogs (pentostatin and cladribine) changed the natural history
32 work has shown that SS1P in combination with pentostatin and cyclophosphamide can result in durable t
33 , sirolimus, mycofenolate mofetil, imatinib, pentostatin and infusion of mesenchymal stem cells have
35 nt of adenosine deaminase in the presence of pentostatin and revealed a protein thermal network that
40 a randomized, intergroup study who received pentostatin as an initial treatment or who crossed over
41 Two hundred forty-one patients treated with pentostatin as initial therapy (n = 154) or who crossed
44 ally, we discuss the differential impacts of pentostatin binding on overall protein flexibility versu
46 of these results, we are currently studying pentostatin, cyclophosphamide, and rituximab (PCR) thera
48 f a phase 2 study evaluating the efficacy of pentostatin, cyclophosphamide, and rituximab in patients
49 to groups to receive saline, bortezomib, the pentostatin/cyclophosphamide (PC) regimen, or the bortez
54 lant Consortium performed a phase 2 trial of pentostatin for steroid-refractory chronic GVHD in 51 ch
60 We examined the toxicity and efficacy of pentostatin in a prospective phase II trial in corticost
64 n the presence of both 1-deaza-adenosine and pentostatin, indicating similar impacts of either ligand
65 Many treatments exist, including cladribine, pentostatin, interferon-alpha, splenectomy, rituximab (m
66 neal cecal slurry) were treated with 1 mg/kg pentostatin intraperitoneally 24 hrs before, or intraven
71 therapy with intravenous alemtuzumab and/or pentostatin, median progression-free survival and overal
74 though the nucleoside analogs cladribine and pentostatin produce high response rates in patients with
76 e results of therapy with new agents such as pentostatin, pulse cyclophosphamide, long-wavelength ult
77 e nucleoside purine analogues cladribine and pentostatin results in lengthy remissions in nearly all
78 a and variant (HCL/HCLv) was to determine if pentostatin-rituximab (DCFR) and bendamustine-rituximab
83 These data indicate that the novel use of pentostatin to prevent systemic inflammatory response sy
84 tients with a confirmed complete response to pentostatin treatment, 5- and 10-year relapse-free survi
88 me were abrogated and survival improved when pentostatin was not given until after signs of the illne