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1 ating with cyclophosphamide, idarubicin, and vincristine.
2 ignificant anticancer agents vinblastine and vincristine.
3 (EdU), and then treated each population with vincristine.
4 nated axons in the sural nerve and toe after vincristine.
5 opathy induced by the chemotherapeutic agent vincristine.
6 at included treatment with 36 to 39 doses of vincristine.
7 ng treatment with doxorubicin, etoposide and vincristine.
8 n the centroblast subtype to doxorubicin and vincristine.
9 ensive anti-cancer compounds vinblastine and vincristine.
10 spect to discontinuation of bleomycin and/or vincristine.
11 luding the anti-cancer drugs vinblastine and vincristine.
12 eukemia cells increased their sensitivity to vincristine.
13 utinib did not alter the pharmacokinetics of vincristine.
14  which the anti-cancer drugs vinblastine and vincristine.
15 er before and (18)F-FDG after treatment with vincristine.
16  combination of cisplatin, fluorouracil, and vincristine.
17 nt and in combination with dexamethasone and vincristine.
18               Nine animals were treated with vincristine (0.75 mug/g/d).
19 nous doxorubicin 50 mg/m(2), and intravenous vincristine 1.4 mg/m(2) [maximum 2.0 mg] all on day 1 of
20 ide 750 mg/m(2), doxorubicin 50 mg/m(2), and vincristine 1.4 mg/m(2) [to a maximum of 2 mg total dose
21 f vincristine intravenously (A+CHP group) or vincristine 1.4 mg/m(2) and a placebo form of brentuxima
22 (1:1) by a minimisation technique to receive vincristine 1.5 mg/m(2) at weeks 1-8, 11, 12, 14, 15, 17
23 ldren <10 kg) intravenous push on day 2; and vincristine (1.5 mg/m(2) per day to a maximum dose of 2
24 [750 mg/m(2)], doxorubicin [50 mg/m(2)], and vincristine [1.4 mg/m(2), up to 2 mg] all on day 1, and
25 surable disease were eligible to receive VI (vincristine, 1.5 mg/m(2) per day intravenously on days 1
26  patients receiving </= or > three cycles of vincristine (5-year PFS difference, -1.3%; 95% CI, -5.6%
27                                              Vincristine, a widely used chemotherapeutic agent, produ
28 re treated with chemotherapy based on either vincristine, actinomycin, and cyclophosphamide or vincri
29 istine, actinomycin, and cyclophosphamide or vincristine, actinomycin, and ifosfamide-based chemother
30  resistant to conventional chemotherapy with vincristine, actinomycin-D, and doxorubicin given singly
31  predominantly axonal damage: Paclitaxel and vincristine affected mostly large myelinated fibers, bor
32 carbazine, lomustine (also called CCNU), and vincristine after radiation therapy at the time of initi
33 ere injected with the chemotherapeutic drug, vincristine, alone or in combination with fractionated i
34 ed 4 weeks of preoperative chemotherapy with vincristine and actinomycin D.
35 EC chemotherapy with a 5-drug combination of vincristine and carboplatin, alternating with cyclophosp
36 phosphamide dose, 26.4 g/m(2)) compared with vincristine and dactinomycin (VA) for patients with subs
37 e may replace ifosfamide in combination with vincristine and dactinomycin (vincristine, dactinomycin,
38 cs were governed by the protonation state of vincristine and doxorubicin and were tunable based on si
39 s were studied with cationic oncology drugs, vincristine and doxorubicin, with a focus on hydrophobic
40           AREN0321 evaluated the activity of vincristine and irinotecan (VI) in patients with newly d
41 ogy Group Protocol AHEP0731 and treated with vincristine and irinotecan (VI).
42  MCT1 inhibition was highly synergistic with vincristine and LDHA inhibition under cell culture condi
43 roteins were sequestered in the cytoplasm by vincristine and paclitaxel but not by an aurora kinase i
44  maintenance with ponatinib 45 mg daily with vincristine and prednisone monthly for 2 years followed
45  that include cyclophosphamide, doxorubicin, vincristine and prednisone, where the majority of dogs a
46  indole alkaloid (MIA)-type anticancer drugs vincristine and vinblastine, we identified a jasmonate-r
47 ids (TIAs), including the chemotherapeutics, vincristine and vinblastine.
48 ressive options, including cyclophosphamide, vincristine, and cyclosporine.
49 ver 70 years) with intrathecal chemotherapy, vincristine, and dexamethasone during induction.
50  treated with modified infusional etoposide, vincristine, and doxorubicin with cyclophosphamide and p
51 ne, and etoposide with or without topotecan, vincristine, and doxorubicin) and achieved an adequate d
52 sed use of common chemotherapies (melphalan, vincristine, and doxorubicin), novel agents (thalidomide
53 doses of pegylated asparaginase, 18 doses of vincristine, and escalated-dose intravenous methotrexate
54 n (cisplatin, carboplatin, cyclophosphamide, vincristine, and etoposide with or without topotecan, vi
55 eived a 3-drug induction with dexamethasone, vincristine, and pegaspargase (PEG) and were then classi
56               Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)-based chemotherapy
57 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) to uncover molecu
58 rd rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP; rituximab 375 mg/
59 of rituximab, gemcitabine, cyclophosphamide, vincristine, and prednisolone (R-GCVP) in patients consi
60 of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone every 21 days (R-CHOP21) r
61 as rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (58%), with local radiation
62 e compared with rituximab, cyclophosphamide, vincristine, and prednisone (adjusted HR, 0.94; 95% CI,
63  treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) +/- rituximab were us
64  etoposide to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) and upfront consolida
65 imab (R) into cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) by Coiffier and colle
66 our cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy as a sta
67 six cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy at 3-wee
68 s of standard cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy plus inv
69 sponse rate to cyclophosphamide, adriamycin, vincristine, and prednisone (CHOP) chemotherapy.
70 A+CHP) versus cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) for the treatment of
71 ive cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or CHOP plus rituxima
72 imens such as cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) remain the standard f
73 evaluation of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) with rituximab in NLP
74 imens, namely cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), nowadays represent t
75 n used in combination with cyclophosphamide, vincristine, and prednisone (CVP) in patients with newly
76 acodynamics of GP2013 plus cyclophosphamide, vincristine, and prednisone (GP2013-CVP) with rituximab-
77 th rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (P = .037), independent of c
78 nutuzumab and cyclophosphamide, doxorubicin, vincristine, and prednisone (R-/G-CHOP) chemotherapy in
79 ed rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) and radiation thera
80 th rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) and the impact of a
81 rd rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) as frontline therap
82 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) at the British Colu
83 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) could decrease rate
84 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has become standard
85 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) in the RICOVER-60 t
86 to rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) on outcomes in prev
87 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) or intensive front-
88 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) or R-CHOP-like ther
89 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treatment failure.
90 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) were assembled on t
91 rd rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP), patients who fail
92 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP)-14 (eight cycles) w
93 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).
94 bination with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).
95 of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).
96 is rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).
97 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP; or variant) across
98 y consisting of rituximab, cyclophosphamide, vincristine, and prednisone (R-CVP).
99 ght cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone [CHOP] or eight cycles of cy
100 (treated with cyclophosphamide, doxorubicin, vincristine, and prednisone [CHOP], n = 270; treated wit
101  [CHOP] or eight cycles of cyclophosphamide, vincristine, and prednisone [CVP]), every 3 weeks during
102 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone [R-CHOP] or rituximab plus c
103 [R-CHOP] or rituximab plus cyclophosphamide, vincristine, and prednisone [R-CVP]) for treatment-naive
104 six cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone administered at an interval
105 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone and 6 cyclophosphamide, doxo
106 th rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone compared with rituximab, cyc
107 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone delivered in a 21-day cycle
108 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone given every 14 days (R-CHOP-
109 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone given every 21 days with int
110 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone immunochemotherapy compared
111 e (BV-CHP) vs cyclophosphamide, doxorubicin, vincristine, and prednisone in the ECHELON-2 trial are p
112 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone on a 14-day schedule (6xR-CH
113 of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone or rituximab, etoposide, pre
114 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone therapy or the like.
115 CHOP (cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone) alternating with R-high-dos
116 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) and R-FM (rituximab plus fl
117 y (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) and the other half with R-A
118 P (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) at the British Columbia Can
119 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy.
120 P (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) clearly show the clinical v
121 P (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) could improve outcomes in p
122 P (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) could overcome these diffic
123 such as CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) for diffuse large B-cell ly
124 dnisone and 6 cyclophosphamide, doxorubicin, vincristine, and prednisone) for DLBCL.
125 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) into maintenance lenalidomi
126 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is standard care for aggres
127 cles of CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) plus radiotherapy (CHOP3RT)
128 ared R-CVP (rituximab plus cyclophosphamide, vincristine, and prednisone) with R-CHOP (rituximab plus
129 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone), with the latter selected t
130 P (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone).
131 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone); this new combination is kn
132 FL treated with rituximab, cyclophosphamide, vincristine, and prednisone, and a clinical trial valida
133 rt treated with rituximab, cyclophosphamide, vincristine, and prednisone, event-free survival has imp
134  A regimen of cyclophosphamide, doxorubicin, vincristine, and prednisone, with (R-CHOP) or without (C
135 otherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone, with or without melatonin.
136 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone.
137 survival over cyclophosphamide, doxorubicin, vincristine, and prednisone.
138 ituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone: OR, 7.09; c-statistic, 0.88
139 ed cyclophosphamide and methotrexate, capped vincristine, and used combination intrathecal chemothera
140 was to characterize paclitaxel-, cisplatin-, vincristine- and bortezomib-induced neuropathy in C57BL/
141 tabolites that includes the anticancer agent vincristine, antimalarial quinine and neurotoxin strychn
142                              Vinblastine and vincristine are condensed from the monoterpenoid indole
143 itumor substances related to vinblastine and vincristine are exclusively found in the Catharanthus ro
144 ore and the Total Neuropathy Score-pediatric vincristine, are promising but require further testing.
145 HOP or in combination with CHP (CHOP without vincristine) as front-line treatment in patients with CD
146 r for the anti-cancer agents vinblastine and vincristine, as well as other biologically active compou
147                               Treatment with vincristine at a dose of 1.5 or 2.0 mg/m2.
148 athway appear to be a feature of vinblastine/vincristine biosynthesis.
149 ne (ABVD) with mechlorethamine, doxorubicin, vincristine, bleomycin, vinblastine, etoposide, and pred
150 h two cycles of cisplatin, fluorouracil, and vincristine can ensure disease control in patients with
151  a WEE1 inhibitor (AZD1775), irinotecan, and vincristine can lead to complete response in multiple rh
152           Conclusion Topotecan combined with vincristine, carboplatin, and aggressive focal therapies
153 eceived six cycles of adjuvant chemotherapy (vincristine, carboplatin, and etoposide).
154 ekly intraperitoneal injections of 1.5 mg/kg vincristine cause pronounced mechanical and heat hyperal
155 t recipient mice and restored sensitivity to vincristine chemotherapy in MLL-rearranged B-ALL patient
156 ddition of PCV (procarbazine, lomustine, and vincristine) chemotherapy to radiotherapy (RT) for patie
157  dose-adjusted EPOCH (etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin) and achi
158                EPOCH (etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin) is a pre
159 dnisone or rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin.
160 ompared dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituxima
161 inations of drugs incorporating doxorubicin, vincristine, cyclophosphamide, ifosfamide, etoposide, an
162 th stage I/II disease received regimen DD4A (vincristine, dactinomycin and doxorubicin) but no radiat
163 andard treatment (nine cycles of ifosfamide, vincristine, dactinomycin with or without doxorubicin, a
164 roved failure-free survival (FFS) rates with vincristine, dactinomycin, and cyclophosphamide (VAC; to
165 mbination with vincristine and dactinomycin (vincristine, dactinomycin, and cyclophosphamide [VAC] v
166 ith stage III/IV disease received regimen M (vincristine, dactinomycin, and doxorubicin alternating w
167 istology Wilms tumor (FHWT) is Regimen DD4A (vincristine, dactinomycin, and doxorubicin) and radiatio
168  treated with 3-drug induction chemotherapy (vincristine, dactinomycin, and doxorubicin) for 6 or 12
169 icin, and etoposide (VIDE) and one course of vincristine, dactinomycin, and ifosfamide (VAI) before e
170 , dactinomycin, and cyclophosphamide [VAC] v vincristine, dactinomycin, and ifosfamide [VAI]) after a
171 treatment of ibrutinib with dexamethasone or vincristine demonstrated synergistic activity against pr
172 odified hyper-cyclophosphamide, doxorubicin, vincristine, dexamethasone (VcR-CVAD) induction chemoimm
173 ivo efficacy of an induction-type regimen of vincristine, dexamethasone, and L-asparaginase against P
174 rafts compared with a combination regimen of vincristine, dexamethasone, and l-asparaginase.
175        Maintenance therapy was dasatinib and vincristine/dexamethasone reinductions for 18 months fol
176                                Bleomycin and vincristine discontinuation because of drug-specific adv
177 2) was associated with impaired flexibility, vincristine dose >/=39 mg/m(2) with peripheral neuropath
178 heral neuropathy and subsequently adjust the vincristine dose accordingly.
179 ranches or distal toe nerve fascicles at the vincristine dose used in this study.
180 reduced by 30% for dexamethasone and 50% for vincristine, doxorubicin, and cyclophosphamide, which sh
181 ients randomly assigned to cyclophosphamide, vincristine, doxorubicin, and dexamethasone (CVAD) induc
182 ycles of hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone (hyper-CVAD)
183 on and lenalidomide in maintenance), and the vincristine, doxorubicin, and dexamethasone (VAD) group
184 rst-line hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone alternating
185 regimen (hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone) on courses
186 B-DLBCLs in both the CHOP (cyclophosphamide, vincristine, doxorubicin, and prednisone) and the rituxi
187 in the National Wilms Tumor Study 5 (NWTS-5; vincristine, doxorubicin, cyclophosphamide, and etoposid
188 a prompted modification of cyclophosphamide, vincristine, doxorubicin, high-dose methotrexate/ifosfam
189 ed with six cycles of cisplatin/fluorouracil/vincristine/doxorubicin (C5VD), and nonresponders receiv
190 tandard imatinib/hyperCVAD (cyclophosphamide/vincristine/doxorubicin/dexamethasone) therapy (arm B) i
191 he response to three chemotherapeutic drugs (vincristine, etoposide and methotrexate).
192 2 groups: group A patients were treated with vincristine, etoposide, and carboplatin (VEC) and group
193 High-dose chemotherapy with a combination of vincristine, etoposide, and carboplatin in patients with
194                               Following IVC (vincristine, etoposide, and carboplatin), adjuvant treat
195 , because in the absence of Nav1.6 channels, vincristine failed to alter TTX-S Na+ current density in
196  chemotherapy: two courses of topotecan plus vincristine followed by three alternating administration
197 ncristine for two courses and topotecan plus vincristine for one course, with optional periocular car
198 ternating administrations of carboplatin and vincristine for two courses and topotecan plus vincristi
199 ating with cyclophosphamide, idarubicin, and vincristine, for stage III retinoblastoma.
200 ing the low-level anticancer vinblastine and vincristine, for which the late biosynthetic steps occur
201  intensive induction chemotherapy containing vincristine, ifosfamide, doxorubicin, and etoposide (VID
202 ts received chemotherapy with six courses of vincristine, ifosfamide, doxorubicin, and etoposide (VID
203 zed, bleomycin was discontinued in 17.6% and vincristine in 32.6%.
204 stigated whether substituting bortezomib for vincristine in frontline therapy with R-CHOP (rituximab,
205                    The role of bleomycin and vincristine in the treatment of patients with advanced H
206 rted NMNAT2-specific neuroprotection against vincristine-induced cell death while four selected NMNAT
207 r, we followed nocodazole-, colchicine-, and vincristine-induced depolymerization events of tyrosinat
208                          Using traumatic and vincristine-induced injury models in neurons, we demonst
209  nerve degeneration is not a prerequisite of vincristine-induced mechanical allodynia in this model.
210 ent and it contributes to the maintenance of vincristine-induced mechanical allodynia.
211                                 Grade 2 to 4 vincristine-induced neuropathy during continuation thera
212  channels are involved in the development of vincristine-induced neuropathy.
213                                              Vincristine-induced peripheral neuropathy was assessed a
214 e-nucleotide polymorphism (SNP) analysis and vincristine-induced peripheral neuropathy were assessed
215 ay be a viable therapeutic option to prevent vincristine-induced peripheral polyneuropathy and possib
216 redominant axonal polyneuropathy that mimics vincristine-induced peripheral polyneuropathy in humans.
217  deletion of SARM1 blocks the development of vincristine-induced peripheral polyneuropathy in mice.
218 ing this pathway prevents the development of vincristine-induced peripheral polyneuropathy.
219                                        Thus, vincristine induces distinct death programs in primary A
220 dria in neuronal cells, whereas eribulin and vincristine inhibited transport only at significantly hi
221 imab vedotin 1.8 mg/kg and a placebo form of vincristine intravenously (A+CHP group) or vincristine 1
222                                              Vincristine is a core chemotherapeutic drug administered
223                                    Liposomal vincristine is also approved for relapsed disease.
224 oxicity profiles, including corticosteroids, vincristine, L-asparaginase, methotrexate, and 6-mercapt
225                               Treatment with vincristine led to reduced tumor growth, which was effic
226 ckdown in combination with either ABT-737 or vincristine markedly reduced leukemia burden in mice and
227 f maintenance therapy with 6-mercaptopurine, vincristine, methotrexate, and prednisone (POMP), with f
228 ormation, had a significant association with vincristine neuropathy (meta-analysis P = 6.3x10(-9)).
229 l that subacute/chronic axon loss induced by vincristine occurs via a SARM1 mediated axonal destructi
230 actinomycin followed by cyclophosphamide and vincristine on alternating weeks (EMA-CO) with an SIR of
231 ous doxorubicin, and 1.4 mg/m(2) intravenous vincristine on day 1, and 40 mg/m(2) oral prednisone on
232 phoblastic leukemia (ALL) cells treated with vincristine only weakly exhibited colocalization between
233  to receive either intravenous bleomycin and vincristine or oral etoposide (the investigational arms)
234 plasma exchange; pulses of cyclophosphamide, vincristine, or cyclosporine A; or salvage splenectomy a
235 ytoreduction by chemotherapy (dexamethasone, vincristine, PEG-asparaginase) resulted in significantly
236 ART (64%, 55 to 73; n=138) and bleomycin and vincristine plus ART (44%, 35 to 53; n=132).
237 arly due to inferiority of the bleomycin and vincristine plus ART arm, as per the recommendations of
238 th oral etoposide plus ART and bleomycin and vincristine plus ART, supporting its use in treating adv
239 tuximab-CHOP (cyclophosphamide, doxorubicin, vincristine, prednisolone)-based chemotherapy were prosp
240 imens such as cyclophosphamide, doxorubicin, vincristine, prednisone (CHOP) and results in a 5-year o
241 or rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP14) induction and a posit
242 rapy regimen (cyclophosphamide, doxorubicin, vincristine, prednisone or cyclophosphamide, vincristine
243 or rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone or salvage immunochemotherapy.
244 4 (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) followed by 3 cycles of ICE (if
245 vincristine, prednisone or cyclophosphamide, vincristine, prednisone), Follicular Lymphoma Internatio
246 mab and CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone)-like chemotherapy, who were enr
247 onal two or four cycles of cyclophosphamide, vincristine, prednisone, and procarbazine were added in
248 side, doxorubicin, and cyclophosphamide with vincristine, prednisone, and rituximab (DA-EPOCH-R) and
249 ed etoposide, doxorubicin, cyclophosphamide, vincristine, prednisone, and rituximab (DA-EPOCH-R) may
250 prednisone, procarbazine, and doxorubicin or vincristine, prednisone, etoposide, and doxorubicin chem
251 1 (TG1; early stages) received two cycles of vincristine, prednisone, procarbazine, and doxorubicin o
252  has involved cyclophosphamide, doxorubicin, vincristine, prednisone-based therapy followed by consol
253 th rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone.
254 nt cohorts (rituximab plus cyclophosphamide, vincristine, prednisone: OR, 2.95; c-statistic, 0.75; P
255 t (n = 138, rituximab plus cyclophosphamide, vincristine, prednisone; n = 45, rituximab plus cyclopho
256 under rituximab-cyclophosphamide-doxorubicin-vincristine-prednisone (R-CHOP) chemotherapy showed a ra
257 ere treated with three cycles of doxorubicin/vincristine/prednisone/cyclophosphamide (AV-PC).
258 py (rituximab, high-dose methotrexate [MTX], vincristine, procarbazine) followed by a novel consolida
259 in, etoposide, doxorubicin cyclophosphamide, vincristine, procarbazine, and prednisone (BEACOPP [68%]
260 n, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone (BEACOPP) was
261 n, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone (BEACOPPesc) a
262 n, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone (eBEACOPP) for
263 n, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone (eBEACOPP) for
264 n, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone at baseline ov
265 n, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone) has significa
266 in, etoposide, adriamycin, cyclophosphamide, vincristine, procarbazine, and prednisone) in the German
267 n, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone), and six cycl
268 n, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone).
269 sine, melphalan, prednisone, epidoxorubicin, vincristine, procarbazine, vinblastine, and bleomycin; C
270  combination of procarbazine, lomustine, and vincristine provide survival benefit.
271 s of asparaginase exposure and dexamethasone/vincristine pulses) compared with historical controls (7
272 sphamide, adriamycin, prednisone, and either vincristine (R-CHOP) or bortezomib (VR-CAP).
273 methotrexate (3.5 g/m(2)), procarbazine, and vincristine (R-MPV).
274 sociated with increased risk and severity of vincristine-related peripheral neuropathy.
275 our cycles of bleomycin or > three cycles of vincristine, respectively.
276 ess the effects of lower CEP72 expression on vincristine sensitivity.
277 that is induced by the chemotherapeutic drug vincristine sulfate (VCR).
278                   Systemic chemotherapy with vincristine sulfate, etoposide, and carboplatin had fail
279 ximab-cyclophosphamide, hydroxydaunorubicin, vincristine sulfate, prednisone (CHOP) or rituximab-CHOP
280 ay for 5 days was the MTD when combined with vincristine, temozolomide and bevacizumab administered o
281 nt with multiagent chemotherapy-carboplatin, vincristine, temozolomide, procarbazine, lomustine, and
282 s of microtubules and the drugs eribulin and vincristine that bind at microtubule ends, on mitochondr
283  and 218 (6.6%) received </= three cycles of vincristine; these were compared with patients receiving
284 ke, indicating that the cytotoxic effects of vincristine took place during G1 Conversely, cells isola
285  symptoms developed faster in paclitaxel and vincristine treated animals compared to cisplatin and bo
286 and medium dorsal root ganglion neurons from vincristine-treated animals revealed a significant upreg
287 es of dorsal root ganglion neurons following vincristine treatment and it contributes to the maintena
288                    Using the same regimen of vincristine treatment in SARM1 knockout mice, the develo
289 hed a mouse model in which repeated systemic vincristine treatment results in the development of sign
290 ts in dorsal root ganglion neurons following vincristine treatment.
291 f life, including peripheral neuropathy from vincristine treatment.
292 ally affected by juvenile irradiation and/or vincristine treatment.
293 mal nerve terminals throughout the course of vincristine treatment.
294          Moreover, co-treatment with ATM and vincristine (VCR), a microtubule inhibitor currently use
295 formation by microtubule inhibitors, such as vincristine (VCR), prevented the "rescue" function of ac
296 py (PCV; procarbazine, lomustine (CCNU), and vincristine) was associated with longer PFS (HR, 0.32; P
297  bioactive compounds such as vinblastine and vincristine, which are classified as terpenoid indole al
298 icrotubule-destabilizing drugs, eribulin and vincristine, which bind preferentially to microtubule en
299  5) or VR-CAP (R-CHOP regimen, but replacing vincristine with bortezomib at a dose of 1.3 mg per squa
300 1-day cycles of cisplatin, fluorouracil, and vincristine within 42 days of resection, consisting of c

 
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