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1 levels of intracellular drug (paclitaxel and vinblastine).
2 nced cell death in vitro in combination with vinblastine.
3 peutic spindle poisons such as paclitaxel or vinblastine.
4  to paclitaxel, docetaxel, epothilone B, and vinblastine.
5 rupting their transport on microtubules with vinblastine.
6 PC-6827, paclitaxel, and colchicine, but not vinblastine.
7 essing breast cancer cells to paclitaxel and vinblastine.
8 mpete with [(3)H]paclitaxel (Taxol) or [(3)H]vinblastine.
9 eatment with the microtubule-modifying agent vinblastine.
10 ylation in KB-3 carcinoma cells treated with vinblastine.
11 rotubule dynamics with low doses of taxol or vinblastine.
12 and even with the mitotic spindle inhibitor, vinblastine.
13 uding paclitaxel, docetaxel, vinorelbine, or vinblastine.
14 ed by vincristine and colchicine, but not by vinblastine.
15 uding the chemotherapeutics, vincristine and vinblastine.
16 terface when compared to the parent compound vinblastine.
17 bule structure by imaging in the presence of vinblastine.
18    We induced leukopenia in guinea pigs with vinblastine (0.7 mg/kg, intravenously, 4 days before) an
19 1 to 4, dacarbazine 800 mg/m2 on day 1 only, vinblastine 1.6 mg/m2 on days 1 to 4, interleukin-2 tota
20 paclitaxel (originally called taxol; 1 muM), vinblastine (1 and 10 muM), colchicine (10 and 100 muM),
21 hed by an ester linkage at the 4-position of vinblastine (1), undergoes rapid cleavage by PSA (T(1/2)
22                     A coumarin derivative of vinblastine, 17-deacetyl-O-(3-carbonylamino-7-diethylami
23                              A series of 180 vinblastine 20' amides were prepared in three steps from
24  methotrexate 30 mg/m(2) days 1, 15, and 22, vinblastine 3 mg/m(2) days 2, 15, and 22, doxorubicin 30
25 clitaxel (3-fold), vincristine (3-fold), and vinblastine (3-4-fold).
26  nor the analog inhibited the binding of [3H]vinblastine, [3H]dolastatin 10, or [8-14C]GTP to tubulin
27 ids, including vincristine, vinorelbine, and vinblastine (4.29- to 6.40-fold), but minimal resistance
28  intermediate iminium ion directly providing vinblastine (40-43%) and leurosidine (20-23%), its natur
29  C (10 mg/m(2) day 1 and every 28 days) plus vinblastine (5 mg/m(2) day 1, day 14, day 28, and day 42
30 received 6 cycles of doxorubicin 25 mg/m(2), vinblastine 6 mg/m(2), and gemcitabine 800 mg/m(2) (1000
31  plus MVP (four cycles of mitomycin 6 mg/m2, vinblastine 6 mg/m2, and cisplatin 50 mg/m2 every 3 week
32                                              Vinblastine (6 mg/m(2)) was administered weekly for 1 ye
33 e MTAs paclitaxel, an assembly promoter, and vinblastine, a disassembly promoter.
34                                 For example, vinblastine, a prototypic drug of this class, induced th
35  the amount of intracellular accumulation of vinblastine, a surrogate marker for the activity of P-gp
36 g radiation, a double-strand break agent, or vinblastine, a tubulin poison.
37 : destabilizing MTAs, such as colchicine and vinblastine, accelerate aging in an EB-dependent manner,
38  compound enhancing 50% of the intracellular vinblastine accumulation in the KB/MDR cells) and 3 time
39 mes higher, based on Amax (the intracellular vinblastine accumulation of the KB/MDR cells caused by t
40                           Cytochalasin D and vinblastine, actin and microtubule inhibitors, respectiv
41                                   Conclusion Vinblastine administered once per week is well tolerated
42 ients treated with neoadjuvant methotrexate, vinblastine, Adriamycin (doxorubicin), and cisplatin, th
43                                              Vinblastine also depolymerizes microtubules but re-aggre
44                                              Vinblastine also promoted Bax activation and Bax oligome
45 r the preparation of previously inaccessible vinblastine analogs and define powerful new methodology
46 difications at C6-C8, were incorporated into vinblastine analogues and used to probe the unusual impo
47 he total synthesis of a systematic series of vinblastine analogues that contain deep-seated structura
48 er cell line, and an important subset of the vinblastine analogues that display little or no differen
49 nit followed by their incorporation into the vinblastine analogues through the use of a single-step b
50  situ oxidation to provide the corresponding vinblastine analogues, their evaluation provided unantic
51 ubstituents, remarkably enhancing potency of vinblastine analogues.
52 ed by CPT are not observed with cisplatin or vinblastine and are not simply due to reduced Top1 activ
53 re commonly displayed resistance to combined vinblastine and corticosteroid therapy (21.9% v 3.3%; P
54 rial movement in astrocytes was inhibited by vinblastine and cytochalasin D, demonstrating that this
55            To reduce doxorubicin, bleomycin, vinblastine and dacarbazine toxicity, the Cancer and Leu
56 ve inhibitors of the binding of radiolabeled vinblastine and dolastatin 10 to tubulin.
57 state cancer with antimitotic agents such as vinblastine and doxorubicin is only marginally effective
58 etoconazole and doxorubicin alternating with vinblastine and estramustine before emergence of a castr
59 etoconazole and doxorubicin alternating with vinblastine and estramustine, given in addition to stand
60 nts in other chemotherapeutic classes (e.g., vinblastine and etoposide) also increased with the mutat
61                                              Vinblastine and other microtubule inhibitors used as ant
62                     The role of single-agent vinblastine and other vinca alkaloid in the management o
63 ulted in a marked increase in sensitivity to vinblastine and paclitaxel, drugs that are known to be m
64 orubicin and greatly enhanced sensitivity to vinblastine and paclitaxel.
65 se nicely on the tubulin-bound structures of vinblastine and phomopsin A.
66  sensitivity of drug-resistant Leishmania to vinblastine and rhodamine 123.
67 sed at 6 mg/kg i.v. with an anticancer drug, vinblastine and shown is the distribution of the precurs
68                                              Vinblastine and vincristine are condensed from the monot
69              Antitumor substances related to vinblastine and vincristine are exclusively found in the
70 e noncompetitively inhibiting the binding of vinblastine and vincristine to beta-tubulin.
71            Moderate inhibition occurred with vinblastine and vincristine, and strong inhibition with
72 nthetic precursor for the anti-cancer agents vinblastine and vincristine, as well as other biological
73 ) is the sole source of the anticancer drugs vinblastine and vincristine, bisindole alkaloids derived
74 lkaloids, including the low-level anticancer vinblastine and vincristine, for which the late biosynth
75 ir dimeric terpenoid indole alkaloids (TIAs) vinblastine and vincristine, which are used in cancer ch
76 the clinically significant anticancer agents vinblastine and vincristine.
77  the potent, expensive anti-cancer compounds vinblastine and vincristine.
78 e alkaloids, including the anti-cancer drugs vinblastine and vincristine.
79 alkaloids, among which the anti-cancer drugs vinblastine and vincristine.
80 orubicin, 10 units/m(2) bleomycin, 6 mg/m(2) vinblastine, and 375 mg/m(2) dacarbazine) or AVD (ABVD m
81 alue 3 times lower than the positive control vinblastine, and against human breast cancer cell lines
82 ycles of PE plus three cycles of ifosfamide, vinblastine, and bleomycin.
83 , epidoxorubicin, vincristine, procarbazine, vinblastine, and bleomycin; CEC) in patients with advanc
84 ma to treatment with doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) alone or to treatmen
85  a series of trials, doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) and mechlorethamine,
86 roup trial comparing doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) and Stanford V regim
87 wo initial cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) and was labeled PET2
88 thotrexate (VBM), or doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) in C studies; and Vb
89  after two cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) in previously untrea
90 ma (HL) treated with doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) in the HAART era acc
91 of chemotherapy with doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) require radiotherapy
92 atients treated with doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) were enrolled retros
93 s Lymphoma) compared doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) with mechlorethamine
94 he majority received doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD)-like chemotherapy.
95  classic combination doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD).
96 were randomly assigned to receive cisplatin, vinblastine, and dacarbazine (CVD) either alone or concu
97 motherapy regimen of doxorubicin, bleomycin, vinblastine, and dacarbazine (or equivalent).
98 nation with standard doxorubicin, bleomycin, vinblastine, and dacarbazine (RABVD) in patients with cl
99      Increasing age, doxorubicin, bleomycin, vinblastine, and dacarbazine as initial therapy, and gra
100 t with two cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine followed by RT is rare.
101 ed with a regimen of doxorubicin, bleomycin, vinblastine, and dacarbazine for Hodgkin disease (HD) an
102  four cycles of ABVD (adriamycin, bleomycin, vinblastine, and dacarbazine) and 30 Gy involved-field r
103  two cycles of ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) as compared with standard
104                ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) chemotherapy is regarded a
105  two cycles of ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) chemotherapy, and then und
106 rentuximab vedotin (BV) and AVD (adriamycin, vinblastine, and dacarbazine) followed by 30 Gy involved
107       Although ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) has been established as th
108 ed 2 cycles of ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) with IFRT.
109  six cycles of ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine), four escalated plus two s
110 umbers and follow-up, adriamycin, bleomycin, vinblastine, and dacarbazine.
111 EACOPP compared with doxorubicin, bleomycin, vinblastine, and dacarbazine; cyclophosphamide, vincrist
112 lating chemotherapy (doxorubicin, bleomycin, vinblastine, and dacarbazine; epirubicin, bleomycin, vin
113 rbazine, prednisone, doxorubicin, bleomycin, vinblastine, and dacarbazine; or standard BEACOPP (P = .
114 substrates used in these studies (verapamil, vinblastine, and digoxin) bind.
115  B conducted a phase 2 trial of doxorubicin, vinblastine, and gemcitabine for newly diagnosed, nonbul
116 such as calcein-AM, bodipy-verapamil, bodipy-vinblastine, and mitoxantrone.
117 crotubule disruptive drugs such as colcemid, vinblastine, and nocodazole.
118 7 were notably more potent than vinorelbine, vinblastine, and paclitaxel in the NCI/ADR-RES and Messa
119 ine, and dacarbazine; epirubicin, bleomycin, vinblastine, and prednisone).
120  many other substrates (including verapamil, vinblastine, and rifampicin) of the well studied multidr
121 nd T-cell lymphoma) resistant to paclitaxel, vinblastine, and teniposide.
122 uppresses on-off kinetics, characteristic of vinblastine, and the other a "pseudo" kinetic stabilizat
123 vide a unique entry into C20' functionalized vinblastines, and afford initial insights into the obser
124 interdimer interface so that it contacts the vinblastine- and dolastatin 10-binding sites believed to
125 g of catharanthine with vindoline to provide vinblastine are described along with key mechanistic and
126 reased resistance of PC-3 cells to Taxol and vinblastine, as assessed by viability and clonogenic sur
127                                The BODIPY FL-vinblastine-based biochemical assay is suitable for high
128                      We describe a BODIPY FL-vinblastine-based human PXR time-resolved fluorescence r
129 valuated in animals rendered leukopenic with vinblastine before graft implantation.
130 nd colchicinoid molecules and a single bound vinblastine between the two heterodimers (Nature (Lond)
131 uorophore is probably on the exterior of the vinblastine binding site.
132  of P-gp inhibitors of digoxin transport and vinblastine binding suggest some commonality in their bi
133 ompound is shown to not significantly affect vinblastine binding to tubulin; however, experiments sug
134 mbly by binding at either the colchicine- or vinblastine-binding site.
135 vinblastine (PAVe) in S studies; MOPP, PAVe, vinblastine, bleomycin, and methotrexate (VBM), or doxor
136                   However, neither taxol nor vinblastine, both of which block microtubule dynamics wh
137 fers resistance to hydrophobic drugs such as vinblastine, but increases the sensitivity of these para
138                                              Vinblastine, but not control agents, induced cleavage of
139 ivatives that match or exceed the potency of vinblastine by as much as 10-fold in cell-based function
140  of the tubulin binding site surrounding the vinblastine C20' center depicted in an X-ray cocrystal s
141 midyl ester (bodipy-FL)-verapamil, bodipy-FL-vinblastine, calcein-AM, bodipy-FL-prazosin, bisantrene,
142             Both 10 mm colchicine and 0.1 mm vinblastine caused AMS to develop in 30.6% and 33.3% of
143 3-null cells but not in p53 wild-type cells, vinblastine caused down-regulation of p21 expression con
144  of neoadjuvant cisplatin, methotrexate, and vinblastine (CMV) chemotherapy in patients with muscle-i
145        Treatment of both types of cells with vinblastine, colchicine, or nocodazole reversed alpha-sy
146         Dose escalation of a folate-targeted vinblastine compound, EC0905, was conducted in dogs with
147 ation of mitosis in nocodazole, colcemid, or vinblastine concentrations that inhibit MT assembly vari
148 571 sensitizes embryos to the toxic compound vinblastine, confirming that one role for the efflux tra
149 r activity and toxicity of a folate-targeted vinblastine conjugate were evaluated in dogs with natura
150 a liposomal delivery system for a prodrug of vinblastine (CPD100) which converts to the parent compou
151 mized to 6 cycles of doxorubicin, bleomycin, vinblastine, dacarbazine (ABVD) alone or 6 cycles of ABV
152 ity of two cycles of doxorubicin, bleomycin, vinblastine, dacarbazine (ABVD) plus 20 Gy involved-fiel
153 ng after 2 cycles of doxorubicin, bleomycin, vinblastine, dacarbazine (ABVD) to guide treatment modif
154 eceived doxorubicin (Adriamycin), bleomycin, vinblastine, dacarbazine chemotherapy along with involve
155 inister the standard doxorubicin, bleomycin, vinblastine, dacarbazine chemotherapy regimen, prescribe
156 n of rituximab-ABVD (doxorubicin, bleomycin, vinblastine, dacarbazine) for stage II-IV untreated clas
157 herapy induction regimen included cisplatin, vinblastine, dacarbazine, decrescendo interleukin-2 (IL-
158 nced progression on or after BCT (cisplatin, vinblastine, dacarbazine, IL-2 9 MU/m(2)/d for 4 days, a
159 ing adjuvant biochemotherapy with cisplatin, vinblastine, dacarbazine, interleukin-2 (IL-2), and inte
160 at baseline and after 2 adriamycin-bleomycin-vinblastine-dacarbazine (ABVD) courses with (18)F-FDG PE
161 0-fold) and define the potential role of the vinblastine Delta(6,7)-double bond.
162 otal synthesis of a systematic series of key vinblastine derivatives is detailed and used to characte
163 ave prepared a new fluorescent derivative of vinblastine designed to retain high affinity for tubulin
164 ently resistant to neoadjuvant methotrexate, vinblastine, doxorubicin and cisplatin chemotherapy, and
165 les of neoadjuvant accelerated methotrexate, vinblastine, doxorubicin, and cisplatin (AMVAC) would be
166 cer, treatment with dose-dense methotrexate, vinblastine, doxorubicin, and cisplatin (ddMVAC) results
167 e for benefit from combination methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC) adjuvant
168  patients received neoadjuvant methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC) chemother
169  basis of reported activity of methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC) or topote
170 ical outcome after neoadjuvant methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC).
171 bine plus cisplatin, high-dose methotrexate, vinblastine, doxorubicin, and cisplatin [high-dose MVAC]
172                                Methotrexate, vinblastine, doxorubicin, and cisplatin and gemcitabine
173 upports the use of neoadjuvant methotrexate, vinblastine, doxorubicin, and cisplatin followed by cyst
174  alone, the use of neoadjuvant methotrexate, vinblastine, doxorubicin, and cisplatin followed by radi
175 ctomy alone or three cycles of methotrexate, vinblastine, doxorubicin, and cisplatin followed by radi
176 mcitabine and cisplatin versus methotrexate, vinblastine, doxorubicin, and cisplatin in locally advan
177 instays of chemotherapy remain methotrexate, vinblastine, doxorubicin, and cisplatin, and gemcitabine
178 with low-risk Hodgkin's disease treated with vinblastine, doxorubicin, methotrexate, and prednisone (
179     Patients received CMT with chemotherapy (vinblastine, doxorubicin, methotrexate, and prednisone [
180  ganglioside levels, restored sensitivity to vinblastine, enhanced vinblastine uptake 3-fold, and dim
181 er ketoconazole/doxorubicin alternating with vinblastine/estramustine (KA/VE) or paclitaxel, estramus
182  and resistance to treatments with TNFalpha, vinblastine, etoposide and gamma-radiation.
183                In contrast to paclitaxel and vinblastine, etoposide does not activate JNK, and gamma-
184 hamine, doxorubicin, vincristine, bleomycin, vinblastine, etoposide, and prednisone (Stanford V).
185 otherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, camptothecin, and Adriamycin) in
186 ubicin, methotrexate, and prednisone [VAMP]; vinblastine, etoposide, prednisone, and doxorubicin; or
187 l-O-(3-carbonylamino-7-diethylaminocoumarin) vinblastine (F-VLB), was prepared by reaction of 17-deac
188 o better regulate the biodistribution of the vinblastine-folate conjugate, EC145, a new folate-spacer
189  and MS/MS imaging experiments by separating vinblastine from an endogenous isobaric lipid.
190  we report the characterization of BODIPY FL-vinblastine, generated by labeling vinblastine with the
191 noterpene precursor of the anti-cancer agent vinblastine, has remained largely unexplored.
192             Many natural products, including vinblastine, have not been easily subjected to simplific
193 tine that matched or exceeded the potency of vinblastine in cell growth inhibition assays.
194  ability to promote uptake of calcein AM and vinblastine in multidrug-resistant cells.
195  ability to promote uptake of calcein AM and vinblastine in multidrug-resistant MDCKII-MDR1 cells, an
196 motherapeutic agents such as doxorubicin and vinblastine in NSCLC.
197  of this study was to assess the activity of vinblastine in therapy-naive children.
198 hetically derived, structurally more complex vinblastines inaccessible from the natural product itsel
199 ncubation of microtubules with 2 or 4 microM vinblastine induced additional lower-affinity eribulin b
200 oposide and cisplatin nor the tubulin-binder vinblastine induced enhanced levels of radiosensitizatio
201                                              Vinblastine induced the translocation of Bax from the cy
202 uding epothilone B analogue (BMS-247550) and vinblastine, induced apoptosis of Bax-positive HCT116 ce
203                    The results indicate that vinblastine-induced apoptosis requires translocation, ac
204           Overexpression of Bcl-xL inhibited vinblastine-induced Bax activation and Bax dimerization
205 ription and protein translation blocked both vinblastine-induced c-Jun expression and apoptotic cell
206 d was found to be highly effective, reducing vinblastine-induced c-Jun expression at both the mRNA an
207  in protein level or nuclear localization of vinblastine-induced c-Jun, or of one of its target genes
208               Lipopolysaccharide-challenged, vinblastine-induced leukopenic guinea pigs exhibit hyper
209 K, ERK, p38(MAPK), or CDK1 failed to inhibit vinblastine-induced phosphorylation of Bcl-xL or Bcl-2.
210                                              Vinblastine-induced spiral formation is strongly inhibit
211  disrupt polymer stability, and compete with vinblastine-induced spiral formation.
212                                              Vinblastine inhibited the binding of crocin to tubulin w
213 herapy consisting of dacarbazine, cisplatin, vinblastine, interleukin-2, IFN alfa-2b (IFN-alpha-2b) a
214           We provide evidence that BODIPY FL-vinblastine is a unique chemical entity different from e
215 results also suggest that the substrate drug vinblastine is released at stages that precede or follow
216 th lack the 6,7-double bond whose removal in vinblastine leads to a 100-fold drop in activity.
217 carboplatin (GC) or methotrexate/carboplatin/vinblastine (M-CAVI).
218 rgo apoptosis by the chemotherapeutic agents vinblastine, melphalan, and cis-platinum.
219 tional five cycles of VACP or five cycles of vinblastine, methotrexate with calcium leucovorin rescue
220                                      Purpose Vinblastine monotherapy has shown promising activity and
221 ine, prednisone, doxorubicin, bleomycin, and vinblastine (MOPP/ABV) have been identified as effective
222 unique chemical entity different from either vinblastine or the fluorophore BODIPY FL in its function
223 H]probe 1 was inhibited by probe 1, HTI-286, vinblastine, or dolastatin 10 (another peptide antimitot
224                   This effect of colchicine, vinblastine, or nocodazole was not linked to a disruptio
225 esencephalic neurons with either colchicine, vinblastine, or nocodazole, each of which disrupts micro
226 (MOPP) or procarbazine, mechlorethamine, and vinblastine (PAVe) in S studies; MOPP, PAVe, vinblastine
227 evidence that c-Jun induction in response to vinblastine plays a proapoptotic role in part via down-r
228 ts, cytoreduction with one or two courses of vinblastine plus ifosfamide plus cisplatin preceded the
229 with irreversible vincristine and reversible vinblastine, pointing to persistent cellular retention a
230 courses of vinblastine+prednisone (Arm A) or vinblastine + prednisone + methotrexate (Arm B).
231 patients received 1 to 2 six-week courses of vinblastine+prednisone (Arm A) or vinblastine + predniso
232                        RO- patients received vinblastine+prednisone throughout.
233 gimens revealed 84% of patients treated with vinblastine/prednisone either did not respond or relapse
234                  Toxicity was worse with the vinblastine/prednisone group as 75% had grade 3-4 neurop
235                                 In contrast, vinblastine/prednisone results in poor overall responses
236  to surgery, curettage, steroids, radiation, vinblastine/prednisone, 2-Chlorodeoxyadenosine (2-CdA),
237           The P-gp inhibitors tariquidar and vinblastine prevented the efflux of rhodamine 123 (rh123
238 e randomization as alternating chlorambucil, vinblastine, procarbazine, and prednisolone (ChlVPP) wit
239 effect profile, the regimen of chlorambucil, vinblastine, procarbazine, and prednisone (ChlVPP) has b
240 ng treatment with the chemotherapeutic agent vinblastine, rapid capillary tube network collapse occur
241            Biochemotherapy involved CVD with vinblastine reduced 25% plus interleukin-2 by 24-hour co
242 icity, and potency to reverse daunomycin and vinblastine resistances.
243 how that EM011 is potently effective against vinblastine-resistant human lymphoblastoid line CEM/VLB1
244 anosomes, and has no effect on cis-platin or vinblastine response.
245 rotubule assembly with low doses of taxol or vinblastine resulted in rapid clearance of microtubules
246                                       Weekly vinblastine seems to be a reasonable alternative to radi
247 ential in activity against a matched pair of vinblastine sensitive and resistant (Pgp overexpressing)
248 phoblastoid line CEM/VLB100 and its parental vinblastine-sensitive line CEM.
249 to colcemid, it did not affect paclitaxel or vinblastine sensitivity, nor did it reduce microtubule a
250  binding indicating that crocin binds at the vinblastine site on tubulin.
251 nough movement of amino acid residues at the vinblastine site to cause the latter compound to bind le
252  into this site, which was also close to the vinblastine site, resulted in enough movement of amino a
253 3342, verapamil, tetraphenylphosphonium, and vinblastine-stimulated ATPase activity.
254                      Doxorubicin, bleomycin, vinblastine sulfate, and dacarbazine (ABVD) is associate
255 Trace RedOrange, BoDipy-verapamil and BoDipy-vinblastine, than any other cell in the embryo, indicati
256                Herein, we detail a synthetic vinblastine that incorporates added benign complexity (A
257 hesized a series of C20' urea derivatives of vinblastine that matched or exceeded the potency of vinb
258 nt tubulin assembly reaction, as occurs with vinblastine (tight spirals) or dolastatin 10 (aggregated
259 h paclitaxel, methotrexate, doxorubicin, and vinblastine to increase Ag presentation to Ag-specific T
260 ally, TTI-237 inhibited the binding of [(3)H]vinblastine to tubulin, but it caused a marked increase
261 an it inhibited the binding of colchicine or vinblastine to tubulin.
262 xoplasmic transport blockers (colchicine and vinblastine) to the sciatic nerve.
263 eling staining revealed fragmented nuclei in vinblastine-treated but not control angiogenic areas.
264                                              Vinblastine-treated cells overexpressing a Ser-62 --> Al
265 solic Bax interacted with Bcl-xL, whereas in vinblastine-treated cells, activated mitochondrial Bax d
266 e mitochondrial fraction in both control and vinblastine-treated cells, indicating that phosphorylati
267 in interactions of Bax, Bcl-2, and Bcl-xL in vinblastine-treated KB-3 cells.
268  demonstrated in mitochondrial extracts from vinblastine-treated, but not control, cells.
269 owth factor-stimulated angiogenesis in vivo, vinblastine treatment also resulted in collapse and apop
270                                              Vinblastine treatment in all cell lines examined causes
271 ating after protease inhibition or prolonged vinblastine treatment strongly resembled AVs that collec
272                                              Vinblastine treatment was also used to halt autophagy an
273 a, underwent multisite phosphorylation after vinblastine treatment, and was strictly monomeric under
274  disruption of microtubules by nocodazole or vinblastine treatment, as well as microtubule stabilizat
275 ules were depleted with either nocodazole or vinblastine treatment, resulting in an increase in Src2
276 osis-inducing ligand (TRAIL), etoposide, and vinblastine treatment, whereas overexpression of IG20 en
277 endent kinase inhibitor) gene promoter after vinblastine treatment.
278 s depleted similarly in both cell lines upon vinblastine treatment.
279 oretic mobilities during the duration of the vinblastine treatment.
280 estored sensitivity to vinblastine, enhanced vinblastine uptake 3-fold, and diminished expression of
281 o determine the efficacy and safety of using vinblastine (Vbl) and methotrexate (Mtx) in children wit
282 s were refractory after at least 1 course of vinblastine (VBL) plus corticosteroid, all had liver and
283                                Most notably, vinblastine (VBL) was found to induce phenotypic and fun
284 ed cytotoxicity to daunorubicin, paclitaxel, vinblastine, vincristine, and etoposide.
285 he commercially important chemotherapy drugs vinblastine, vincristine, and other synthetic derivative
286  door to new strategies for the synthesis of vinblastine, vincristine, and related anticancer agents.
287 d with VBM) or mechlorethamine, doxorubicin, vinblastine, vincristine, bleomycin, etoposide, and pred
288 ughout the pathway appear to be a feature of vinblastine/vincristine biosynthesis.
289                                              Vinblastine was administered once per week at a dose of
290  (MIA)-type anticancer drugs vincristine and vinblastine, we identified a jasmonate-regulated basic h
291             Their sensitivities to Taxol and vinblastine were enhanced by hPXR ablation.
292 le key C20' urea and thiourea derivatives of vinblastine were prepared from 20'-aminovinblastine that
293 hemotherapeutics (e.g. DOX, daunorubicin, or vinblastine) were required to be Pgp substrates and also
294                       This is in contrast to vinblastine which strongly stimulates large spiral polym
295 f c-Jun induced by the microtubule inhibitor vinblastine, which strongly induced c-Jun expression, wa
296             The newly discovered ultrapotent vinblastines, which may look highly unusual upon first i
297 uptake of calcein AM and inhibited efflux of vinblastine with IC(50)'s of approximately 2 microM in M
298 BODIPY FL-vinblastine, generated by labeling vinblastine with the fluorophore 4,4-difluoro-5,7-dimeth
299                          The distribution of vinblastine within the ventricles of the brain is also d
300 rbazine, prednisone, doxorubicin, bleomycin, vinblastine) without involved field radiation therapy (I

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