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1 29 to doxorubicin and 128 to gemcitabine and docetaxel).
2 irradiation or chemotherapy (gemcitabine or docetaxel).
3 umetinib + docetaxel; 254 received placebo + docetaxel).
4 .9% with ganetespib and docetaxel v 25% with docetaxel).
5 ilarly in mice in the presence or absence of docetaxel.
6 pared with 5% (3-7) in patients treated with docetaxel.
7 prostate cancer cells that were resistant to docetaxel.
8 ab or placebo in addition to trastuzumab and docetaxel.
9 eceived a relative dose intensity >= 85% for docetaxel.
10 t prostate cancer (mCRPC) and synergism with docetaxel.
11 tumor cell proliferation compared with free docetaxel.
12 tant prostate cancer previously treated with docetaxel.
13 nib + docetaxel and 256 to receive placebo + docetaxel.
14 ab and 425 patients were assigned to receive docetaxel.
15 atients received second-line nintedanib plus docetaxel.
16 xicity compared with equimolar doses of free docetaxel.
17 QR, 2.3-7.3; 95% CI, 2.8-5.6) with placebo + docetaxel.
18 line plus paclitaxel, and anthracycline plus docetaxel.
19 espib and docetaxel and 337 were assigned to docetaxel.
20 d cell survival and increased sensitivity to docetaxel.
21 , showed effective intracellular delivery of docetaxel.
22 0.71) for nivolumab and 0.80 (0.61-1.04) for docetaxel.
23 s, especially among those treated with early docetaxel.
25 higher were more frequent with selumetinib + docetaxel (169 adverse events [67%] for selumetinib + do
28 nts received vinorelbine, 343 (23%) received docetaxel, 283 (19%) received gemcitabine, and 497 (33%)
29 rexate (40-60 mg/m(2) of body surface area), docetaxel (30-40 mg/m(2)), or cetuximab (250 mg/m(2) aft
30 in versus those who received gemcitabine and docetaxel (46.3% [95% CI 37.5-54.6] vs 46.4% [37.5-54.8]
31 kg volume equivalent followed by intravenous docetaxel 75 mg/m(2) (60 mg/m(2) in Korea, Taiwan, and J
32 (2) (C20) or 25 mg/m(2) (C25) is superior to docetaxel 75 mg/m(2) (D75) in terms of OS in patients wi
33 erapy (intravenous pemetrexed 500 mg/m(2) or docetaxel 75 mg/m(2) [investigator choice], every 21 day
34 ously receive either atezolizumab 1200 mg or docetaxel 75 mg/m(2) every 3 weeks by permuted block ran
35 physician's choice of a taxane (intravenous docetaxel 75 mg/m(2) every 3 weeks or intravenous paclit
36 nce per week for 6 weeks then 1 week off; or docetaxel 75 mg/m(2) for at least 60 min every 3 weeks),
38 ganetespib 150 mg/m(2) on days 1 and 15 with docetaxel 75 mg/m(2) on day 1 of a 21-day cycle or to do
40 e web response system to receive intravenous docetaxel 75 mg/m(2) plus either intravenous ramucirumab
41 arboplatin, and trastuzumab plus pertuzumab (docetaxel 75 mg/m(2); carboplatin area under the concent
42 oadjuvant CHT with androgen deprivation plus docetaxel (75 mg/m(2) body surface area every 3 weeks fo
44 Patients received up to ten 21-day cycles of docetaxel (75 mg/m(2) intravenous, day 1) and prednisolo
45 cycles 2-8) in conjunction with neoadjuvant docetaxel (75 mg/m(2) on day 1 of cycles 1-4) and FEC (f
46 of vinorelbine (30 mg/m(2) on days 1 and 8), docetaxel (75 mg/m(2) on day 1), gemcitabine (1200 mg/m(
47 e randomly assigned to receive six cycles of docetaxel (75 mg/m(2)) and cyclophosphamide (600 mg/m(2)
48 nd extensive prior treatment including prior docetaxel (84%), cabazitaxel (48%), and abiraterone and/
49 d extensive prior treatment, including prior docetaxel (84%), cabazitaxel (48%), and abiraterone or e
50 ata available for analysis; g differentiated docetaxel (a US Food and Drug Administration-approved th
52 ave a predictive impact on chemotherapy with docetaxel, a widely used drug in patients with metastati
53 trial highlights a differential response to docetaxel according to BMI, which calls for a body compo
55 esistant prostate cancer cells and tumors to docetaxel, allowing a four-fold reduction in effective d
56 (MEK) inhibitor selumetinib + docetaxel with docetaxel alone as a second-line therapy for advanced KR
57 espib did not improve outcomes compared with docetaxel alone for any secondary end point, including s
60 associated with longer overall survival than docetaxel among patients with previously treated non-sma
61 e response rate was 20.1% with selumetinib + docetaxel and 13.7% with placebo + docetaxel (difference
62 ile range [IQR], 1.5-5.9) with selumetinib + docetaxel and 2.8 months (IQR, 1.4-5.5) with placebo + d
65 1.7-4.8; 95% CI, 2.7-4.1) with selumetinib + docetaxel and 4.5 months (IQR, 2.3-7.3; 95% CI, 2.8-5.6)
66 .7 months (IQR, 3.6-16.8) with selumetinib + docetaxel and 7.9 months (IQR, 3.8-20.1) with placebo +
67 ratio, patients who had previously received docetaxel and an androgen-signaling-targeted inhibitor (
70 and some of their constituents interact with docetaxel and cabazitaxel on CRPC cells in culture and i
72 )F-FDG PET to assess response to combination docetaxel and carboplatin therapy in a co-clinical trial
73 acid) (PLGA) core and lipid layer containing docetaxel and clinically used inhibitor of sphingosine k
75 ne-free chemotherapy standard (six cycles of docetaxel and cyclophosphamide [TC]) in the routine trea
76 tate cancer who were previously treated with docetaxel and had progression within 12 months while rec
78 ns indicate rapid emergence of resistance to docetaxel and increased sensitivity to carboplatin, ther
79 tivity (compared with administration of free docetaxel and non-targeted nanotherapeutic controls) in
81 nd custirsen group (n=501) compared with the docetaxel and prednisone alone group (n=499) were neutro
86 Sphere, comprising 476 patients treated with docetaxel and prednisone from the ASCENT2 trial, 526 pat
87 the effect of custirsen in combination with docetaxel and prednisone on overall survival in patients
88 ETATION: Addition of custirsen to first-line docetaxel and prednisone was reasonably well tolerated,
90 nd custirsen vs 22.0 months [19.5-24.0] with docetaxel and prednisone; hazard ratio [HR] 0.93, 95% CI
91 rative cytostatic effect in combination with docetaxel and prevents adaptation and cell cycle re-entr
93 tant prostate cancer previously treated with docetaxel and the alternative androgen signalling-target
94 cancer who had been previously treated with docetaxel and the alternative androgen-signaling-targete
95 atient-derived xenografts (PDX) sensitive to docetaxel and their counterparts that developed resistan
96 phamide), followed by 3 cycles of concurrent docetaxel and trastuzumab, followed by maintenance trast
97 s frequent and correlates with resistance to docetaxel and worst clinical outcomes in patients treate
98 interventions (prednisone, mitoxantrone, and docetaxel) and off-treatment data when on-study treatmen
102 therapy (40 [34%] to pemetrexed, 73 [63%] to docetaxel, and three [3%] discontinued before receiving
103 e events were lower with nivolumab than with docetaxel (any grade, 68% v 88%; grade 3 to 4, 10% v 55%
104 cluding paclitaxel and the second-generation docetaxel are currently limited by severe adverse effect
105 10.5 months (95% CI, 8.6 to 12.2 months) in docetaxel arm (hazard ratio [HR], 1.11; 95% CI, 0.899 to
106 spib and docetaxel arm and 4.3 months in the docetaxel arm (HR, 1.16; 95% CI, 0.96 to 1.403; P = .119
107 urvival was 4.2 months in the ganetespib and docetaxel arm and 4.3 months in the docetaxel arm (HR, 1
108 I, 9.0 to 12.3 months) in the ganetespib and docetaxel arm compared with 10.5 months (95% CI, 8.6 to
109 /kg loading dose and 6 mg/kg thereafter; and docetaxel at 75 mg/m(2), escalating to 100 mg/m(2) if to
110 data to investigate whether the efficacy of docetaxel-based chemotherapy differs from non-docetaxel-
111 ocetaxel-based chemotherapy differs from non-docetaxel-based chemotherapy in patients with breast can
112 (CHT) with androgen-deprivation therapy plus docetaxel before RP would improve biochemical progressio
113 cancer cells more migratory and resistant to docetaxel, cabazitaxel, and cisplatin chemotherapy.
114 linically relevant anticancer drug payloads (docetaxel, cabazitaxel, and gemcitabine) were successful
115 ne, enzalutamide, apalutamide, darolutamide, docetaxel, cabazitaxel, radium-223, and sipuleucel-T hav
116 A second random assignment (R-C) compared docetaxel-capecitabine with an anthracycline-based regim
118 g loading dose, 420 mg maintenance doses) or docetaxel, carboplatin, and trastuzumab plus pertuzumab
119 group and 123 (55.7%) of 221 patients in the docetaxel, carboplatin, and trastuzumab plus pertuzumab
120 tuzumab emtansine plus pertuzumab (n=223) or docetaxel, carboplatin, and trastuzumab plus pertuzumab
121 most common grade 3-4 adverse events in the docetaxel, carboplatin, and trastuzumab plus pertuzumab
122 [1%] of 223 patients vs 11 [5%] of 219 with docetaxel, carboplatin, and trastuzumab plus pertuzumab)
123 emotherapy plus dual HER2-targeted blockade (docetaxel, carboplatin, and trastuzumab plus pertuzumab)
124 treatment, compared with patients receiving docetaxel, carboplatin, and trastuzumab plus pertuzumab,
125 her trastuzumab emtansine plus pertuzumab or docetaxel, carboplatin, and trastuzumab plus pertuzumab.
126 of FDG-PET to assess response to combination docetaxel/carboplatin therapy in a co-clinical trial inv
127 itivity to carboplatin, therefore sequential docetaxel/carboplatin treatment could improve survival i
128 se who had received previous treatments with docetaxel, CD137 agonists, anti-CTLA4, or therapies targ
129 a new molecular mechanism of prostate cancer docetaxel chemoresistance mediated by the mammalian targ
131 These findings suggest that continuation of docetaxel chemotherapy contributes to the survival benef
135 combination, patients on DPL received fewer docetaxel cycles (median, 6) vs 8 cycles in the control
137 arms, we investigated whether the number of docetaxel cycles administered to patients deriving clini
139 s, patients who received a greater number of docetaxel cycles had superior OS; patients who received
141 n which g was used as the endpoint, compared docetaxel data with mitoxantrone data and showed that sm
143 blockade of pertuzumab and trastuzumab, with docetaxel, demonstrating an 8-year landmark overall surv
144 y patients who would benefit from concurrent docetaxel, demonstrating the feasibility and potential v
145 cell lung cancer, addition of selumetinib to docetaxel did not improve progression-free survival comp
147 nd 7.9 months (IQR, 3.8-20.1) with placebo + docetaxel (difference, 0.9 months; HR, 1.05 [95% CI, 0.8
148 and 2.8 months (IQR, 1.4-5.5) with placebo + docetaxel (difference, 1.1 months; hazard ratio [HR], 0.
149 metinib + docetaxel and 13.7% with placebo + docetaxel (difference, 6.4%; odds ratio, 1.61 [95% CI, 1
151 ogy Research (USOR) 06-090 compared TC6 with docetaxel, doxorubicin, and cyclophosphamide (TAC6).
155 s) at low concentrations in conjunction with docetaxel (DTX) to overcome drug resistance of triple ne
158 resistance against the chemotherapeutic drug docetaxel due to MCL1 upregulation but remain sensitive
162 urthermore, mice treated with alphavbeta3-MP-docetaxel exhibited a significant decrease in bone-resid
163 of 126 patients who received gemcitabine and docetaxel), febrile neutropenia (26 [20%] and 15 [12%]),
164 nts in patients who received gemcitabine and docetaxel, fever (18 [12%] and 19 [15%]), and neutropeni
165 f fluorouracil, leucovorin, oxaliplatin, and docetaxel (FLOT) followed by surgery and 4 postoperative
167 ed induction chemotherapy with cisplatin and docetaxel, followed by concomitant chemoradiation therap
169 ious localised disease treatment or previous docetaxel for metastatic castration-sensitive prostate c
170 and those who received 4 or fewer cycles of docetaxel for other reasons, minimizing the effect of co
171 o to first-line therapy with trastuzumab and docetaxel for patients with locally recurrent, unresecta
172 evaluated the combination of ganetespib and docetaxel for second-line therapy of patients with advan
174 0.27) for nivolumab and 0.43 (0.29-0.65) for docetaxel; for stable disease versus progressive disease
175 Continuous wave laser-induced release of docetaxel from a nanoshell-based DNA host complex showed
177 2 in the atezolizumab group and n=110 in the docetaxel group) or non-squamous (0.73 [0.60-0.89]; n=31
178 nce in DFS or OS according to BMI in the non-docetaxel group, while reduced DFS and OS were observed
182 therapy groups, 7.7 months (6.7-9.2) for the docetaxel groups, and 10.8 months (9.4-12.3) for the ant
183 therapy groups, 2.7 months (1.9-2.9) for the docetaxel groups, and 3.0 months (2.7-3.9) for the anti-
185 de mice, RAD001 alone or in combination with docetaxel has suppressed tumour growth, VEGF expression
187 -risk nonmetastatic prostate cancer, CT with docetaxel improved OS from 89% to 93% at 4 years, with i
189 greater antitumor activity than 10 mg/kg of docetaxel in A549 non-small cell lung, as well as MDA-MB
190 A2 mutation showed a response rate of 25% to docetaxel in comparison to 71.1% in men with wildtype BR
191 and docetaxel with placebo, trastuzumab, and docetaxel in patients with HER2-positive metastatic brea
192 onger overall survival with nivolumab versus docetaxel in patients with previously treated advanced n
193 h nivolumab and/or ipilimumab, everolimus or docetaxel in phase 3 clinical trials, revealing the impo
194 evant improvement of overall survival versus docetaxel in previously treated non-small-cell lung canc
195 favorable tolerability profile compared with docetaxel in previously treated patients with advanced N
196 We assessed its efficacy and safety versus docetaxel in previously treated patients with non-small-
197 e of the prodrug, reduced exposure of active docetaxel in the circulation (compared with administrati
200 or, prolonged overall survival compared with docetaxel in two independent phase III studies in previo
207 ch as methotrexate, doxorubicin, paclitaxel, docetaxel, irinotecan and its important metabolite 7-eth
209 une checkpoint inhibitor after chemotherapy, docetaxel is recommended; in patients with nonsquamous N
210 the best of our knowledge, ramucirumab plus docetaxel is the first regimen in a phase 3 study to sho
212 a simple self-assembling process to prepare docetaxel-loaded hyaluronic acid (HA) nanocapsules by us
213 month PSA </= 0.2 ng/mL was more likely with docetaxel, low-volume disease, prior local therapy, and
214 mucirumab plus docetaxel versus placebo plus docetaxel (median 4.07 months [95% CI 2.96-4.47] vs 2.76
215 was improved with atezolizumab compared with docetaxel (median overall survival was 13.8 months [95%
216 ility to various anticancer drugs, including docetaxel (microtubule stabilizer), gemcitabine (nucleos
217 xty-three patients were randomly assigned to docetaxel (n = 41) or cabazitaxel (n = 22); 44.4% receiv
218 oved with atezolizumab (n=241) compared with docetaxel (n=222; median overall survival was 15.7 month
219 were randomly allocated to ramucirumab plus docetaxel (n=263) or placebo plus docetaxel (n=267) and
220 e randomly allocated either ramucirumab plus docetaxel (n=263) or placebo plus docetaxel (n=267).
221 rumab plus docetaxel (n=263) or placebo plus docetaxel (n=267) and comprised the intention-to-treat p
223 did not alter the tumor growth inhibition by docetaxel of xenografted 22Rv1 cells, ellagic acid has t
225 ies obtained 2 to 3 days after initiation of docetaxel or cabazitaxel in 2 patients with castration-r
226 tained 2 to 5 days after their first dose of docetaxel or cabazitaxel were processed to assess microt
228 's choice of standard doses of methotrexate, docetaxel, or cetuximab intravenously (standard-of-care
229 ), while the other half received 3 cycles of docetaxel plus capecitabine followed by 3 cycles of cycl
230 ed the efficacy and safety of treatment with docetaxel plus either ramucirumab-a human IgG1 VEGFR-2 a
231 re treated in phase III clinical trials with docetaxel plus prednisone (DP) or a DP-containing regime
234 on adverse events of grade 3 or worse in the docetaxel, prednisone and custirsen group (n=501) compar
235 he MAINSAIL trial, 598 patients treated with docetaxel, prednisone or prednisolone, and placebo in th
237 d for 214 (43%) of 501 patients treated with docetaxel, prednisone, and custirsen and 181 (36%) of 49
238 lled to the trial, of whom 510 were assigned docetaxel, prednisone, and custirsen and 512 were alloca
239 andomly assigned 1:1 centrally to either the docetaxel, prednisone, and custirsen combination or doce
240 s were attributable to 23 (5%) deaths in the docetaxel, prednisone, and custirsen group and 24 (5%) d
242 survival 23.4 months [95% CI 20.9-24.8] with docetaxel, prednisone, and custirsen vs 22.0 months [19.
243 study of 1059 patients with mCRPC receiving docetaxel, prednisone, and lenalidomide (DPL) or docetax
244 the ASCENT2 trial, 526 patients treated with docetaxel, prednisone, and placebo in the MAINSAIL trial
245 tic encapsulating a hydrolytically sensitive docetaxel prodrug and conjugated to an antibody specific
247 s in the risk of death with nivolumab versus docetaxel remained similar to those reported in the prim
248 fication is associated with the emergence of docetaxel resistance and carboplatin responsiveness in T
249 ntify mutations of key genes associated with docetaxel resistance in nine endometrial cancer cell lin
253 nt efficacy and survival in both taxane- and docetaxel-resistant in vivo anticancer mouse efficacy mo
254 stem cell niche in patient-derived cells, in docetaxel-resistant spheres and in an in vitro model.
255 Cs derived from prostate cancer patients, on docetaxel-resistant spheres with stem cell characteristi
257 lification was validated in a second pair of docetaxel-sensitive/resistant BRCA1-mutated PDXs and aft
259 iopsies after treatment with leuprolide plus docetaxel showed extensive microtubule bundling as did b
260 nal follow-up supports that ramucirumab plus docetaxel significantly improves progression-free surviv
261 oshamide (C)(600) followed by four cycles of docetaxel (T)(100) or six cycles of T(75)C(600) (adminis
262 s in vitro due to uMUC1 downregulation after docetaxel therapy was paralleled by in vivo imaging stud
264 CA2 mutation does not preclude a response to docetaxel, there is overall a significant correlation be
265 therapy, whereas it was only 0.3 QALMs when docetaxel + trastuzumab was used as a systemic therapy.
266 ced HER2-positive breast cancer treated with docetaxel, trastuzumab, and pertuzumab or placebo, highe
268 evident in PCa xenografts 2 to 3 days after docetaxel treatment but was decreased or lost with acqui
269 ng, disease progression following first-line docetaxel treatment established by radiographic evidence
270 tant BRCA1-mutated PDXs and after short-term docetaxel treatment in several TNBC/BRCA1-mutated PDXs a
271 nt prostate cancer that had progressed after docetaxel treatment with a Karnofsky performance status
276 e-fluorouracil, leucovorin, oxaliplatin, and docetaxel) trial is a prospective, phase 2 trial of 252
277 hibitors should preferably be avoided during docetaxel use in patients with breast cancer who are und
280 antly in patients allocated ramucirumab plus docetaxel versus placebo plus docetaxel (median 4.07 mon
281 l survival with pertuzumab, trastuzumab, and docetaxel versus placebo, trastuzumab, and docetaxel wer
282 (169 adverse events [67%] for selumetinib + docetaxel vs 115 adverse events [45%] for placebo + doce
283 n in the risk of death with nivolumab versus docetaxel was 28% (hazard ratio, 0.72; 95% CI, 0.62 to 0
286 uzumab were given until disease progression; docetaxel was given for six cycles, or longer at the inv
287 uent to response at 6 months on nivolumab or docetaxel was longer than after progressive disease at 6
288 biopsies 2 to 3 days after the first dose of docetaxel was markedly lower in 4 nonresponding patients
289 ial growth factor receptor 2 antagonist-plus docetaxel was previously reported to improve progression
290 or targeted delivery of the chemotherapeutic docetaxel, we showed that bone tumor burden could be red
291 overall survival rates with nivolumab versus docetaxel were 23% (95% CI, 16% to 30%) versus 8% (95% C
292 d docetaxel versus placebo, trastuzumab, and docetaxel were maintained after a median of more than 8
293 ety profiles of pertuzumab, trastuzumab, and docetaxel were maintained in the overall safety populati
294 -TGBF and GS-Wnt mice were more resistant to docetaxel, whereas organoids from the CIN tumors were mo
295 response compared with patients treated with docetaxel, which was associated with a long-term surviva
296 tosterone suppression, with or without early docetaxel, will improve survival in men with metastatic,
297 ring androgen-deprivation therapy (ADT) plus docetaxel with ADT alone for initial metastatic hormone-
298 kinase kinase (MEK) inhibitor selumetinib + docetaxel with docetaxel alone as a second-line therapy
300 y and safety of pertuzumab, trastuzumab, and docetaxel with placebo, trastuzumab, and docetaxel in pa