ライフサイエンスコーパス: induction chemotherapy

1 and 3D measurements) at diagnosis and after induction chemotherapy.

2 group progressed during the fourth cycle of induction chemotherapy.

3 He had an incomplete response to induction chemotherapy.

4 e was controlled after cisplatin-gemcitabine induction chemotherapy.

5 Cytarabine is a key constituent of remission induction chemotherapy.

6 ts when adding gemtuzumab ozogamicin (GO) to induction chemotherapy.

7 r PTCL patients who are chemosensitive after induction chemotherapy.

8 es of complete remission after one course of induction chemotherapy.

9 nts also received intensive or non-intensive induction chemotherapy.

10 ults who are not candidates for conventional induction chemotherapy.

11 ns when assessing for molecular responses to induction chemotherapy.

12 atients receiving idiotype vaccination after induction chemotherapy.

13 vaccination regardless of their response to induction chemotherapy.

14 ation based on response to a single cycle of induction chemotherapy.

15 observed with the addition of lintuzumab to induction chemotherapy.

16 ly advanced non-small-cell lung cancer after induction chemotherapy.

17 Forty-two percent of patients responded to induction chemotherapy.

18 pulation, best predicted patient response to induction chemotherapy.

19 ccurs in vivo in human lung cancer following induction chemotherapy.

20 ulness of CRc attained immediately following induction chemotherapy.

21 nd 2300 white) with de novo AML who received induction chemotherapy.

22 One patient was PET-negative after induction chemotherapy.

23 ed randomly to standard- or intensive-timing induction chemotherapy.

24 erlying hematological malignancies receiving induction chemotherapy.

25 were recommended before (t0) and after (t2) induction chemotherapy.

26 PBL were initially treated with surgery and induction chemotherapy.

27 e myeloma patients who achieve a response to induction chemotherapy.

28 fractionation radiotherapy, and the role of induction chemotherapy.

29 c acid-lowering agent for 5 to 7 days during induction chemotherapy.

30 dow before initiation of standard, multidrug induction chemotherapy.

31 acute myelogenous leukemia and treated with induction chemotherapy.

32 elate with prognostic factors or response to induction chemotherapy.

33 arabinoside (Ara-C), a primary component of induction chemotherapy.

34 acute myelogenous leukemia (AML) response to induction chemotherapy.

35 ients without minimal residual disease after induction chemotherapy.

36 lete, and sustained molecular response after induction chemotherapy.

37 good histologic response (good response) to induction chemotherapy.

38 cally advanced NSCLC underwent surgery after induction chemotherapy.

39 ve a high rate of complete remission (CR) to induction chemotherapy.

40 oncomitant chemoradiotherapy with or without induction chemotherapy.

41 tical data review within 21 days of starting induction chemotherapy.

42 are treated with curative intent and offered induction chemotherapy.

43 ly increased in bone marrow adipocytes after induction chemotherapy.

44 s shows the superiority of Tax-PF over PF as induction chemotherapy.

45 from patients with persistent disease after induction chemotherapy.

46 -2.00]; p=0.04) and receipt of non-intensive induction chemotherapy (1.97 [1.25-3.10]; p=0.003) were

47 After induction chemotherapy 163 of 189 (84.0%) underwent defi

48 Thirty-nine patients completed induction chemotherapy: 19 had a partial response, seven

49 [78%] vs 422 [76%]; p=0.43) or non-intensive induction chemotherapy (215 [50%] vs 195 [46%]; p=0.18).

50 antly reduced the frequency of resistance to induction chemotherapy (31% versus 47%, P =.0077).

51 eater than 50% response at the primary after induction chemotherapy; 43 went on to receive definitive

52 acid groups for patients receiving intensive induction chemotherapy (432 patients [78%] vs 422 [76%];

53 After induction chemotherapy, 54.7% of patients underwent comp

54 iferative neoplasms in blast phase receiving induction chemotherapy (55%), low-intensity therapy (16%

55 At remission, after course 1 induction chemotherapy, a > 3 log reduction in RUNX1-RUN

56 Induction chemotherapy added to concomitant chemoradioth

57 vant chemotherapy alone (0.87, 0.68-1.12) or induction chemotherapy alone (0.96, 0.80-1.16).

58 Toxicity was similar to that of standard induction chemotherapy alone.

59 concomitant chemotherapy (30.8% v 20.8% with induction chemotherapy and 16.9% with RT alone).

60 in the study, 58 had a complete response to induction chemotherapy and 252 had a partial response.

61 tion of healthy persons, appeared both after induction chemotherapy and after allogeneic HSCT.

62 We evaluated paclitaxel-based induction chemotherapy and chemoradiotherapy in patients

63 Here we review the results of both induction chemotherapy and chemoradiotherapy trials in p

64 AML) and developed methods to mimic standard induction chemotherapy and efficiently monitor therapy r

65 valuated by magnetic resonance imaging after induction chemotherapy and HFEBRT at a dose of 72 Gy.

66 mic and radiation therapy such as the use of induction chemotherapy and sequential chemotherapy and r

67 between the presence of activated ILCs after induction chemotherapy and the absence of acute graft-ve

68 systemic lymphoma, the low response rate to induction chemotherapy and the significant number of pat

69 approaches (one without fluorouracil) using induction chemotherapy and then definitive chemoradiothe

70 Trials investigating taxane inclusion in induction chemotherapy and trials of epidermal growth fa

71 cer Group study 3891 received five cycles of induction chemotherapy and were randomized either to mye

72 etween patients with nonresponding tumors to induction chemotherapy and WNT ( P = .143) or MYCC/MYCN

73 ients in our series, 192 (92%) received only induction chemotherapy, and 18 (9%) required additional

74 All patients underwent induction chemotherapy, and 52% received chemoradiation

75 tients with aggressive malignancies received induction chemotherapy, and all patients received conven

76 erebrospinal fluid (CSF) at diagnosis, after induction chemotherapy, and during follow-up.

77 gic subgroup, MYCC/ MYCN status, response to induction chemotherapy, and histologic subtype may serve

78 Organ preservation is possible using induction chemotherapy, and improved survival results ha

79 leukemia cells were incubated with standard induction chemotherapy, and individual cell stiffness wa

80 ukemic cells after 2 to 3 weeks of remission-induction chemotherapy, and these patients have an excel

81 Patients with RS who are sensitive to induction chemotherapy appear to benefit from consolidat

82 rvival, with induction group and response to induction chemotherapy as stratification parameters.

83 Response to induction chemotherapy as studied in this trial was not

84 (mean age, 50.8 years) treated with standard induction chemotherapy at a single site starting in Marc

85 tocol consisting of dexamethasone-containing induction chemotherapy, autologous stem-cell transplanta

86 Leukemia Group B 39801, we evaluated whether induction chemotherapy before concurrent chemoradiothera

87 l features of early treatment failure during induction chemotherapy before protocol radiation therapy

88 Induction chemotherapy before surgery may yield a surviv

89 10) were reviewed in 29 patients undergoing induction chemotherapy before surgery.

90 atients with ALL showing a rapid response to induction chemotherapy benefit from early intensive post

91 599 newly diagnosed AML patients treated by induction chemotherapy between 2000 and 2009.

92 If there is stable disease after 6 months of induction chemotherapy but unacceptable toxicities, radi

93 After induction chemotherapy, but before HDC, bronchoalveolar

94 ry was achieved in 46% of patients receiving induction chemotherapy, but remissions were not durable

95 The ability to determine response to induction chemotherapy by means of noninvasive monitorin

96 Induction chemotherapy, C/T or C/N, was followed by esca

97 TPF induction chemotherapy can be delivered safely with a ci

98 od performance status (PS) were treated with induction chemotherapy (carboplatin area under the curve

99 2-HG decrease was more rapid with induction chemotherapy compared with DNA-methyltransfera

100 th WT1 mutations had an inferior response to induction chemotherapy compared with wild-type cases (co

101 e investigated longitudinally the effects of induction chemotherapy, conditioning radiochemotherapy,

102 Induction chemotherapy consisted of carboplatin (area un

103 Induction chemotherapy consisted of two cycles of carbop

104 Toxicities during induction chemotherapy consisted primarily of grade 3 or

105 103 patients received induction chemotherapy, consisting of ketoconazole and d

106 in, and ifosfamide [VAI]) after an intensive induction chemotherapy containing vincristine, ifosfamid

107 signed to receive three additional cycles of induction chemotherapy (control group) or one additional

108 one marrow samples obtained after the second induction chemotherapy course.

109 e after completion of a predefined number of induction chemotherapy cycles, has two principal paradig

110 nt was initially comprised of five cycles of induction chemotherapy (cyclophosphamide, doxorubicin, a

111 Toxicity was low, and induction chemotherapy did not preclude delivery of conc

112 re, suggesting that an intervention, such as induction chemotherapy, directed at improving distant co

113 phase 3 trial comparing three cycles of TPF induction chemotherapy (docetaxel 75 mg/m(2), followed b

114 d, diagnosed between 2001 and 2007) received induction chemotherapy, dose-escalated hyperfractionated

115 Patients underwent induction chemotherapy during which peripheral-blood ste

116 Following induction chemotherapy, eligible patients underwent a si

117 y have a competitive fitness advantage after induction chemotherapy, expand, and persist long after t

118 ysis of the CGH findings in patients in whom induction chemotherapy failed compared with those in who

119 Induction chemotherapy failed to induce remission in 3 o

120 Moreover, induction chemotherapy failing to restore normal vascula

121 y (control group) or one additional cycle of induction chemotherapy followed by autologous stem-cell

122 rognostic value of metabolic response during induction chemotherapy followed by bimodality/trimodalit

123 i-institutional trial evaluates taxane-based induction chemotherapy followed by CCR for organ preserv

124 ce noted between those patients treated with induction chemotherapy followed by chemoradiotherapy and

125 ous phase II study had shown the efficacy of induction chemotherapy followed by chemoradiotherapy and

126 ogic response rate at the primary site after induction chemotherapy followed by chemoradiotherapy for

127 More patients had febrile neutropenia in the induction chemotherapy followed by chemoradiotherapy gro

128 (IQR 39-63), 41 patients had died-20 in the induction chemotherapy followed by chemoradiotherapy gro

129 that the three-step strategy of preoperative induction chemotherapy followed by chemoradiotherapy res

130 docetaxel, cisplatin, and fluorouracil (TPF) induction chemotherapy followed by concurrent chemoradio

131 using this kind of a sequential schedule of induction chemotherapy followed by concurrent chemoradio

132 We conducted a phase II study of induction chemotherapy followed by concurrent chemoradio

133 aryngeal cancer treated with this regimen of induction chemotherapy followed by definitive chemoradio

134 Thus, induction chemotherapy followed by HCT has the potential

135 tly from the proportions in the groups given induction chemotherapy followed by radiotherapy (75 perc

136 t administration of cisplatin is superior to induction chemotherapy followed by radiotherapy or radio

137 advanced neuroblastoma, we used a program of induction chemotherapy followed by tandem high-dose, mye

138 an preservation) to receive either TPF or PF induction chemotherapy, followed by chemoradiotherapy wi

139 ere are data from clinical trials to support induction chemotherapy, followed by radiotherapy (prefer

140 njunction with the first course of intensive induction chemotherapy for acute myeloid leukaemia (excl

141 xis with levofloxacin in children undergoing induction chemotherapy for ALL.

142 o standard 3 + 7 daunorubicin and cytarabine induction chemotherapy for AML resulted in an encouragin

143 eight patients given six cycles of intensive induction chemotherapy for high-risk neuroblastoma were

144 no benefit for patients receiving intensive induction chemotherapy for high-risk neuroblastoma.

145 lidation chemoradiotherapy after a course of induction chemotherapy for locally advanced pancreatic c

146 for use in a phase III comparative study of induction chemotherapy for patients with acute myeloid l

147 d capecitabine-based chemoradiotherapy after induction chemotherapy for patients with locally advance

148 poside and high-dose ifosfamide is effective induction chemotherapy for patients with metastatic oste

149 of platelet transfusions; they also received induction chemotherapy for similar durations and had sim

150 compromised woman with neutropenia following induction chemotherapy for treatment of acute myelogenou

151 thoracic radiation therapy (TRT), following induction chemotherapy, for treatment of locally advance

152 row samples collected on day 19 of remission-induction chemotherapy from 248 children with newly diag

153 During induction chemotherapy, grade 3/4 granulocytopenia occur

154 clearance of their founding AML clone after induction chemotherapy had a concomitant expansion of a

155 of patients had grade 3 or 4 toxicity during induction chemotherapy, half of which was hematologic.

156 PURPOSE Cisplatin plus fluorouracil (PF) induction chemotherapy has been compared with taxane (do

157 efore definitive locoregional management, or induction chemotherapy, has been a theoretically attract

158 squamous NSCLC, particularly those receiving induction chemotherapy, have sufficiently common BM rate

159 f worse outcome with concomitant relative to induction chemotherapy (HR, 1.25; 95% CI, 0.98 to 1.61;

160 samples, 15 with inferior necrosis following induction chemotherapy (Huvos I/II) and 15 with superior

161 /II) and 15 with superior necrosis following induction chemotherapy (Huvos III/IV), was conducted usi

162 on was inversely associated with response to induction chemotherapy (IC) (P = .01), chemotherapy/radi

163 Induction chemotherapy (IC) before radiotherapy lowers d

164 whether complete clinical response (cCR) to induction chemotherapy (IC) could select patients with H

165 TAX 324 was a phase III trial comparing induction chemotherapy (IC) with docetaxel, cisplatin, a

166 value of early assessment (after 1 cycle of induction chemotherapy [IC]) with (18)F-FDG PET/CT and d

167 Questions regarding the role of induction chemotherapy (ICT) and a higher radiation dose

168 disease, we conducted a phase II trial with induction chemotherapy (ICT) consisting of six weekly cy

169 Despite decades of research, the role of induction chemotherapy (ICT) in the treatment of locally

170 fractory patients and those who responded to induction chemotherapy identified a single gene, interle

171 s indicate that preleukemic HSCs can survive induction chemotherapy, identifying these cells as a res

172 homa, determine whether additional cycles of induction chemotherapy improve the complete response (CR

173 -independent carcinoma of the prostate after induction chemotherapy, improved overall survival.

174 Dysphagia improved or resolved after induction chemotherapy in 13 (81%) of 16 patients who re

175 efficacy of adding gemtuzumab ozogamicin to induction chemotherapy in adult patients with acute myel

176 rials in which it was combined with standard induction chemotherapy in adults have produced conflicti

177 ence of persistent or relapsed disease after induction chemotherapy in AML necessitates a better unde

178 ted ABD as a predictor of a poor response to induction chemotherapy in an independent series of patie

179 (18)F-FDG PET for monitoring the response to induction chemotherapy in HNSCC or for assessing treatme

180 correlated with residual viable tumor after induction chemotherapy in locally advanced NSCLC.

181 appropriate for response consolidation after induction chemotherapy in older patients with advanced d

182 appropriate for response consolidation after induction chemotherapy in older patients with advanced d

183 predicted an improved outcome with high-dose induction chemotherapy in patients with AML.

184 etic priming with decitabine before standard induction chemotherapy in patients with less-than-favora

185 sidual disease (MRD) detection at the end of induction chemotherapy in pediatric patients with newly

186 roach that merits reassessment is the use of induction chemotherapy in the setting of locally advance

187 therapy following primary surgery of OPSCC, induction chemotherapy in the treatment of OPSCC, and th

188 Earlier studies of preoperative (induction) chemotherapy in resectable NSCLC demonstrated

189 Response to induction chemotherapy included partial response rate of

190 One hundred patients received induction chemotherapy including 4 cycles of continuous

191 relapse after one or two cycles of previous induction chemotherapy, including at least one cycle of

192 However, it remains unknown how induction chemotherapy influences the clonal evolution o

193 not demonstrate any benefit to the use of ME induction chemotherapy instead of AD in older patients w

194 Early response to induction chemotherapy is a predictor of outcome in acut

195 Early response to induction chemotherapy is an important prognostic factor

196 me to clearance of circulating blasts during induction chemotherapy is an independent prognostic mark

197 Resistance to intensive induction chemotherapy is the major cause of death in el

198 Response to induction chemotherapy may affect OS only for continuati

199 nalysis showed that magnitude of response to induction chemotherapy may affect the OS benefit as a re

200 soon after HDT suggest that more aggressive induction chemotherapy may be warranted.

201 Induction chemotherapy may contribute to local failure b

202 rent chemoradiation show that the three-drug induction chemotherapy may improve survival particularly

203 ns of gemtuzumab ozogamicin as an adjunct to induction chemotherapy may yet be a viable option in old

204 All patients were treated with six cycles of induction chemotherapy, myeloablative consolidation, and

205 were evaluated at diagnosis (n = 280), after induction chemotherapy (n = 237), and after an autologou

206 After induction chemotherapy, no evidence of MD of tumor cells

207 o 10(-3) at the end of 4 weeks of multiagent induction chemotherapy now receive intensified treatment

208 Patients received up to two 28-day cycles of induction chemotherapy of fluorouracil, leucovorin, and

209 Patients received two 28-day cycles of induction chemotherapy of fluorouracil, paclitaxel, and

210 Grade 3 or 4 toxicities during induction chemotherapy on arm B consisted mainly of neut

211 er way, which use idiotype vaccination after induction chemotherapy; one trial completed accrual in e

212 parameter for treatment stratification after induction chemotherapy or for evaluation of adjuvant new

213 We included patients receiving intensive induction chemotherapy or non-intensive treatment.

214 f circulating leukemic blasts in response to induction chemotherapy or prednisone is one of the most

215 nsplantation, hypomethylating agent therapy, induction chemotherapy, or enrollment in a clinical tria

216 sis in patients, show a dramatic response to induction chemotherapy owing to robust activation of the

217 However, it is unclear whether induction chemotherapy per se is effective when compared

218 However, little is known concerning the role induction chemotherapy plays in its development.

219 ed docetaxel plus cisplatin and fluorouracil induction chemotherapy plus chemoradiotherapy had a sign

220 ents who received cisplatin and fluorouracil induction chemotherapy plus chemoradiotherapy.

221 We found that patients after induction chemotherapy plus G-CSF had similar overall su

222 Initial response to induction chemotherapy predicts failure-free survival (F

223 PTCL patients with responsive disease after induction chemotherapy proceeded to AHCT.

224 alysis showed that, in general, a successful induction chemotherapy produces a reduction of 2 to 3 lo

225 blood at diagnosis and in bone marrow during induction chemotherapy provides prognostic information t

226 Complete or partial responders to induction chemotherapy received 54 Gy in 27 fractions, a

227 tients with complete or partial responses to induction chemotherapy received 54 Gy radiation, and 20

228 Adding GO (3 mg/m(2)) to induction chemotherapy reduces relapse risk and improves

229 cutaneous rituximab (1400 mg), stratified by induction chemotherapy regimen (cyclophosphamide, doxoru

230 This intensified induction chemotherapy regimen is feasible and tolerable

231 imum-tolerated dose (MTD) of cisplatin in an induction chemotherapy regimen of docetaxel, cisplatin,

232 Objective response rate to the induction chemotherapy regimen was 90%; overall median s

233 old with ALL were treated with a four-agent induction chemotherapy regimen.

234 We randomly assigned 302 patients to receive induction chemotherapy regimens consisting of cytosine a

235 ing was a determinant of initial response to induction chemotherapy, relapse after remission, and req

236 The addition of induction chemotherapy remains an appropriate approach f

237 Intensified induction chemotherapy resulted in a high response rate

238 Induction chemotherapy resulted in eight complete and 21

239 nts with acute myelogenic leukemia receiving induction chemotherapy, risks for C. kefyr colonization

240 0) were treated with five to seven cycles of induction chemotherapy (rituximab, MTX, procarbazine, an

241 Taxane-based induction chemotherapy seems promising in phase II studi

242 Patients who are candidates for induction chemotherapy should be treated with TPF.

243 reated with standard-dose daunorubicin-based induction chemotherapy, suggesting that DNMT3A(R882) cel

244 SUVmax) remaining in the primary tumor after induction chemotherapy-%SUVremaining = SUVmax(t2)/SUVmax

245 Twenty-four patients received AML-like induction chemotherapy that resulted in no complete remi

246 After induction chemotherapy, the metabolic change in (11)C-ac

247 On admission for induction chemotherapy, the patient was noted to have an

248 AML) whose disease is refractory to standard induction chemotherapy therapy or who experience relapse

249 er with disease controlled after 4 months of induction chemotherapy, there was no significant differe

250 ly salvage surgery after the single cycle of induction chemotherapy, three patients (3%) had late sal

251 The relative efficacy of the addition of induction chemotherapy to chemoradiotherapy compared wit

252 The addition of induction chemotherapy to concurrent chemoradiotherapy a

253 this review we summarise data for the use of induction chemotherapy to define better which patients w

254 undergo a bone marrow biopsy 7-10 days after induction chemotherapy to evaluate treatment effectivene

255 nt failure rates, we added a brief course of induction chemotherapy to TFHX.

256 ndomly assigned in a 1:1 ratio to concurrent induction chemotherapy (two cycles of cisplatin [50 mg/m

257 Delaying induction chemotherapy until molecular testing results r

258 Intensive induction chemotherapy using a regimen consisting of car

259 icantly improved LFS compared with RT alone (induction chemotherapy v RT alone: hazard ratio [HR], 0.

260 randomly assigned to one of two regimens of induction chemotherapy (vincristine, cisplatin, cyclopho

261 They were treated with 3-drug induction chemotherapy (vincristine, dactinomycin, and d

262 nse rate (partial and complete responses) to induction chemotherapy was 89%.

263 The major response rate to induction chemotherapy was 89%; 90% of patients had a co

264 Induction chemotherapy was allowed.

265 e efficacy of lintuzumab in combination with induction chemotherapy was compared with chemotherapy al

266 Induction chemotherapy was generally followed by radiati

267 EP induction chemotherapy was given to 23.1% of high-risk p

268 Response to induction chemotherapy was partial response 52% and comp

269 The addition of lintuzumab to salvage induction chemotherapy was safe, but did not result in a

270 motherapy failed compared with those in whom induction chemotherapy was successful identified the abs

271 Induction chemotherapy was two cycles of cisplatin 100 m

272 After two or three cycles of induction chemotherapy, we randomly assigned 72 patients

273 onstrating less than complete response after induction chemotherapy were encouraged to undergo second

274 The most common grade 3 events during induction chemotherapy were leucopenia (17 [39%]) and ne

275 ts who had a complete or partial response to induction chemotherapy were then randomly assigned to re

276 Patients received two cycles of induction chemotherapy with 175 mg/m(2) paclitaxel and c

277 ith high-risk neuroblastoma includes initial induction chemotherapy with a 21-day interval between in

278 dard treatment paradigm for AML is remission induction chemotherapy with an anthracycline/cytarabine

279 es from 175 adult AML patients who underwent induction chemotherapy with anthracycline and cytarabine

280 After two cycles of induction chemotherapy with carboplatin-paclitaxel, HART

281 Induction chemotherapy with cisplatin plus fluorouracil

282 ients then received two courses of remission induction chemotherapy with daunorubicin, ara-C, and eto

283 cell carcinoma of the head and neck compared induction chemotherapy with docetaxel plus cisplatin and

284 udy showed a significant survival benefit of induction chemotherapy with docetaxel, cisplatin, and fl

285 stage IIIA/B NSCLC were randomly assigned to induction chemotherapy with either carboplatin (area und

286 To establish the safety and efficacy of induction chemotherapy with infusional fluorouracil (FU)

287 improved survival with the addition of GO to induction chemotherapy with little additional toxicity.

288 age 61 to 75 years were randomly assigned to induction chemotherapy with mitoxantrone, cytarabine, an

289 tment consisted of intensive alkylator-based induction chemotherapy with or without autologous bone m

290 Thus, we studied the use of induction chemotherapy with or without conservation lary

291 were randomly assigned to receive identical induction chemotherapy with or without thalidomide, are

292 Induction chemotherapy with PFL followed by concurrent c

293 Patients received induction chemotherapy with R-MPV (five to seven cycles)

294 e the potential benefits of combining CHOP-R induction chemotherapy with RIT consolidation and/or ext

295 Induction chemotherapy with the three-drug regimen docet

296 assigned (in a 1:1 ratio) to receive either induction chemotherapy with three cycles of TPF followed

297 Induction chemotherapy with TPF provides long-term survi

298 Induction chemotherapy with weekly cisplatin 30 mg/m2 an

299 IENTS AND METHODS Patients received the same induction chemotherapy, with random assignment (N = 379)

300 If there is local disease progression after induction chemotherapy, without metastasis, then radiati