ライフサイエンスコーパス: myelosuppression

1 Toxicity consisted primarily of myelosuppression.

2 tion and, unlike ganciclovir, does not cause myelosuppression.

3 ced susceptibility to 5-fluorouracil-induced myelosuppression.

4 The most common grade 3/4 toxicity was myelosuppression.

5 The major toxicity was myelosuppression.

6 e > or = 3 toxicities were related mostly to myelosuppression.

7 obust recovery from cyclophosphamide-induced myelosuppression.

8 /m2 with dose-limiting toxicities limited to myelosuppression.

9 l to accelerate hemangiogenic recovery after myelosuppression.

10 sembly and remodeling of BM neovessels after myelosuppression.

11 All patients had anticipated myelosuppression.

12 patients (36%) received AHSCT for prolonged myelosuppression.

13 sis under physiological conditions and after myelosuppression.

14 and FGF-4 diminished thrombocytopenia after myelosuppression.

15 consists mainly of moderate but controllable myelosuppression.

16 The most frequent side effect was myelosuppression.

17 balanced hematopoietic reconstitution after myelosuppression.

18 es were supraventricular tachyarrhythmia and myelosuppression.

19 duce remissions but entails risks related to myelosuppression.

20 ith minimal bladder irritation and tolerable myelosuppression.

21 e but thereby increased chemotherapy-induced myelosuppression.

22 nadir was minimized, even with BSO-enhanced myelosuppression.

23 insufficiency, polydipsia, paresthesias, and myelosuppression.

24 s treatment can be administered with minimal myelosuppression.

25 indolent lymphoma with minimal toxicity and myelosuppression.

26 xposure correlated well with the severity of myelosuppression.

27 otoxicity, liver function abnormalities, and myelosuppression.

28 primates after high-dose, radiation-induced myelosuppression.

29 he potential to cause clinically significant myelosuppression.

30 ted at all dose levels, with no grade 3 or 4 myelosuppression.

31 eys administered MPO after radiation-induced myelosuppression.

32 store TMZ sensitivity, but causes off-target myelosuppression.

33 d cycling state after 5-fluorouracil-induced myelosuppression.

34 sed 14 d after therapy to abrogate prolonged myelosuppression.

35 icities observed were fatigue and reversible myelosuppression.

36 the most frequent grade 3 to 4 toxicity was myelosuppression.

37 ads to lymphocyte depletion with low risk of myelosuppression.

38 The primary toxicity is myelosuppression.

39 le to rescue hematopoiesis in the setting of myelosuppression.

40 nly significant toxicity was mild, transient myelosuppression.

41 potential to cause peripheral neuropathy and myelosuppression.

42 Skin and mucosal toxicities (2% grade 3) and myelosuppression (55% grade 3 or 4) were the most common

43 s/m2 daily, mainly because of reductions for myelosuppression (70% of cases); the median ara-C dose w

44 well tolerated but resulted in more frequent myelosuppression; 82% of patients continue to receive 60

45 eated with higher paclitaxel doses died from myelosuppression after the first administration.

46 ion and repopulating potential in vivo after myelosuppression and accelerates HSC expansion during in

47 histocompatibility complex barriers, without myelosuppression and by using moderate doses of bone mar

48 oxicities associated with this agent include myelosuppression and cardiotoxicity; however, the genes

49 oxantrone arm, which was offset by increased myelosuppression and deaths in CR.

50 Common toxicities were myelosuppression and diarrhea.

51 The DLTs were mainly myelosuppression and diarrhea.

52 ient mice are resistant to chemokine-induced myelosuppression and do not show a synergistic growth re

53 The absence of significant myelosuppression and encouraging clinical responses sugg

54 de >/=3 drug-related adverse events included myelosuppression and fatigue.

55 Toxicokinetic analysis of CPA-induced myelosuppression and granulocytopenia showed that at hig

56 sible in a community-based setting; however, myelosuppression and hospitalizations for treatment of n

57 acodynamic effect that augments RAPA-induced myelosuppression and hyperlipidemia.

58 ytic leukemia (CLL) but can have significant myelosuppression and immunosuppression that may require

59 owing to increased toxicity from overlapping myelosuppression and immunosuppression.

60 cause of increased toxicity from overlapping myelosuppression and immunosuppression.

61 Toxicity was predominantly myelosuppression and included grade 3/4 neutropenia in 5

62 A to potentiate two RAPA-mediated toxicities-myelosuppression and increased serum cholesterol/low-den

63 Myelosuppression and infection remain the most significa

64 main complication of therapy was related to myelosuppression and infection.

65 patients has been restricted by substantial myelosuppression and infection.

66 Myelosuppression and infections were uncommon.

67 ot improved due to mortality associated with myelosuppression and its sequelae.

68 coupled with markedly reduced potential for myelosuppression and MAOI.

69 halidomide and BCNU was well tolerated; mild myelosuppression and mild to moderate sedation were the

70 Myelosuppression and monoamine oxidase inhibition (MAOI)

71 posure, oral administration of TMC mitigated myelosuppression and mortality in mice.

72 ell (HSPC) function and mitigates IR-induced myelosuppression and mortality.

73 Toxicity was mainly mild and/or reversible myelosuppression and mucositis; however, four patients d

74 anti-CD45 antibody are sufficient to achieve myelosuppression and myeloablation with less nonhematolo

75 patients in phase 2, we noted a high rate of myelosuppression and myelosuppression-related toxic effe

76 Myelosuppression and nephrotoxicity were not observed.

77 rase inhibitors has been limited somewhat by myelosuppression and other side effects.

78 Myelosuppression and other significant organ toxicities

79 Toxicity, especially myelosuppression and pneumonitis, was more pronounced in

80 iry cell leukemia (HCL), are associated with myelosuppression and profound and prolonged immunosuppre

81 regimen was well tolerated, with acceptable myelosuppression and rare treatment-related diarrhea.

82 apy tolerance was determined by the observed myelosuppression and recovery following each cycle.

83 t was associated with side effects including myelosuppression and recurrence of severe GVHD.

84 se-limiting toxicities on this schedule were myelosuppression and renal dysfunction.

85 c deaths were documented and were related to myelosuppression and sepsis in one patient and pneumonia

86 Myelosuppression and stomatitis were dose-limiting toxic

87 Severe myelosuppression and stomatitis/esophagitis were the mos

88 this study was to determine risk factors for myelosuppression and the need for AHSCT after (131)I-MIB

89 diarrhea, anorexia, and dehydration, whereas myelosuppression and thrombocytopenia were more prominen

90 herapy to determine whether it could prevent myelosuppression and to determine the antitumor activity

91 n of NAC to perfuse bone marrow and minimize myelosuppression and toxicity to visceral organs could b

92 ost common grade 3 to 4 adverse effects were myelosuppression and transient elevation of transaminase

93 Myelosuppression and weight loss exhibited a haploinsuff

94 ignificantly reduced aggressiveness, reduced myelosuppression, and a more differentiated phenotype.

95 clonal antibodies YTH 24.5 and YTH 54.12 for myelosuppression, and alemtuzumab (anti-CD52) and fludar

96 oxicity of 90Y ibritumomab tiuxetan has been myelosuppression, and concern has been expressed about t

97 Common adverse events were rash, myelosuppression, and constitutional symptoms.

98 state conditions, after chemotherapy-induced myelosuppression, and during bone marrow transplantation

99 d in higher rates of venous thromboembolism, myelosuppression, and infections versus placebo + dexame

100 arrow microvascular reconstruction following myelosuppression, and limited the extent of revasculariz

101 apy, with increased p53-dependent apoptosis, myelosuppression, and mortality.

102 xicity was significantly greater (infection, myelosuppression, and mucositis) in the six-drug arm.

103 toring, managing common side effects such as myelosuppression, and potential drug interactions.

104 rovided protection from chemotherapy-induced myelosuppression, and proviral integration site analysis

105 ld prevent p53-dependent apoptosis, decrease myelosuppression, and reduce the need for platelet trans

106 Severe myelosuppression, and stomatitis or esophagitis were the

107 ghtly superior biodistribution profile, less myelosuppression, and superior efficacy.

108 The most common toxicity was myelosuppression, and the median daily dose of lenalidom

109 nts in the T discontinued MMF for infection, myelosuppression, and/or gastrointestinal disturbances.

110 s: 2 mg/m(2) for solid tumors, the DLT being myelosuppression; and 40 mg/m(2) for acute leukemia, the

111 ated with alemtuzumab administration include myelosuppression as well as profound cellular immune dys

112 adaches (3%), cardiovascular events (3%),and myelosuppression-associated complications (3% to 14%).

113 occurred in four patients in the context of myelosuppression-associated infectious complications.

114 has been hampered by acquired resistance and myelosuppression attributed to a 'synthetic lethal toxic

115 was well tolerated at all dose levels, with myelosuppression being the major side effect.

116 toxicities were observed at any level, with myelosuppression being the most frequent toxicity.

117 Nevertheless, only two patients developed myelosuppression (both grade 2).

118 pression in bone marrow stem cells to reduce myelosuppression brought about by alkylating agents, to

119 volvement was a risk factor for higher grade myelosuppression but could be identified by PSMA imaging

120 rm HU toxicities primarily include transient myelosuppression, but long-term HU risks have not been d

121 The primary toxicity was myelosuppression, but the MTD was not defined because do

122 ation is used to rescue cancer patients from myelosuppression caused by high-dose chemotherapy.

123 ortant limitation of this approach is severe myelosuppression caused by many of these drug combinatio

124 The myelosuppression caused by this agent has led to the dev

125 ociated with a higher incidence of grade 3/4 myelosuppression, constitutional symptoms, and GI and de

126 JAK2 inhibitors with the potential for less myelosuppression continue to be investigated.

127 vents, such as prolonged periods of profound myelosuppression, contribute to AML treatment-related mo

128 Myelosuppression, determined by peripheral blood cell co

129 The expected myelosuppression developed after busulfan but then persi

130 l within the first 28 days; however, grade 3 myelosuppression developed after day 28 in all 13 patien

131 tion-time curve (P = .0015), but severity of myelosuppression did not.

132 Myelosuppression due to pegylated interferon (peg-IFN) i

133 tal body irradiation (TBI) can induce lethal myelosuppression, due to the sensitivity of proliferatin

134 te constitutional symptoms, chronic fatigue, myelosuppression, elevated liver enzyme levels, and neur

135 Anticipated rates of myelosuppression, fatigue, and expected regimen-specific

136 e of 600 mg PO bid resulted in side effects (myelosuppression, fatigue, neurotoxicity, rash, or leg p

137 The most common toxicities were myelosuppression, febrile neutropenia, and fatigue.

138 d Notch signaling improves HSPC function and myelosuppression following IR exposure.

139 ve an increased risk of chemotherapy-induced myelosuppression following treatment.

140 (211)At was more effective at producing myelosuppression for the same quantity of injected radio

141 e most frequently observed toxicity included myelosuppression, gastrointestinal symptoms, and asympto

142 Myelosuppression, GI, and hepatic toxicities were common

143 Toxicity is limited to temporary myelosuppression, governed by the administered activity

144 Main side effects were myelosuppression (grade 3 or 4 anemia, 14%; and thromboc

145 , affecting single patients at the MTD, were myelosuppression (grade 4), raised bilirubin, vomiting,

146 The principal toxicity was myelosuppression; grade 4 neutropenia was more frequent

147 Myelosuppression, graft-versus-host disease (GVHD), and

148 Myelosuppression was common, but prolonged myelosuppression (> 42 days) was rare.

149 le profile of adverse events, but reversible myelosuppression has occurred in patients receiving high

150 Nineteen patients experienced myelosuppression higher than grade 2, most frequently th

151 0 mCi/m(2) was associated with dose-limiting myelosuppression; however, up to three doses of 30 mCi/m

152 Despite expected mild myelosuppression, hydroxyurea was not associated with an

153 d patients had relatively high incidences of myelosuppression, hyperbilirubinemia, and elevated hepat

154 n of HU results in significant but transient myelosuppression in advanced-phase CML.

155 esent an underlying mechanism for developing myelosuppression in alcohol-abusing hosts with severe ba

156 e (Fapy)] and is associated with significant myelosuppression in dose-intensive therapies.

157 f the antigens that triggers T cell-mediated myelosuppression in MDS.

158 tentially decreasing cumulative drug-induced myelosuppression in patients with cancer.

159 a first-line chemotherapy drug, often causes myelosuppression in patients, thus limiting its effectiv

160 FLT3, induced spleen responses with limited myelosuppression in phase 1/2 trials.

161 clophosphamide dose was decreased because of myelosuppression in the early part of the study.

162 cocutaneous toxicity in the FAP arm and more myelosuppression in the M-VAC arm.

163 lacebo plus letrozole, with a higher rate of myelosuppression in the ribociclib group.

164 The major toxicity was myelosuppression in three of five patients at 1500 mg/m(

165 th grade 3 or grade 4 adverse events (mainly myelosuppression) in less than 10% of patients.

166 lerated recovery of haematopoiesis following myelosuppression, in part through protection of the BM m

167 Following sublethal radiation-induced myelosuppression, in vivo overexpression of murine IL-17

168 suited to help manage radiation victims, as myelosuppression is a frequent complication of radiation

169 Myelosuppression is a life-threatening complication of a

170 PRRT-induced myelosuppression is almost invariably reversible and rar

171 achieving symptomatic response without undue myelosuppression is challenging.

172 Myelosuppression is mild and uncommon.

173 ietic stem cell (HSC) regeneration following myelosuppression is not well understood.

174 Myelosuppression is the dose-limiting toxicity for many

175 Most data indicate that myelosuppression is the same or less pronounced among th

176 Toxicity, especially myelosuppression, is significant.

177 ated and produced a noncumulative, transient myelosuppression late in the 28-day cycle.

178 The most common toxicities were myelosuppression (leukopenia, neutropenia, and thrombocy

179 Myelosuppression limited further dose escalation, howeve

180 Significant myelosuppression limited the ability to coadminister ABT

181 Myelosuppression may be the dose-limiting toxicity in pe

182 At a paclitaxel dose of 60 mg/m(2)/wk, myelosuppression, mostly neutropenia, was relatively mil

183 Side effects were myelosuppression, mucositis, and hearing deficits; neuro

184 ecause of lack of improvement in GVHD (n=5), myelosuppression (n=2), seizure (n=2), and attending phy

185 Severe myelosuppression (neutropenia that was protracted and/or

186 st adverse events (AEs) were consistent with myelosuppression; nonhematologic AEs included fatigue, n

187 0K) overexpression prevented the substantial myelosuppression normally associated with this drug comb

188 To overcome the myelosuppression observed by chemotherapeutic alkylating

189 The increased myelosuppression observed is at least partially because

190 Reversible grade 4 myelosuppression occurred in all patients, but no deaths

191 Clinically significant myelosuppression occurred in less than 10% of patients i

192 Myelosuppression occurred in most patients, but toxic de

193 Myelosuppression occurred sporadically at all dose level

194 atment toxicities were confined to transient myelosuppression of grade 3 or 4 in 15.3% (leukopenia) a

195 did not induce the toxicity (cardiotoxicity/myelosuppression) of paclitaxel in mice.

196 Despite the severe myelosuppression, only 34 (11%) of 307 courses were asso

197 ors in response to hematopoietic stress from myelosuppression or after transplantation.

198 associated with patients experiencing severe myelosuppression or cardiac toxicity following treatment

199 cantly extended survival without evidence of myelosuppression or cardiac toxicity.

200 nce of toxicity to major organs, the minimal myelosuppression or immunosuppression, and the antineopl

201 cell count and platelet recoveries following myelosuppression or radiotherapy.

202 in combination to produce renal dysfunction, myelosuppression, or hyperlipidemia, with their correspo

203 sed renal function, previous therapy-induced myelosuppression, or major coexisting illnesses to recei

204 on new JAK inhibitors with potentially less myelosuppression( pacritinib) or even activity for anemi

205 In group A, dose-limiting myelosuppression persisted despite de-escalation of TOPO

206 Proximal myopathy, erectile dysfunction, and myelosuppression precluded the administration of multipl

207 Myelosuppression, predominately neutropenia, was the pri

208 When G-CSF was not used, myelosuppression prevented escalation beyond the startin

209 The most frequent adverse events included myelosuppression, rash, fatigue, and musculoskeletal sym

210 and dose-limiting toxicities on cycle 1 were myelosuppression, rash, nausea, vomiting, and diarrhea.

211 Radium-223 was associated with low myelosuppression rates and fewer adverse events.

212 overall and in subgroups, but with increased myelosuppression, reducing participation in the consolid

213 we noted a high rate of myelosuppression and myelosuppression-related toxic effects; therefore, we am

214 rdens in patients, but it produces prolonged myelosuppression requiring hematopoietic stem cell trans

215 Prolonged myelosuppression resulted in significant treatment delay

216 ntly less stomatitis/mucositis (P <.001) and myelosuppression, resulting in fewer episodes of febrile

217 Chemotherapy- or radiation-induced myelosuppression results in apoptosis of cycling hematop

218 osteosarcoma, despite significant associated myelosuppression sometimes complicated by infection and

219 reover, during emergency situations, such as myelosuppression, Stat5a/b-mutant mice failed to produce

220 xicities included infection, cardiotoxicity, myelosuppression, stomatitis, and reversible increases i

221 Grade 3/4 myelosuppression TEAEs were reported in 41% of patients;

222 growth, which may result in relatively less myelosuppression than quizartinib.

223 This schedule was also associated with more myelosuppression than the schedule of OSI-211 administer

224 ose and was more predictive of the degree of myelosuppression than was PZA dose.

225 s may contribute to the patient variation in myelosuppression that occurs after treatment with microt

226 esponse, with a safety profile that included myelosuppression, the cytokine release syndrome, and neu

227 een groups, with the most frequent including myelosuppression, thrombocytopenia, anemia, nausea, vomi

228 Common adverse events were myelosuppression, transient indirect hyperbilirubinemia,

229 Frequent toxicities included myelosuppression, vomiting, sensory neuropathy, and otot

230 Myelosuppression was acceptable with grade 3/4 neutropen

231 Dose-limiting myelosuppression was associated with both an increased 2

232 Myelosuppression was common but not dose-limiting.

233 Myelosuppression was common, but prolonged myelosuppress

234 Myelosuppression was common.

235 As a result, myelosuppression was comparable to that produced by full

236 Severe myelosuppression was consistently experienced by heavily

237 Myelosuppression was dose limiting and 35 mg/m(2)/dose x

238 Myelosuppression was dose limiting at 75 mCi/m(2), and t

239 Myelosuppression was dose-limiting, consisting of thromb

240 Myelosuppression was frequent.

241 Myelosuppression was mild and infrequent.

242 Myelosuppression was mild.

243 oxicities were mainly hematologic; prolonged myelosuppression was not observed.

244 Clinically significant myelosuppression was not observed; hematologic toxicity

245 No grade 4 toxicity or clinically relevant myelosuppression was noted.

246 ell tolerated, but mild to severe reversible myelosuppression was noted.

247 namic relation between systemic exposure and myelosuppression was noted.

248 Grade 3 to 4 myelosuppression was observed in 28% of patients in the

249 On testing this system in vivo, decreased myelosuppression was observed in mice transplanted with

250 Dose-limiting pneumonitis or myelosuppression was observed in three of three patients

251 Although myelosuppression was prolonged following the administrat

252 In the MPT patients, dose-limiting myelosuppression was reached at 80 mg/m2, with six patie

253 Grade 3-4 myelosuppression was reported in 33 (26%) of 128 patient

254 Grade 3 or 4 myelosuppression was seen in 30 patients, primarily in a

255 DLT caused by myelosuppression was seen in two of six patients treated

256 Myelosuppression was seen with 68% of patients who exper

257 As expected, myelosuppression was severe in both groups; however, >/=

258 currence of clinically significant grade 3/4 myelosuppression was shorter in the twice-daily group (1

259 trate that thrombopoietic recovery following myelosuppression was significantly enhanced in mice defi

260 and thrombocytopenia (four [31%] patients); myelosuppression was similar in each cohort.

261 Myelosuppression was similar to that expected with pacli

262 Myelosuppression was the DLT.

263 Reversible myelosuppression was the main adverse event and was more

264 Toxicities were manageable; myelosuppression was the main toxicity (25% and 14% of p

265 Myelosuppression was the main toxicity with 88% with >/=

266 Myelosuppression was the main toxicity.

267 Myelosuppression was the major adverse effect, with neut

268 Myelosuppression was the major dose-limiting toxicity.

269 Myelosuppression was the major toxicity, and two patient

270 Myelosuppression was the major toxicity, as has been rep

271 Myelosuppression was the major toxicity; 58% of carbopla

272 Myelosuppression was the most common toxicity.

273 Myelosuppression was the most common toxicity.

274 Myelosuppression was the most frequent toxicity: grade 3

275 Myelosuppression was the most frequently observed toxici

276 Myelosuppression was the predominant toxicity.

277 Reversible myelosuppression was the primary toxicity noted with (90

278 Myelosuppression was the primary toxicity to TC.

279 Myelosuppression was the principal toxicity.

280 similar to the FOLFOX4 regimen, except that myelosuppression was uncommon with XELOX (grade 3 or 4 n

281 Acute toxicity, including myelosuppression, was mild.

282 Acute toxicity, including myelosuppression, was mild.

283 phil recovery after cyclophosphamide-induced myelosuppression, was normal.

284 ciclovir discontinuation, renal function and myelosuppression were also assessed.

285 rate, but rates of peripheral neuropathy and myelosuppression were increased.

286 Regimen toxicities and myelosuppression were mild, allowing 53% of eligible pat

287 Fatigue and myelosuppression were the most common treatment-related

288 e competitive repopulation and recovery from myelosuppression were the same as for wild type.

289 topenia are the only factors contributing to myelosuppression, whereas splenectomy may exert a protec

290 e most common and dose-limiting toxicity was myelosuppression, which consisted of neutropenia that wa

291 The dose-limiting toxicity was myelosuppression, which included neutropenia and thrombo

292 syndrome (H-ARS) is characterized by severe myelosuppression, which increases the risk of infection,

293 The primary toxicity of (131)I-MIBG is myelosuppression, which might necessitate autologous hem

294 and docetaxel causes significant reversible myelosuppression, which was dose limiting but led to no

295 Toxicity consisted primarily of myelosuppression, which was manageable.

296 There was more myelosuppression with DC but no additional mortality.

297 neuropathy during thalidomide maintenance vs myelosuppression with MPR.

298 thout HCT rescue demonstrated dose-dependent myelosuppression with subsequent autologous recovery, an

299 All 17 evaluable patients developed myelosuppression, with a median time to recovery of 22 d

300 Toxicities have primarily included prolonged myelosuppression, with a potential risk of treatment-ass