ライフサイエンスコーパス: myelosuppression

1 nd enhances hematopoietic recovery following myelosuppression.

2 to predict their mechanisms and magnitude of myelosuppression.

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

4 ads to lymphocyte depletion with low risk of myelosuppression.

5 The primary toxicity is myelosuppression.

6 n, as well as BM recovery after drug-induced myelosuppression.

7 nly significant toxicity was mild, transient myelosuppression.

8 potential to cause peripheral neuropathy and myelosuppression.

9 Toxicity consisted primarily of myelosuppression.

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

11 ced susceptibility to 5-fluorouracil-induced myelosuppression.

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

13 The major toxicity was myelosuppression.

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

15 obust recovery from cyclophosphamide-induced myelosuppression.

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

17 l to accelerate hemangiogenic recovery after myelosuppression.

18 sembly and remodeling of BM neovessels after myelosuppression.

19 Use of thiopurines may be limited by myelosuppression.

20 All patients had anticipated myelosuppression.

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

22 sis under physiological conditions and after myelosuppression.

23 and FGF-4 diminished thrombocytopenia after myelosuppression.

24 consists mainly of moderate but controllable myelosuppression.

25 The most frequent side effect was myelosuppression.

26 balanced hematopoietic reconstitution after myelosuppression.

27 duce remissions but entails risks related to myelosuppression.

28 ith minimal bladder irritation and tolerable myelosuppression.

29 e but thereby increased chemotherapy-induced myelosuppression.

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

31 insufficiency, polydipsia, paresthesias, and myelosuppression.

32 s treatment can be administered with minimal myelosuppression.

33 indolent lymphoma with minimal toxicity and myelosuppression.

34 xposure correlated well with the severity of myelosuppression.

35 otoxicity, liver function abnormalities, and myelosuppression.

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

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

38 eys administered MPO after radiation-induced myelosuppression.

39 le to rescue hematopoiesis in the setting of myelosuppression.

40 es were supraventricular tachyarrhythmia and myelosuppression.

41 he potential to cause clinically significant myelosuppression.

42 e of various hematologic problems, including myelosuppression.

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

44 ation and HSC dysfunction observed following myelosuppression.

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

46 sed 14 d after therapy to abrogate prolonged myelosuppression.

47 icities observed were fatigue and reversible myelosuppression.

48 europathy (occurring in 81% of patients) and myelosuppression (48%), although common, were manageable

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

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

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

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

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

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

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

56 Common toxicities were myelosuppression and diarrhea.

57 The DLTs were mainly myelosuppression and diarrhea.

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

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

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

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

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

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

64 owing to increased toxicity from overlapping myelosuppression and immunosuppression.

65 cause of increased toxicity from overlapping myelosuppression and immunosuppression.

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

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

68 Myelosuppression and infection remain the most significa

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

70 patients has been restricted by substantial myelosuppression and infection.

71 Myelosuppression and infections were uncommon.

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

73 coupled with markedly reduced potential for myelosuppression and MAOI.

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

75 Myelosuppression and monoamine oxidase inhibition (MAOI)

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

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

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

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

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

81 Myelosuppression and nephrotoxicity were not observed.

82 Es) were as expected in R/R AML and included myelosuppression and nonhematologic AEs, such as infecti

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

84 Myelosuppression and other significant organ toxicities

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

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

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

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

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

90 Myelosuppression and stomatitis were dose-limiting toxic

91 Severe myelosuppression and stomatitis/esophagitis were the mos

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

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

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

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

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

97 Myelosuppression and weight loss exhibited a haploinsuff

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

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

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

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

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

103 eatment-emergent adverse events were nausea, myelosuppression, and fatigue.

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

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

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

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

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

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

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

111 Severe myelosuppression, and stomatitis or esophagitis were the

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

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

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

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

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

117 therapy leads to leukemia clearance, without myelosuppression, as demonstrated by the engraftment and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 Thiopurine-induced myelosuppression, defined as a decline in absolute white

134 Myelosuppression, determined by peripheral blood cell co

135 The expected myelosuppression developed after busulfan but then persi

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

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

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

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

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

141 Data cutoff for myelosuppression endpoints was July 30, 2018, and for an

142 No significant differences were observed in myelosuppression endpoints with trilaciclib plus gemcita

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

144 The most common AEs included myelosuppression, fatigue, and nausea/vomiting.

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

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

147 mechanism through which HCMV induces global myelosuppression following HSCT while maintaining lifelo

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

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

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

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

152 Myelosuppression, GI, and hepatic toxicities were common

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

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

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

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

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

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

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

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

161 0 mCi/m(2) was associated with dose-limiting myelosuppression; however, up to three doses of 30 mCi/m

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 Myelosuppression is a life-threatening complication of a

179 PRRT-induced myelosuppression is almost invariably reversible and rar

180 achieving symptomatic response without undue myelosuppression is challenging.

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

182 Myelosuppression is one of the most common and severe ad

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

184 Toxicity, especially myelosuppression, is significant.

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

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

187 Myelosuppression limited further dose escalation, howeve

188 Significant myelosuppression limited the ability to coadminister ABT

189 Myelosuppression may be the dose-limiting toxicity in pe

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

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

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

193 Severe myelosuppression (neutropenia that was protracted and/or

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

195 0K) overexpression prevented the substantial myelosuppression normally associated with this drug comb

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

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

198 Myelosuppression occurred in most patients, but toxic de

199 Myelosuppression occurred sporadically at all dose level

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

201 ssor NGFI-A binding protein (NAB1) to induce myelosuppression of uninfected CD34(+) hematopoietic pro

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

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

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

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

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

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

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

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

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

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

212 Myelosuppression, predominately neutropenia, was the pri

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

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

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

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

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

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

219 herapies to augment HSC DNA repair following myelosuppression remain undeveloped.

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

221 Prolonged myelosuppression resulted in significant treatment delay

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

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

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

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

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

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

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

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

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

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

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

233 iants are associated with thiopurine-induced myelosuppression (TIM).

234 relative to c-Kit kinase, which might reduce myelosuppression toxicity.

235 Common adverse events were myelosuppression, transient indirect hyperbilirubinemia,

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

237 Myelosuppression was acceptable with grade 3/4 neutropen

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

239 Myelosuppression was common but not dose-limiting.

240 Myelosuppression was common, but prolonged myelosuppress

241 Myelosuppression was common.

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

243 Severe myelosuppression was consistently experienced by heavily

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

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

246 Myelosuppression was dose-limiting, consisting of thromb

247 Myelosuppression was frequent.

248 Myelosuppression was mild and infrequent.

249 Myelosuppression was mild.

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

251 Clinically significant myelosuppression was not observed; hematologic toxicity

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

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

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

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

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

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

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

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

260 Myelosuppression was seen with 68% of patients who exper

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

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

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

264 Myelosuppression was similar to that expected with pacli

265 Myelosuppression was the DLT.

266 Reversible myelosuppression was the main adverse event and was more

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

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

269 Myelosuppression was the major adverse effect, with neut

270 Myelosuppression was the major toxicity, and two patient

271 Myelosuppression was the major toxicity, as has been rep

272 Myelosuppression was the major toxicity; 58% of carbopla

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 phil recovery after cyclophosphamide-induced myelosuppression, was normal.

283 ove predictive understanding of drug-induced myelosuppression, we developed a quantitative systems ph

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