ライフサイエンスコーパス: CIPN

1 CIPN affects sensory neurons through neuroinflammatory m

2 CIPN and RagA translation are strongly attenuated by gen

3 CIPN investigations in preclinical model systems have fo

4 CIPN may involve multiple areas of the peripheral nervou

5 CIPN must be assessed earlier in the clinical pathway, a

6 CIPN often affects unmyelinated nociceptive sensory term

7 CIPN often persists long after treatment completion and

8 CIPN was assessed via PROMs (European Organization for R

9 CIPN was measured using composite neurological grading s

10 CIPN+ had significantly worse self-report and objectivel

11 CIPN+ reported significantly more disability and 1.8 tim

12 CIPN-sx increase from baseline to 1 month was significan

13 CIPN-sx were evaluated with the self-reported Functional

14 Most participants had grade 1 CIPN or higher (238 [71.5%] participants).

15 ange predicted subsequent onset of grade 2-3 CIPN during the remainder of the trial (mean treatment d

16 es the priming associated with CIPN, and (3) CIPN also produces opioid-induced hyperalgesia (OIH).

17 There was no evidence that ALC affected CIPN at 12 weeks; however, ALC significantly increased C

18 the mechanisms of CIPN and analgesia against CIPN remains unclear.

19 uced robust neuroprotection in an aggressive CIPN model utilizing the frontline anticancer drug, pacl

20 Gait was slower among CIPN+, with those women taking significantly more, but s

21 rons from cisplatin-induced cytotoxicity and CIPN in mice.

22 tween pre-chemotherapy physical function and CIPN in patients with pancreatic cancer.

23 d dorsal root ganglion neuroinflammation and CIPN-related pain behaviors in mice.

24 treatment of peripheral neuropathies such as CIPN.

25 monstrated best ability to accurately assess CIPN (convergent validity), especially the PRO-CTCAE com

26 cians with valuable information in assessing CIPN morbidity.

27 sense knockdown of nociceptor MOR attenuates CIPN, (2) and attenuates the priming associated with CIP

28 The mean (SD) baseline CIPN scores were 8.1 (5.6) in the exercise intervention

29 ted the best ability to discriminate between CIPN severity (known-groups validity) and to detect chan

30 sessed to elucidate the relationship between CIPN and previously reported cancer treatment-related br

31 ted after-discharges in rats with bortezomib CIPN.

32 a therapeutic strategy for alleviating both CIPN and enhancing the efficacy of chemotherapy in TNBC

33 DRG neuronal Ca(2+) activity elevated by CIPN was attenuated by LY379268 and meclizine, but not b

34 he distribution and pain percept as shown by CIPN patients.

35 action, diverse chemotherapeutics can cause CIPN through a converged pathway-an active axon degenera

36 nce for new target mechanisms that may cause CIPN.

37 Cytotoxic drugs that cause CIPN exert their effects by increasing oxidative stress,

38 m-based chemotherapeutic drug known to cause CIPN, possibly by causing oxidative stress damage to pri

39 Among other substances, oxaliplatin causes CIPN in up to 80% of treated patients.

40 , common chemotherapeutics known for causing CIPN, without reducing their anticancer effectiveness.

41 ent endpoints to systematically characterize CIPN recovery in mice exposed to the antitubulin cancer

42 at for the group that received chemotherapy, CIPN-sx were positively associated with cerebral perfusi

43 pared women self-reporting symptoms of CIPN (CIPN+) with asymptomatic women (CIPN-) on the following:

44 c Bonferroni correction were used to compare CIPN between patients according to blood-based factor no

45 ed with neurotoxic chemotherapy will develop CIPN, and there is considerable variability in its sever

46 more, but slower and shorter, steps than did CIPN- (all P < .05).

47 t and objectively measured function than did CIPN-, with the exception of maximal leg strength and ba

48 ly suggests that MNK1-eIF4E signaling drives CIPN and that a drug in human clinical trials, eFT508, m

49 CS) may be used at the subclinical and early CIPN stage, to assess the extent of large nerve fibre da

50 y trials related to treatment of established CIPN, are included in this update.

51 nt- completely reverses signs of established CIPN, including mechanical allodynia, spontaneous pain,

52 candidates because they reverse established CIPN and may enhance anti-tumor effects of chemotherapy.

53 Given that stress exacerbates CIPN, and that the therapeutic effect of duloxetine is t

54 With regard to the treatment of existing CIPN, the best available data support a moderate recomme

55 ource of dietary fiber, with HRQoL, fatigue, CIPN, and gastrointestinal symptoms in CRC survivors fro

56 HRQoL, fatigue, CIPN, and gastrointestinal symptoms were measured by val

57 ercise intervention vs attention control for CIPN in patients who were diagnosed with ovarian cancer.

58 male), 32 met the predetermined criteria for CIPN symptoms.

59 re are no efficacious FDA-approved drugs for CIPN.

60 development of successful interventions for CIPN and other neurodegenerative disorders.

61 Risk mitigation for CIPN involves preemptive reduction of cumulative dose or

62 more, they suggest prevention strategies for CIPN in patients through the use of early, short-term tr

63 d dorsal horn (DH; another key structure for CIPN pain response) tissues from vehicle and paclitaxel

64 is no approved pharmacological treatment for CIPN available.

65 Duloxetine is the only treatment for CIPN currently recommended by the American Society of Cl

66 No effective treatment for CIPN exists, short of dose-reduction which worsens cance

67 rrently, there is no effective treatment for CIPN.

68 rges by DRG neurons to promote recovery from CIPN.

69 Remarkably, 47% of women in our sample had CIPN symptoms many years after treatment, together with

70 In CIPN, mitochondrial dysfunction is characterized by defi

71 g 1 (SARM1) is responsible for axonopathy in CIPN.

72 del was used to assess the 6-month change in CIPN between the exercise intervention and attention con

73 Change in CIPN was the primary outcome in this secondary analysis.

74 hways in macrophages may be sex-dimorphic in CIPN.

75 r, our understanding of sexual dimorphism in CIPN remains unclear.

76 ling mechanisms underlying sex dimorphism in CIPN, which may inspire the development of more precise

77 therapeutic effect of a single AIBP dose in CIPN was associated with anti-inflammatory and cholester

78 E, present in dorsal root ganglion (DRG), in CIPN.

79 signaling, supports the role of Hedgehog in CIPN.

80 Double immunofluorescence in CIPN rats showed that Nav1.7 was upregulated in small DR

81 esis that microglia are causally involved in CIPN, and that gut bacteria are drivers of this phenotyp

82 esic priming (priming), which also occurs in CIPN, we determined, using male rats, whether (1) antise

83 xcitability of primary afferents and pain in CIPN.

84 standing of axonal degeneration processes in CIPN will provide important information regarding the de

85 g that senescent-like neurons play a role in CIPN pathogenesis.

86 in DRG cells also have an important role in CIPN.

87 udies suggest that lipids may play a role in CIPN.

88 the involvement of astrocytes and Sparcl1 in CIPN.

89 ptors, we also evaluated the role of TLR4 in CIPN at the cellular level, using patch-clamp electrophy

90 this study, we examined the role of TLR9 in CIPN induced by paclitaxel in WT and Tlr9 mutant mice of

91 weeks; however, ALC significantly increased CIPN by 24 weeks.

92 hemotherapy reported significantly increased CIPN-sx from baseline to 1 month, with partial recovery

93 wing that a nutritional supplement increased CIPN.

94 nduced CIPN, in rats with bortezomib-induced CIPN it only produced a temporary attenuation.

95 the mechanisms driving chemotherapy-induced CIPN is urgently needed to facilitate the development of

96 , we used a mouse model of cisplatin-induced CIPN using male and female mice to test agonists of mGlu

97 o develop paclitaxel- or oxaliplatin-induced CIPN posttreatment.

98 Paclitaxel-induced CIPN caused macrophage infiltration to DRGs in both sexe

99 reversed oxaliplatin- and paclitaxel-induced CIPN, in rats with bortezomib-induced CIPN it only produ

100 odels of oxaliplatin- and paclitaxel-induced CIPN.

101 A predictive biomarker for dose-limiting CIPN could improve treatment outcomes by allowing provid

102 subscales (p < 0.05) at 10 weeks, with lower CIPN symptoms for 3X/week groups versus 2X/week groups.

103 like neuronal cells may effectively mitigate CIPN, we used a pharmacological 'senolytic' agent, ABT26

104 dysregulated activation could help mitigate CIPN in patients with cancer who are receiving paclitaxe

105 also positively correlated with the 6-month CIPN sensory and autonomic subscales.

106 , week-12 scores were 0.9 points lower (more CIPN) with ALC than placebo (95% CI, -2.2 to 0.4; P = .1

107 Chemotherapy-Induced Peripheral Neuropathy (CIPN) -20 instruments during the entire course of therap

108 Chemotherapy-induced peripheral neuropathy (CIPN) accompanied by chronic neuropathic pain is a major

109 Chemotherapy-induced peripheral neuropathy (CIPN) affects ~68% of patients undergoing chemotherapy,

110 chemotherapy-induced peripheral neuropathy (CIPN) after the neurotoxic treatment.

111 chemotherapy-induced peripheral neuropathy (CIPN) and may be important for developing effective prev

112 chemotherapy-induced peripheral neuropathy (CIPN) and to test whether this is matched by changes in

113 Chemotherapy-induced peripheral neuropathy (CIPN) arises from collateral damage to peripheral affere

114 Chemotherapy-induced peripheral neuropathy (CIPN) impacts a growing number of cancer survivors and t

115 ith cisplatin-induced peripheral neuropathy (CIPN) in mice.

116 chemotherapy-induced peripheral neuropathy (CIPN) in wild-type mice, but AIBP failed to reverse allo

117 Chemotherapy-induced peripheral neuropathy (CIPN) is a common adverse effect experienced by cancer p

118 Chemotherapy-induced peripheral neuropathy (CIPN) is a common adverse effect of neurotoxic chemother

119 Chemotherapy-induced peripheral neuropathy (CIPN) is a common dose-limiting side effect experienced

120 Chemotherapy-induced peripheral neuropathy (CIPN) is a common dose-limiting side effect of several a

121 Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating adverse effect of neurotoxic can

122 chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating dose-dependent and therapy-limit

123 Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating side effect of many cancer treat

124 Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating side effect that occurs in many

125 Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting side effect of chemotherapy tre

126 Chemotherapy-induced peripheral neuropathy (CIPN) is a major adverse effect of paclitaxel.

127 Chemotherapy-induced peripheral neuropathy (CIPN) is a major cause of disability in cancer survivors

128 Chemotherapy-induced peripheral neuropathy (CIPN) is a major cause of morbidity and the main cause o

129 Chemotherapy-induced peripheral neuropathy (CIPN) is a major side effect from cancer treatment with

130 Chemotherapy-induced peripheral neuropathy (CIPN) is a major side effect in cancer patients undergoi

131 Chemotherapy-induced peripheral neuropathy (CIPN) is a major unmet medical need with limited treatme

132 Chemotherapy-induced peripheral neuropathy (CIPN) is a prevalent side effect of widely used platinum

133 Chemotherapy-induced peripheral neuropathy (CIPN) is a serious therapy-limiting side effect of commo

134 Chemotherapy-induced peripheral neuropathy (CIPN) is a severe and painful adverse reaction of cancer

135 Chemotherapy-induced peripheral neuropathy (CIPN) is a substantial adverse effect of anticancer trea

136 Chemotherapy-induced peripheral neuropathy (CIPN) is common and leads to suboptimal treatment.

137 Chemotherapy-induced peripheral neuropathy (CIPN) is one of the most frequently reported adverse eff

138 chemotherapy-induced peripheral neuropathy (CIPN) is poorly understood.

139 Chemotherapy-induced peripheral neuropathy (CIPN) is the most prevalent and limiting side effect of

140 Chemotherapy-induced peripheral neuropathy (CIPN) is the most prevalent neurological complication of

141 Chemotherapy-induced peripheral neuropathy (CIPN) may persist after treatment ends and may lead to f

142 Chemotherapy-induced peripheral neuropathy (CIPN) occurs commonly in cancer patients and is individu

143 Chemotherapy-induced peripheral neuropathy (CIPN) remains a pressing clinical problem; however, our

144 chemotherapy-induced peripheral neuropathy (CIPN) remains a significant challenge in the treatment o

145 chemotherapy-induced peripheral neuropathy (CIPN), a serious treatment-limiting side effect for whic

146 Chemotherapy induced peripheral neuropathy (CIPN), a toxic side effect of some cancer treatments, ne

147 chemotherapy-induced peripheral neuropathy (CIPN), agents such as paclitaxel are known to elicit chr

148 chemotherapy-induced peripheral neuropathy (CIPN), and gastrointestinal problems.

149 Chemotherapy-induced peripheral neuropathy (CIPN), characterized by pain and numbness in hands and f

150 Chemotherapy-induced peripheral neuropathy (CIPN), one of the most common and severe adverse effects

151 chemotherapy-induced peripheral neuropathy (CIPN), the most common treatment-limiting side effect of

152 chemotherapy-induced peripheral neuropathy (CIPN), which can last for months to years after treatmen

153 chemotherapy-induced peripheral neuropathy (CIPN), which is often accompanied by pain.

154 nst cisplatin-induced peripheral neuropathy (CIPN).

155 chemotherapy-induced peripheral neuropathy (CIPN).

156 chemotherapy-induced peripheral neuropathy (CIPN).

157 emotherapy-induced peripheral neurotoxicity (CIPN) is a common dose-limiting side effect of several a

158 emotherapy-induced peripheral neurotoxicity (CIPN).

159 emotherapy-induced peripheral neurotoxicity (CIPN).

160 As such, the assessment of CIPN remains critically important in both research and c

161 Attenuation of CIPN by cyclopamine (intradermal and intraganglion), whi

162 The prevalence and burden of CIPN late effects will likely increase as cancer surviva

163 ngs identify PN as a critical determinant of CIPN, while providing the rationale toward development o

164 itaxel treatment, prevent the development of CIPN in mice at the sensory-motor and cellular level.

165 and RAGE AS-ODN prevented the development of CIPN induced by all three chemotherapy drugs.

166 AEG-1 deletion prevented the development of CIPN pathologies induced by PAC, as well as oxaliplatin

167 icularly in myeloid cells, in development of CIPN.

168 e underlying mechanism in the development of CIPN.

169 therapy for the debilitating side effect of CIPN.

170 aliplatin, and prevented the exacerbation of CIPN by sound stress.

171 The hallmark of CIPN is degeneration of long axons required for transmis

172 oward understanding the functional impact of CIPN symptoms on cancer survivors.

173 rs are associated with a higher incidence of CIPN development.

174 Interaction of CIPN-sx perfusion effects with known chemotherapy-associ

175 in participants who reported high levels of CIPN symptoms compared with those who reported low level

176 en those who reported high and low levels of CIPN symptoms using linear regressions.

177 mpared with those who reported low levels of CIPN symptoms.

178 ide evidence that an underlying mechanism of CIPN is sustained mTORC1 activation driven by MNK1-eIF4E

179 dimorphism with regards to the mechanisms of CIPN and analgesia against CIPN remains unclear.

180 Currently the molecular mechanisms of CIPN are not understood, and there are no available trea

181 yte-intrinsic IRE1alpha as a key mediator of CIPN and suggests that targeting its dysregulated activa

182 hether TRPA1 acted as a critical mediator of CIPN by bortezomib or oxaliplatin in a mouse model syste

183 of mechanical allodynia in a mouse model of CIPN and was advanced into preclinical development.

184 Here, we have used a model of CIPN in Drosophila melanogaster to identify genetic chan

185 In a mouse paclitaxel model of CIPN we determined that Sarm1 knockout mice prevented lo

186 ng both sexes of animals in the modelling of CIPN, ensuring that outcome measures align with those mo

187 an refine our approaches in the modelling of CIPN.

188 nsive summary of the use of animal models of CIPN, we have identified areas in which the value of pre

189 validity) and to detect changes at onset of CIPN development (responsiveness), especially for EORTC-

190 fore demonstrates a circadian oscillation of CIPN and its underlying transcriptomic landscape.

191 s) and trended toward stronger prediction of CIPN that remained unresolved at the end of the study.

192 ses, and 28 primary trials for prevention of CIPN in addition to 14 primary trials related to treatme

193 of acetyl-l-carnitine for the prevention of CIPN in patients with cancer should be discouraged.

194 on of susceptible patients and prevention of CIPN through the targeting of mitochondria.SIGNIFICANCE

195 We also demonstrate the prevention of CIPN with our two new orally active PNDCs, SRI6 and SRI1

196 no agents recommended for the prevention of CIPN.

197 clinically recommended for the prevention of CIPN.

198 agents are recommended for the prevention of CIPN.

199 Core measurement properties of CIPN outcome measures were evaluated.

200 The resolution of CIPN is associated with normalization of the cisplatin-i

201 entified a novel mechanism for resolution of CIPN that requires CD8(+) T cells and endogenous IL-10.

202 s to Rag1(-/-) mice normalized resolution of CIPN.

203 ogenous interleukin (IL)-10 to resolution of CIPN.

204 servation that stress may impact response of CIPN to duloxetine, open new approaches to the treatment

205 itors, the mechanisms underlying reversal of CIPN need to be identified.

206 The findings showed that the severity of CIPN at 6-month follow-up was significantly associated w

207 Furthermore, the development and severity of CIPN in patients with gynecological cancer were associat

208 significantly attenuated behavioral signs of CIPN.

209 nd compared women self-reporting symptoms of CIPN (CIPN+) with asymptomatic women (CIPN-) on the foll

210 indings suggest that the sensory symptoms of CIPN are an indicator of an increased risk of falling an

211 In most patients, symptoms of CIPN subside after treatment completion.

212 ancer survivors with and without symptoms of CIPN to identify targets for functional rehabilitation.

213 are not capable of reversing the symptoms of CIPN.

214 ent, 47% of women still reported symptoms of CIPN.

215 ine, open new approaches to the treatment of CIPN and other stress-associated pain syndromes.

216 romising candidate for clinical treatment of CIPN conditions due to its efficacy and optimized pharma

217 ontrolled trials (RCTs) for the treatment of CIPN.

218 ffective for the prevention and treatment of CIPN.

219 sia (anti-hyperalgesia) for the treatment of CIPN.SIGNIFICANCE STATEMENT Painful chemotherapy-induced

220 Research on CIPN mechanism is extensive but has produced only few cl

221 imodal testing is recommended as the optimal CIPN assessment strategy, employing objective NCS and ot

222 thic pain conditions given the limited other CIPN treatment options.

223 It more robustly attenuated oxaliplatin CIPN in male rats, while it was more effective for pacli

224 inflammatory mediator PGE(2) and paclitaxel CIPN, in a sex-specific fashion.

225 , while it was more effective for paclitaxel CIPN in females.

226 associated with oxaliplatin- and paclitaxel-CIPN.

227 rs in chemotherapy-induced neuropathic pain (CIPN) caused by paclitaxel treatment.

228 therapy-induced peripheral neuropathic pain (CIPN) is a common and severe debilitating side effect of

229 nt of chemotherapy-induced neuropathic pain (CIPN), a major dose-limiting toxicity of widely used che

230 ts use for patients with established painful CIPN.

231 n resolution pathways may explain persistent CIPN.

232 Posttreatment CIPN severity was compared with blood-based factors with

233 fied areas in which the value of preclinical CIPN studies might be increased.

234 n Carba1 as a promising candidate to prevent CIPN, with potential to enhance both cancer treatment ou

235 chondrial function is anticipated to prevent CIPN.

236 s could provide effective therapy to prevent CIPN.

237 ar effects of cisplatin and drugs preventing CIPN pain.

238 as a key underlying mechanism of preventing CIPN, warranting future investigation of SIRT2 activatio

239 y objective was to determine if ALC prevents CIPN as measured by the 11-item neurotoxicity (NTX) comp

240 by oxidative stress by-products in producing CIPN.

241 DRGs and their subsequent activation promote CIPN.

242 show that macrophage TLR9 signaling promotes CIPN in male mice only.

243 ndering an inflammatory milieu that promotes CIPN.

244 o evaluate the use of mangafodipir to reduce CIPN.

245 ons in rats with confirmed bortzomib-related CIPN showed an increase in number of evoked discharges t

246 DRGs from male rats with paclitaxel-related CIPN and from male and female humans with cancer-related

247 (SymptomCare@Home) used a series of relevant CIPN questions to track symptoms on a 0 to 10 ordinal sc

248 control significantly improved self-reported CIPN among patients who were treated for ovarian cancer.

249 At 6 months, the self-reported CIPN score was reduced by 1.3 (95% CI, -2.3 to -0.2) poi

250 o nasal administrations of MSC fully reverse CIPN and the associated mitochondrial abnormalities via

251 Moreover, WT MSC do not reverse CIPN in mice lacking IL-10 receptors on peripheral senso

252 ing domain did not bind microglia or reverse CIPN allodynia.

253 C6 inhibition is a novel strategy to reverse CIPN without negatively interfering with tumor growth, b

254 RAGE AS-ODN, in contrast, reversed CIPN induced by all three chemotherapy drugs.

255 with an HDAC6 inhibitor apparently reverses CIPN.

256 nce of DRG senescent neuronal cells reverses CIPN, suggesting that senescent-like neurons play a role

257 10 days were considered to have significant CIPN symptoms and were compared with those patients who

258 However, in a substantial subgroup, CIPN persists long into survivorship.

259 In that CIPN model, the irreversible SARM1 inhibitors prevented

260 group receiving chemotherapy indicated that CIPN-sx and associated perfusion changes from baseline t

261 We showed that CIPN was alleviated upon GCV administration to p16-3MR m

262 Although the CIPN trials are inconclusive regarding tricyclic antidep

263 w the current evidence on techniques for the CIPN assessment in the clinical and experimental setting

264 for the field, confirms many findings in the CIPN literature and also find extensive evidence for new

265 Notably, the CIPN phenotype was abolished completely in mice that wer

266 hemotherapy may be predictive factors of the CIPN severity 6 months after the commencement of chemoth

267 stion that the massage program targeting the CIPN-affected area directly provided 3X a week for 4 wee

268 Here, we report that the CIPN-causing drug bortezomib (Bort) promotes delta 2 tub

269 This CIPN hypersensitivity phenotype that was stably establis

270 Thus, CIPN is one of most common causes of dose reduction and

271 uroinflammatory response that contributes to CIPN development and maintenance.

272 lecular and cellular mechanisms that lead to CIPN are still poorly understood.

273 logical changes in spinal cord are linked to CIPN, but the causative mediators and mechanisms remain

274 erestingly, the contribution of microglia to CIPN appears to be limited.

275 e allelic variability with susceptibility to CIPN.

276 mutated in patients who were susceptible to CIPN but not in controls (p = 8 x 10(-3)).

277 e chemotherapeutic agent paclitaxel triggers CIPN by altering IP3 receptor phosphorylation and intrac

278 t mouse to examine the mechanisms underlying CIPN and identify protective pathways.

279 We used CIPN as a clinical model to investigate the association

280 ver, we have determined a mechanism by which CIPN develops and have discovered that lithium and ibudi

281 10, was highly significantly associated with CIPN (p = 5 x 10(-4)).

282 tial prechemotherapy factors associated with CIPN development.

283 ) and attenuates the priming associated with CIPN, and (3) CIPN also produces opioid-induced hyperalg

284 nts outside normative ranges associated with CIPN.

285 ric analyses and tested for association with CIPN-sx in the patients who received chemotherapy.

286 y blood-based and clinical associations with CIPN development.

287 nd 1.8 times the risk of falls compared with CIPN- ( P < .0001).

288 No associations were found with CIPN and gastrointestinal symptoms.

289 al care for falls (8 of 32 participants with CIPN symptoms [25.0%] vs 6 of 84 participants without CI

290 The participants with CIPN symptoms were more likely than the participants wit

291 The participants with CIPN symptoms were nearly 3 times more likely to report

292 imate was larger among the 127 patients with CIPN symptoms at enrollment (-2.0; 95% CI, -3.6 to -0.5

293 s mechanical hyperalgesia (OIH) in rats with CIPN, suggesting the presence of OIH.

294 ntials in DRG neurons occurring in rats with CIPN, while intrathecal injection of ProTx II significan

295 l or near fall than the participants without CIPN symptoms (hazard ratio, 2.67 [95% CI, 1.62-4.41]; P

296 toms [25.0%] vs 6 of 84 participants without CIPN symptoms [7.1%]; P = .01).

297 re more likely than the participants without CIPN symptoms to obtain medical care for falls (8 of 32

298 oms of CIPN (CIPN+) with asymptomatic women (CIPN-) on the following: maximal leg strength, timed cha

299 s with low hemoglobin pretreatment had worse CIPN posttreatment (median [IQR] composite neurological

300 , several factors were associated with worse CIPN (F4,315 = 18.6; P < .001; r2 = .19) including for l