ライフサイエンスコーパス: CIPN

1 CIPN investigations in preclinical model systems have fo

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

3 CIPN+ had significantly worse self-report and objectivel

4 CIPN+ reported significantly more disability and 1.8 tim

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

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

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

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

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

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

11 ted after-discharges in rats with bortezomib CIPN.

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

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

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

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

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

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

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

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

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

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

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

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

24 is no approved pharmacological treatment for CIPN available.

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

26 rges by DRG neurons to promote recovery from CIPN.

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

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

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

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

31 wing that a nutritional supplement increased CIPN.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 no agents recommended for the prevention of CIPN.

60 clinically recommended for the prevention of CIPN.

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

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

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

64 significantly attenuated behavioral signs of CIPN.

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

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

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

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

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

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

71 ffective for the prevention and treatment of CIPN.

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

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

74 n resolution pathways may explain persistent CIPN.

75 s could provide effective therapy to prevent CIPN.

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

77 by oxidative stress by-products in producing CIPN.

78 o evaluate the use of mangafodipir to reduce CIPN.

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

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

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

82 10 days were considered to have significant CIPN symptoms and were compared with those patients who

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

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

85 Although the CIPN trials are inconclusive regarding tricyclic antidep

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

87 This CIPN hypersensitivity phenotype that was stably establis

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

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

90 e allelic variability with susceptibility to CIPN.

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

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

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

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

95 10, was highly significantly associated with CIPN (p = 5 x 10(-4)).

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

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

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

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

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

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

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

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

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

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