ライフサイエンスコーパス: nonresponding

1 n, which often consists of a mixture of both nonresponding and reactivating cells that in turn contai

2 troduction of new drug classes and driven by nonresponding and treatment-naive patients.

3 for their ability to discern responding from nonresponding cancers.

4 e and increased expression with treatment in nonresponding cases.

5 sponsiveness was partially reversible, where nonresponding CD19 cells spontaneously recover their sig

6 e largely stochastic with a subpopulation of nonresponding cells across all the stimulation condition

7 Ectopic expression of CD44 in nonresponding cells conferred responsiveness, while gene

8 es could be developed based on findings from nonresponding cells exposed to reactivation stimuli.

9 Furthermore, a suppressive effect of nonresponding cells was not observed.

10 cin-induced NFAT activity allows survival of nonresponding cells.

11 ias in auxin distribution to create a local, nonresponding cytokinin source within the root vascular

12 tly lower baseline MP concentration than did nonresponding eyes.

13 response and therapeutic strategies for the nonresponding fraction are both limited.

14 vant chemotherapy treatment can discriminate nonresponding from responding patients.

15 N1 and CLMP expression were downregulated in nonresponding hairdressers and patients with mild ACD.

16 For the nonresponding hand, CSE variability also decreased, but

17 an also be increased early during therapy in nonresponding HL patients with the addition of involved-

18 ing, whereas 10% of those with high m6Ascore nonresponding (in cohort GSE63557).

19 efficacy of T-cell-based immunotherapies in nonresponding individuals.

20 Low/nonresponding kidney transplant recipients receiving sta

21 im of this work was to characterize PSMA-TAT-nonresponding lesions by targeted next-generation sequen

22 d biopsies with histologic validation of the nonresponding lesions in 7 of these nonresponding patien

23 Selective targeting of nonresponding lesions may be a reasonable approach to ex

24 primary tumor and nodal metastases; whereas nonresponding lesions tend to reveal only a slight incre

25 take can discriminate between responding and nonresponding lesions with an area under the curve of 0.

26 identified decreased expression of CXCR3 in nonresponding mice and showed that tumors grown in Cxcr3

27 ine was greater at the start of treatment in nonresponding patients (1.9 +/- 1.3 mg/dL) than in respo

28 istance (TDR) mutations are transmitted from nonresponding patients (defined as patients with no init

29 nd area under the curve values compared with nonresponding patients (P < .0001 for each).

30 a significantly higher overall survival than nonresponding patients (stable or progressive disease) (

31 alone did not predict response, because most nonresponding patients also exhibited 2-HG suppression.

32 ly higher in the responding patients than in nonresponding patients at month (M)12, M36, and M60.

33 ntained anti-HBs level of >/=10 mIU/mL.Among nonresponding patients at week 4, who received further v

34 significant improvement in responding versus nonresponding patients by landmark analysis (14.6 v 7.5

35 4V was positively associated with the PVL of nonresponding patients carrying M184V (RR, 1.50 per 100

36 (0.82 +/- 0.28 v 0.39 +/- 0.29, P <.016) in nonresponding patients compared with patients responding

37 on of responding patients (CRs plus PRs) and nonresponding patients did not show any significant diff

38 y-phase clinical development, and predicting nonresponding patients early in treatment.

39 s in distinguishing responding patients from nonresponding patients early on.

40 r effects of PD-1 blockade, whereas FMT from nonresponding patients failed to do so.

41 Despite this, ex vivo responding and nonresponding patients had substantial frequencies of te

42 foot may require revascularization, and some nonresponding patients may benefit from selected adjunct

43 Nonresponding patients received a second course of thera

44 of therapeutic activity in responding versus nonresponding patients remain poorly understood.

45 Nonresponding patients reported preserved QOL during the

46 More nonresponding patients required dialysis or mechanical v

47 re higher but not statistically increased in nonresponding patients versus those responding to treatm

48 val rates in the responding patients and the nonresponding patients were 100% and 36.5%, respectively

49 (18)F-FDG was able to identify early nonresponding patients with a 97% negative predictive va

50 ociate with tumor nonresponse (P = .004) and nonresponding patients with metastatic spread (P = .04).

51 ore hydrophobic amino acid pairs in HCV from nonresponding patients, and these hydrophobic interactio

52 ther MAPK pathway effectors were enriched in nonresponding patients, consistent with RAS signaling co

53 In these nonresponding patients, effector and regulatory T cells

54 ding patients is diluted by large numbers of nonresponding patients, or a beneficial effect in respon

55 In nonresponding patients, the risk of residual tumor at su

56 n of the nonresponding lesions in 7 of these nonresponding patients.

57 st dose of docetaxel was markedly lower in 4 nonresponding patients.

58 arly-phase trials and utility for predicting nonresponding patients.

59 considered only in targeted subsets such as nonresponding patients.

60 ereas the negative tests were obtained in 10 nonresponding patients.

61 rated to inform empiric treatment changes in nonresponding patients.

62 irectly inform escalation of treatment among nonresponding patients.

63 ficantly different between responding versus nonresponding patients.

64 Patients with nonresponding PB had a significantly higher progression

65 The two nonresponding PDXs showed hypermutated genomes with enri

66 PT treatment resulted in both responding and nonresponding populations of cells upon stimulation.

67 Sites with persistent nonresponding probing depths and signs of inflammation f

68 Responding, but not nonresponding, samples exhibited basal AKT phosphorylati

69 plicitly attributed the historical trends of nonresponding species to any specific factor.

70 advance, minimizing discussion of apparently nonresponding species.

71 tigen-specific CD4(+) T cells rather than to nonresponding T cells.

72 rties of cells historically considered to be nonresponding to growth factor signals.

73 and 9-ketooctadecatrienoic acid-insensitive nonresponding to oxylipins (noxy) mutants showed the imp

74 Previous studies using nonresponding to oxylipins (noxy), a series of Arabidops

75 eceptor-positive breast cancer, many of them nonresponding to prior treatment with tamoxifen.

76 ication of ~20% of human HCCs that, although nonresponding to single agents, could benefit from the p

77 Three subgroups had nonresponding trajectories: 2 with high baseline symptom

78 nature (n = 32) discriminated responding and nonresponding tumors (mean homologous recombination defi

79 significantly lower (18)F-FDG activity than nonresponding tumors (scores 3 and 4: SUVmax, 4.2 [range

80 he presence of T cell exhaustion pathways in nonresponding tumors and T cell activation in responding

81 ned gene expression patterns in controls and nonresponding tumors compared with tumors undergoing reg

82 as not able to differentiate responding from nonresponding tumors early after treatment.

83 as not able to differentiate responding from nonresponding tumors early after treatment.

84 flare on day 1 was adequate to discriminate nonresponding tumors from responding tumors.

85 uptake to distinguish between responding and nonresponding tumors need to be validated for different

86 Furthermore, early identification of nonresponding tumors provides the opportunity to adjust

87 Responding and nonresponding tumors showed consistent differences in th

88 YL719 demonstrated suppression of pRB, while nonresponding tumors showed sustained or increased level

89 ere was no association between patients with nonresponding tumors to induction chemotherapy and WNT (

90 n CD8 T cell infiltrate among responding and nonresponding tumors, objective response rate, overall s

91 When compared with controls or nonresponding tumors, the expression of adipocyte-relate

92 poorly differentiated between responding and nonresponding tumors.

93 ponding tumors when compared with control or nonresponding tumors.

94 Skin conductance nonresponding was associated with negative and total sym

95 PBMC, Leptospira-responding, and Leptospira nonresponding WC1+ gammadelta T cells to examine the pot