ライフサイエンスコーパス: nonresponding

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

2 for their ability to discern responding from nonresponding cancers.

3 e and increased expression with treatment in nonresponding cases.

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

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

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

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

8 tly lower baseline MP concentration than did nonresponding eyes.

9 vant chemotherapy treatment can discriminate nonresponding from responding patients.

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

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

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

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

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

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

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

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

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

19 4V was positively associated with the PVL of nonresponding patients carrying M184V (RR, 1.50 per 100

20 (0.82 +/- 0.28 v 0.39 +/- 0.29, P <.016) in nonresponding patients compared with patients responding

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

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

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

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

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

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

27 Nonresponding patients received a second course of thera

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

29 Nonresponding patients reported preserved QOL during the

30 More nonresponding patients required dialysis or mechanical v

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

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

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

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

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

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

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

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

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

40 considered only in targeted subsets such as nonresponding patients.

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

42 Patients with nonresponding PB had a significantly higher progression

43 The two nonresponding PDXs showed hypermutated genomes with enri

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

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

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

47 advance, minimizing discussion of apparently nonresponding species.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 poorly differentiated between responding and nonresponding tumors.

65 ponding tumors when compared with control or nonresponding tumors.

66 Skin conductance nonresponding was associated with negative and total sym