ライフサイエンスコーパス: tumor escape

1 ffects, including autoimmune pathogenesis or tumor escape.

2 essarily ends in either tumor elimination or tumor escape.

3 ced immune suppression that likely underlies tumor escape.

4 ic T cell tolerance plays a critical role in tumor escape.

5 D8(+) effector T cells, thus contributing to tumor escape.

6 sensitization is a predominant mechanism of tumor escape.

7 single epitope, there is always the risk of tumor escape.

8 nto the model altered the timing and mode of tumor escape.

9 ls (MDSCs), is one of the main mechanisms of tumor escape.

10 ells (ImC) is one of the major mechanisms of tumor escape.

11 ys can subvert the effector phase and enable tumor escape.

12 nce is a result of lymphocyte dysfunction or tumor escape.

13 T cell tolerance is a critical element of tumor escape.

14 antigen presentation may play a key role in tumor escape.

15 infiltrated by CD8+ T cells, contributing to tumor escape.

16 paration and may minimize the risk of clonal tumor escape.

17 tions in tumor-specific antigens may lead to tumor escape.

18 fibroblasts to investigate the mechanisms of tumor escape after VEGF inactivation.

19 in defective T cell priming, also leading to tumor escape and growth.

20 Tumor escape and recurrence are major impediments for su

21 ntenance and growth, loss of p53 facilitates tumor escape and the acquisition of oncogene independenc

22 Tumors escape antiangiogenic therapy by activation of pr

23 ere are 2 prevailing hypotheses on how these tumors escape antiangiogenic therapy: switch to VEGF-ind

24 hen stromal cells are not destroyed, and the tumor escapes as Ag loss variants.

25 t work has suggested two broad categories of tumor escape based on cellular and molecular characteris

26 essor cells (MDSC) play an important role in tumor escape by suppressing T-cell responses.

27 We identified a novel mechanism of tumor escape by which VEGF-A directly triggers Treg prol

28 The ability to block tumor escape depends on a better understanding of cellul

29 city in vivo was an important determinant of tumor escape following CTL-based immunotherapy.

30 r suppressor p53 remain a vital mechanism of tumor escape from apoptosis and senescence.

31 differentiation is an important mechanism of tumor escape from immune control.

32 t protection against cancer and facilitating tumor escape from immune destruction.

33 umor T cells has been hypothesized to permit tumor escape from immune destruction.

34 mor-induced immunosuppression and subsequent tumor escape from immune recognition and elimination.

35 This suggests that tumor escape from immune surveillance may have occurred

36 This mechanism could contribute to tumor escape from immune surveillance.

37 ing immune infiltrate, and (3) mechanisms of tumor escape from immune surveillance.

38 of these cells is an important mechanism of tumor escape from immune system control.

39 PD-1(+) T lymphocytes plays a major role in tumor escape from immune system during cancer progressio

40 Therefore, in general, tumor escape from immune-mediated clearance is not attri

41 cient in cytolysis, a defect that may permit tumor escape from immune-mediated destruction.

42 proposed by several groups as a mechanism of tumor escape from immunological detection.

43 is frequently associated with mechanisms of tumor escape from immunosurveillance.

44 develop strategies to override mechanisms of tumor escape from oncogene dependence.

45 The result is tumor escape from the host immune system.

46 Significantly, no tumors escaped from dormancy without HSP27 expression.

47 however, a better understanding of how these tumors escape immune surveillance is required to enhance

48 flammatory infiltrate, suggesting that these tumors escape immune surveillance.

49 focal, nonmetastatic Stat3-deficient mammary tumors escaped immune surveillance after a long latency

50 In tumors escaping immunologic rejection, the expression of

51 y its soluble receptor may explain how CD30+ tumors escape immunosurveillance and may be related to t

52 e elucidated genetic determinants underlying tumor escape in a transgenic mouse model of Wnt pathway-

53 s, and its interaction with PD-1 resulted in tumor escape in experimental models.

54 on and the design of inhibitors that prevent tumor escape in quiescence.

55 sponses, we found that IFN-gamma can promote tumor escape in the CT26 colon carcinoma by down-regulat

56 Tumor escape is accomplished through the activation of o

57 These epidermal-derived tumors escape local immune surveillance and infiltrate t

58 tion may represent a previously unrecognized tumor escape mechanism that facilitates tumor progressio

59 than one target specific inhibitors based on tumor escape mechanism, genetic, epigenetic and molecula

60 ne and are therefore considered an important tumor escape mechanism.

61 Altogether our data propose a novel tumor escape-mechanism based on the modulation of chemok

62 d clinical efficacy to date, possibly due to tumor escape mechanisms that inhibit NK cell function.

63 By removing these tumor escape mechanisms, sildenafil enhances intratumora

64 The establishment of tumor escape mutants, which can be driven by innate and/

65 ; core or rim injections alone may result in tumor escape, particularly in a well-vascularized tumor;

66 une-privileged site within the eye develop a tumor escape phenotype in the absence of selective T cel

67 vileged environment within the eye induces a tumor escape phenotype that is not driven by selective T

68 We show that brain tumors escape pro-inflammatory M1 conversion of microgli

69 rsistence strikingly parallels mechanisms of tumor escape, prompting investigations into the generati

70 ce of these molecules and their relevance in tumor escape remain unknown.

71 suppressed in vivo and how MITF-low cells in tumors escape senescence are poorly understood.

72 Nevertheless, Tag-expressing solid tumors escape the immune surveillance and are devoid of

73 Finally, in an in vivo model of tumor escape, there was complete ACAR-mediated tumor cle

74 mited by levels of natural antibodies and by tumor escape through elimination of antigen-positive cel

75 reted by tumor-infiltrating T cells promotes tumor escape through the down-regulation of the endogeno

76 Tumor escape variants (TEV) recovered from the lungs of

77 ry disease and the emergence of antigen-loss tumor escape variants after treatment demonstrate the ne

78 However, antigen-loss tumor escape variants and the absence of currently targe

79 Tumor escape variants are likely to emerge after treatme

80 Although our data regarding "tumor escape" were inconclusive, some patients had growi

81 both promoted rapid, EMT-associated mammary tumor escape, whereas isolated p16 Ink4a deficiency fail

82 Simply put, there is no need for tumor escape without immunological pressure.