ライフサイエンスコーパス: anti-tumour

1 g of the processes that regulate the pro- or anti-tumour activities of Th17 cell and IL-17 will allow

2 cabozantinib and BEZ235, also showed minimal anti-tumour activities.

3 rent species of brown algae showed selective anti-tumour activity against different types of cancer,

4 de derivative (MM41) has significant in vivo anti-tumour activity against the MIA PaCa-2 pancreatic c

5 D4A also has more potent anti-tumour activity against xenograft tumours than abir

6 INTERPRETATION: Pembrolizumab showed anti-tumour activity and acceptable safety in patients w

7 4)-abiraterone (D4A), which has even greater anti-tumour activity and is structurally similar to endo

8 y progressing tumours in humans counter this anti-tumour activity by shedding the soluble major histo

9 e shown that high levels of lymphocytes with anti-tumour activity can be raised in cancer-bearing pat

10 ageable toxicity profile and provides robust anti-tumour activity in patients with advanced melanoma.

11 ppears to be well tolerated and might confer anti-tumour activity in patients with PD-L1-positive mal

12 tecan-temozolomide-dinutuximab shows notable anti-tumour activity in patients with relapsed or refrac

13 The anti-tumour activity of CC-885 is mediated through the c

14 hat REGgamma knockdown markedly improves the anti-tumour activity of energy metabolism inhibitors in

15 iet containing geranylgeraniol can limit the anti-tumour activity of pitavastatin and diet should be

16 Conversely, the anti-tumour activity of single-targeted ErbB agents incl

17 We assessed the safety and anti-tumour activity of standard-dose pembrolizumab in c

18 ivation of p53 could influence the selective anti-tumour activity of this therapeutic approach.

19 stat in this combination and the preliminary anti-tumour activity of this treatment.

20 in vivo studies are warranted to explore the anti-tumour activity of tivozanib in combinatorial appro

21 vealed that normal epithelial cells exert an anti-tumour activity on prostate carcinoma cells.

22 responses, five partial responses); and the anti-tumour activity was enriched in patients with known

23 umours and has shown preclinical synergistic anti-tumour activity when combined with cisplatin.

24 s is the first targeted agent to show robust anti-tumour activity with acceptable tolerability across

25 In vivo, S63845 shows potent anti-tumour activity with an acceptable safety margin as

26 nts are still being monitored for safety and anti-tumour activity.

27 r beneficial biological activities including anti-tumour activity.

28 NO) (3, TriplatinNC), which exhibits in vivo anti-tumour activity.

29 t they are well tolerated at doses that have anti-tumour activity.

30 hat these agents are well tolerated and have anti-tumour activity.

31 ta exist on the role of this zinc ion in the anti-tumour activity.

32 new cereblon modulator, CC-885, with potent anti-tumour activity.

33 ble tolerability and preliminary evidence of anti-tumour activity.

34 egulating PTEN or molecules that enhance its anti-tumour activity.

35 y paradoxical effects of TNFalpha as both an anti-tumour agent and a mediator of tumour growth.

36 ibe the mechanism of action of the selective anti-tumour agent erastin, involving the RAS-RAF-MEK sig

37 in the synthesis of the naturally occurring anti-tumour agent neopeltolide and in a single-step ster

38 ough doxorubicin (DOX) is a highly effective anti-tumour agent used to treat a variety of cancers, DO

39 Bisnaphthalimide intercalators are anti-tumour agents composed of two planar rings linked b

40 ivity of the enzyme to the DNA intercalating anti-tumour agents m-AMSA and ellipticine, but confer re

41 rticles as carriers for targeted delivery of anti-tumour agents.

42 The enzyme may have anti-tumour and anti-inflammatory effects in colon and i

43 rees with anti-inflammatory, anti-oxidative, anti-tumour and neuroprotective properties.

44 operties (anti-inflammatory, anti-microbial, anti-tumour, anti-oxidative and anti-ageing).

45 Nearly all anti-tumour antibodies are of a single class-namely, IgG

46 making it a novel and attractive target for anti-tumour approaches.

47 s the in vivo proliferation, persistence and anti-tumour capacity of adoptively transferred CD8(+) T

48 that can be presented to CTLs; the resulting anti-tumour CTL responses may provide part of the body's

49 We investigated the effect of the anti-tumour drug taxol, a known microtubule polymerizing

50 Taxol, a first-line anti-tumour drug, has low effectiveness against colorect

51 Many antimicrobial and anti-tumour drugs elicit hormetic responses characterise

52 A synergetic anti-tumour effect for Trypsinogen and Chymotrypsinogen

53 have produced a consistent demonstration of anti-tumour effect in a small percentage of patients.

54 ed siRNA treatment, leading to a synergistic anti-tumour effect in combination with paclitaxel.

55 This anti-angiogenic and anti-tumour effect is more robust than that observed wit

56 Ras 3'UTR showed very significantly that the anti-tumour effect of miR-193a-3p is via specific direct

57 ex response that could improve or impede the anti-tumour effect of serine and glycine starvation.

58 ion of macrophage phenotype could produce an anti-tumour effect.

59 nd 72h release half-lives did not achieve an anti-tumour effect.

60 calicheamicin exerts strong antigen-specific anti-tumour effects against human tumour xenografts in p

61 To test its anti-tumour effects in vitro C. microphysa pepsin-digest

62 e mechanisms by which CD40 activation exerts anti-tumour effects include inhibition of tumour cell pr

63 led CREB3L1 has been proposed to explain the anti-tumour effects of doxorubicin.

64 Moreover, tivozanib synergistically enhanced anti-tumour effects of EGFR-directed therapies including

65 In vivo, IRF8 is essential for the anti-tumour effects of Th9 cells in mouse melanoma model

66 suberoylanilide hydroxamic acid (SAHA), have anti-tumour effects, as they can inhibit cell growth, in

67 a pepsin-digested extract had the ability to anti-tumour effects.

68 e TNBC response induced by hypoxia and exert anti-tumour effects.

69 GFR blockade by tivozanib may yield stronger anti-tumour efficacy and circumvent resistance to EGFR-d

70 to tumours is believed to improve both their anti-tumour efficacy and their safety.

71 cal evidence of 5-FU delivery to tumours and anti-tumour efficacy following oral CAP administration t

72 e the pharmacokinetics, pharmacodynamics and anti-tumour efficacy of the first specific inhibitor, an

73 heavily on murine models for evaluating the anti-tumour efficacy of therapies.

74 Ultimately, a significant increase in anti-tumour efficacy resulted from this strategy.

75 netic studies were implemented and the PRP's anti-tumour efficacy was explored against orthotopic pan

76 old increases in T-cell priming and enhanced anti-tumour efficacy while greatly reducing systemic tox

77 nase (ALK) inhibitor, which has shown robust anti-tumour efficacy, along with intracranial activity,

78 ypsinogen A with potent in vitro and in vivo anti-tumour efficacy.

79 ally engineering macrophages to perform such anti-tumour functions as inducing cell lysis and inhibit

80 er, here we show that miR-22 is an essential anti-tumour gatekeeper in de novo acute myeloid leukaemi

81 Anti-tumour immune activation by checkpoint inhibitors l

82 ha chain on regulatory T cells mitigates the anti-tumour immune response and its expression on vascul

83 s a critical role for Id1 in suppressing the anti-tumour immune response during tumour progression an

84 The enhanced anti-tumour immune response has two underpinnings.

85 re long-envisioned as optimal targets for an anti-tumour immune response, their systematic discovery

86 enotype and stimulation of a T-cell-mediated anti-tumour immune response.

87 omitant blockade of CTLA-4 and PD-1 improves anti-tumour immune responses and synergistically eradica

88 asis, but is required by Treg cells to limit anti-tumour immune responses and to cure established inf

89 thin the malignant cells, and stimulation of anti-tumour immune responses via activation of dendritic

90 of CEACAM1 and TIM-3 leads to enhancement of anti-tumour immune responses with improved elimination o

91 utaneous SCCs, and contribute to ineffective anti-tumour immune responses, thereby permitting SCC dev

92 yet, excessive Treg cell activities suppress anti-tumour immune responses.

93 oadly applicable treatment that can generate anti-tumour immunity 'on demand' for oncologists in a va

94 also represent a major barrier to effective anti-tumour immunity and sterilizing immunity to chronic

95 simple, safe and robust strategy in boosting anti-tumour immunity for cancer immunotherapy.

96 Effective anti-tumour immunity in humans has been associated with

97 reatic cancer, and blockade of CCR2 restores anti-tumour immunity in preclinical models.

98 reprogrammed into indispensable mediators of anti-tumour immunity in the absence of RIP3 or Mincle.

99 ITR-mediated iTreg to Th9 induction enhances anti-tumour immunity in vivo.

100 esponses to parasites and viruses as well as anti-tumour immunity induced by therapeutic vaccines.

101 This lack of anti-tumour immunity is attributed to an absence of cell

102 Cancer cells elude anti-tumour immunity through multiple mechanisms, includ

103 Specific and protective anti-tumour immunity was generated with these materials,

104 with oncolytic viruses can lead to systemic anti-tumour immunity, although the appropriate targets f

105 e tumour cell cycle arrest, but also promote anti-tumour immunity.

106 is an upstream regulator of radiation-driven anti-tumour immunity.

107 cells, thereby enhancing suppression of Th1 anti-tumour immunity.

108 both a consequence of and key contributor to anti-tumour immunity.

109 crucial role in regulating autoimmunity and anti-tumour immunity.

110 , and are thought to have a critical role in anti-tumour immunity; however, the interaction between N

111 n may represent a viable strategy to improve anti-tumour immunotherapy.

112 Highly avid anti-tumour lymphocytes can be isolated from immunized p

113 Anti-tumour necrosis factor (TNF) agents have revolution

114 ients with rheumatoid arthritis treated with anti-tumour necrosis factor (TNF) drugs do not respond b

115 o potentially induce rheumatic diseases were anti-tumour necrosis factor (TNF) drugs, oncology drugs,

116 -dose glucocorticoids and an antimetabolite, anti-tumour necrosis factor (TNF) monoclonal antibodies

117 idylcholine to promote barrier function, new anti-tumour necrosis factor agents, B-cell (anti-CD20) d

118 ment escalation during the 12 study weeks to anti-tumour necrosis factor alpha (TNFalpha) agents, imm

119 opensity-score matching tested the effect of anti-tumour necrosis factor alpha (TNFalpha) therapy exp

120 mpounds such as ranibizumab and bevacizumab, anti-tumour necrosis factor alpha antibodies such as inf

121 mpared with traditional DMARD-experienced or anti-tumour necrosis factor biological drug-experienced

122 Anti-tumour necrosis factor drugs were most commonly stu

123 study to show that timely escalation with an anti-tumour necrosis factor therapy on the basis of clin

124 The anti-tumour necrosis factor-alpha infliximab and adalimu

125 Anti-tumour necrosis factor-alpha therapies have set a n

126 e clinical efficacy of an important class of anti-tumour poisons.

127 Ia HDAC inhibition as a means to harness the anti-tumour potential of macrophages to enhance cancer t

128 e pentacyclic acridinium salt RHPS4 displays anti-tumour properties in vitro as well as in vivo and i

129 calinium, a DNA bis-intercalator with strong anti-tumour properties.

130 Mechanistically, loss of Grail enhances anti-tumour reactivity and functionality of CD8(+) T cel

131 , PLX4032, demonstrated an unprecedented 80% anti-tumour response rate among patients with B-RAF(V600

132 692/29 showed good anti-tumour responses in vivo and is a strong therapeuti

133 ched the clinic but have failed to show good anti-tumour responses with an acceptable level of toxici

134 ng surface MHC-I corresponded with effective anti-tumour responses.

135 ink between lipid dysregulation and impaired anti-tumour surveillance.

136 r, the mechanisms by which radiation induces anti-tumour T cells remain unclear.

137 monitor the kinetics and distribution of the anti-tumour T-cell response before and after vaccination

138 lie the presence or absence of a spontaneous anti-tumour T-cell response in subsets of cases, therefo

139 nt induction of potent, durable and specific anti-tumour T-cell responses in a melanoma model.

140 ckpoint blockade (ICB) therapies can unleash anti-tumour T-cell responses.

141 e myeloid cells and their ability to inhibit anti-tumour T-cell responses.

142 'neosubstrate' selectivity, and identify an anti-tumour target rendered druggable by cereblon modula

143 o be an effective and well tolerated in vivo anti-tumour treatment.

144 a promising approach to establish an in-situ anti-tumour vaccine.