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 hile isolates LB4 and LB41 showed pronounced anti-tumour activity against HepG2 cells.

5 K) A, B, and C, which has been shown to have anti-tumour activity against NTRK gene fusion-positive s

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

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

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

9 velumab combined with axitinib has promising anti-tumour activity and acceptable toxicity in patients

10 hibitors) is associated with higher rates of anti-tumour activity and immune-related toxicities, when

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

12 tion of sotorasib once per day showed modest anti-tumour activity and manageable safety in these heav

13 stuzumab deruxtecan and were included in the anti-tumour activity and safety analyses sets.

14 Anti-tumour activity and safety were analysed in all pat

15 Anti-tumour activity and safety were analysed in all tre

16 Anti-tumour activity and safety were assessed in all par

17 nt offers encouraging anti-proliferative and anti-tumour activity and was well tolerated, both as a s

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

19 , 2014, and May 29, 2019, were evaluable for anti-tumour activity by the March 10, 2020, data cutoff

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

21 At the cutoff date for anti-tumour activity data (Dec 15, 2017), median study f

22 rally administered cyclin A/Bi showed robust anti-tumour activity in chemotherapy-resistant SCLC pati

23 The BCL-2 inhibitor venetoclax has a high anti-tumour activity in chronic lymphocytic leukaemia, a

24 sine-kinase inhibitor, has shown encouraging anti-tumour activity in heavily pre-treated patients wit

25 CLXL and BIM-MCL1 interactions, with durable anti-tumour activity in models with AKT inhibitor acquir

26 tane showed preliminary signs of encouraging anti-tumour activity in patients with advanced hormone r

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

28 Lenvatinib plus pembrolizumab showed anti-tumour activity in patients with advanced recurrent

29 Enobosarm has anti-tumour activity in patients with ER-positive, HER2-

30 ess the safety, tolerability and preliminary anti-tumour activity in patients with MSI colorectal can

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

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

33 re, in clinical trials, AMG 510 demonstrated anti-tumour activity in the first dosing cohorts and rep

34 ls that were expanded with H9T showed robust anti-tumour activity in vivo in mouse models of melanoma

35 ) into T cells (which we show lead to strong anti-tumour activity in vivo) and also transduce natural

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

37 The anti-tumour activity of effector T cells can be therapeu

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

39 of a phase 2 study, in which we assessed the anti-tumour activity of golidocitinib in a large multina

40 verse human and mouse tumours and limits the anti-tumour activity of IL-18 in mice.

41 ever, there is a lack of methods to validate anti-tumour activity of NK cells in vivo.

42 echanism of action, we aimed to evaluate the anti-tumour activity of PD-1 blockade with EGFR inhibiti

43 We assessed the safety and anti-tumour activity of pembrolizumab, a programmed cell

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

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

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

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

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

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

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

51 ERV-reactive antibodies exert anti-tumour activity that extends survival in the mouse

52 that ID3 is sufficient to confer this potent anti-tumour activity to mouse bone-marrow-derived macrop

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

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

55 ergic receptors (alpha2-AR) have very strong anti-tumour activity when used as monotherapies in multi

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

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

58 itors and monoclonal antibodies, have a high anti-tumour activity, are well tolerated, and have a low

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

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

61 r beneficial biological activities including anti-tumour activity.

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

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

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

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

66 eckpoint inhibition to revive their inherent anti-tumour activity.

67 to the induction of natural killer (NK) cell anti-tumour activity.

68 rial antigen targeted approaches, to improve anti-tumour activity.

69 that avoids enhanced toxicity but maintains anti-tumour activity.

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

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

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

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

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

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

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

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

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

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

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

81 d death ligand 1 or IFNGR1 elicited a robust anti-tumour and/or anti-metastatic effect.

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

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

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

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

86 cgamma receptors (FcgammaR), in turn driving anti-tumour CD8(+) T cells from an exhausted effector-li

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

88 LNCs delivered by Ho-MN exhibited remarkable anti-tumour destruction (85.84%) after irradiation with

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

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

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

92 g cancer immunotherapy provides a short-term anti-tumour effect at the cost of diminishing efficacy d

93 A synergetic anti-tumour effect for Trypsinogen and Chymotrypsinogen

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

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

96 h KRASG12C inhibitors elicited a substantial anti-tumour effect in LUAD and PDAC.

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

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

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

100 autoimmunity-was sufficient to produce this anti-tumour effect, showing that it is not the mere loss

101 tion, few studies have reported its abscopal anti-tumour effect, which has limited its further clinic

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

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

104 2 production ex vivo, and enhanced antiviral/anti-tumour effector function after TCR engagement.

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

106 fficiently targets tumours, mediating robust anti-tumour effects in a diverse set of preclinical canc

107 Doxycycline has anti-tumour effects in a range of tumour systems.

108 meric antigen receptor (CAR) T cells mediate anti-tumour effects in a small subset of patients with c

109 MCL1 inhibition exhibits anti-tumour effects in MCL1-gained mCRPC models.

110 ing in an enzyme capable of mediating strong anti-tumour effects in mice.

111 Unlike wild-type IL-18, DR-18 exerted potent anti-tumour effects in mouse tumour models by promoting

112 nst cancer antigens have demonstrated potent anti-tumour effects in pre-clinical studies.

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

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

115 Accordingly, the anti-tumour effects of autophagy inhibition are reversed

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

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

118 t that treatment with CP-673451 improves the anti-tumour effects of temozolomide in vivo using a subc

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

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

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

122 for tumour control and induction of systemic anti-tumour effects.

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

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

125 r haematological malignancies with increased anti-tumour efficacy and reduced toxicity are developed,

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

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

128 CBD-IL-12-armoured CAR-T cells showed potent anti-tumour efficacy in a 22Rv1 xenograft while reducing

129 wth(1-6) and its inhibition has demonstrated anti-tumour efficacy in combination with targeted therap

130 pecificity, are stable in plasma and improve anti-tumour efficacy in mice with non-small cell lung tu

131 ed to o2R T cells, o9R T cells have superior anti-tumour efficacy in two recalcitrant syngeneic mouse

132 ssion of KRAS(G12C) tumours and improved the anti-tumour efficacy of chemotherapy and targeted agents

133 hat increased ferroptosis contributes to the anti-tumour efficacy of immunotherapy.

134 e and talazoparib significantly improved the anti-tumour efficacy of LuTate alone.

135 ti-tumor xenograft studies demonstrated high anti-tumour efficacy of PRP against tumours induced by B

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

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

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

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

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

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

142 ith CD4(+) and CD8(+) T cells-contributed to anti-tumour efficacy.

143 CAR-T cells targeting nfP2X7 exhibit robust anti-tumour efficacy.

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

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

146 gic signalling in CD8(+) T cells rejuvenates anti-tumour functions.

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

148 ntain expression of crucial pro-inflammatory/anti-tumour genes with time.

149 Anti-tumour immune activation by checkpoint inhibitors l

150 nment (TME), alleviating fibrosis, promoting anti-tumour immune cell phenotypes, and enhancing the ef

151 mune checkpoint blockers, and thus activates anti-tumour immune memory to effectively inhibit tumour

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

153 e NSCLC as an immunomodulator to enhance the anti-tumour immune response associated with the anti-PD-

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

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

156 er ablation of a primary tumour thanks to an anti-tumour immune response stimulated by cryoablation.

157 tic inactivation of PI3Kbeta led to a robust anti-tumour immune response that abrogated tumour growth

158 ontrol over the location and duration of the anti-tumour immune response, CAR T cell therapy still fa

159 types block the development of an effective anti-tumour immune response, including inhibition of the

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

161 BCG also stimulates an anti-tumour immune response, which urologists have harne

162 -CTLA4 antibodies), and leads to an enhanced anti-tumour immune response.

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

164 with checkpoint blockade therapy to enhance anti-tumour immune response.

165 tein 2 (BTNL2) is a potent suppressor of the anti-tumour immune response.

166 immune adjuvants release to provoke a potent anti-tumour immune response.

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

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

169 e spatio-temporal dynamics of CCR7(+) DCs in anti-tumour immune responses remain unclear.

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

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

172 hexa-acylated LPS was required for effective anti-tumour immune responses, and LPS-binding antibiotic

173 sm by which VISTA may engender resistance to anti-tumour immune responses, as well as an unexpectedly

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

175 apy-free treatment combination that triggers anti-tumour immune responses, we conducted a phase 2 stu

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

177 accumulate in metastatic lesions to promote anti-tumour immune responses.

178 une stimulatory molecules, thereby promoting anti-tumour immune responses.

179 tile strategy for the generation of adaptive anti-tumour immune responses.

180 accination, do not typically generate robust anti-tumour immune responses.

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

182 uppressing local steroidogenesis can augment anti-tumour immunity against TNBC.

183 2 as a target for bolstering T-cell-mediated anti-tumour immunity and CAR T-cell therapy against soli

184 ulsive guidance molecule b (RGMb) to promote anti-tumour immunity and identify bacterial species that

185 ade synergistically enhanced T cell-mediated anti-tumour immunity and induced ferroptosis in tumour c

186 cancer cells induce T-cell and IFN-dependent anti-tumour immunity and inhibit tumour growth in mice.

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

188 ly, therapeutic CXCL13 treatment potentiates anti-tumour immunity and synergizes with ICB.

189 HECTD2 expression is associated with weaker anti-tumour immunity and unfavourable outcome of PD-1 bl

190 ibroblasts (CAFs) and their direct impact on anti-tumour immunity are uncharacterized.

191 danger detector NKG2D-a critical mediator of anti-tumour immunity by cytotoxic lymphocytes, such as N

192 lenide-bridged organosilica generates robust anti-tumour immunity by exploiting the capacity of prima

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

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

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

196 ized the field of oncology, inducing durable anti-tumour immunity in solid tumours.

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

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

199 promotes effector CD8(+) T cell function and anti-tumour immunity in vivo.

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

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

202 Thus, effective anti-tumour immunity is constrained by inhibitory checkp

203 d IL-18, completely abrogated the protective anti-tumour immunity observed with TIM-3 deletion in DCs

204 the mechanisms via which CAFs influence the anti-tumour immunity remain poorly understood.

205 nts is variable and how gut bacteria promote anti-tumour immunity remains unclear.

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

207 owing that microglia are critical to promote anti-tumour immunity to suppress BCBM.

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

209 MP-AMP signalling during viral infection and anti-tumour immunity(1-5).

210 other immune subsets may also contribute to anti-tumour immunity(11-15), although these have been le

211 ith Alzheimer's disease, atherosclerosis and anti-tumour immunity(2-5), affect COVID-19 outcome in a

212 PI3Kdelta inhibitors (PI3Kdeltai) can induce anti-tumour immunity(4,5), its effect on solid tumours i

213 nteraction with lymphocytes as components of anti-tumour immunity(5), which LSCs must escape to induc

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

215 ic PD-1 inhibition to expand TILC2s, augment anti-tumour immunity, and enhance tumour control, identi

216 D8(+) T lymphocytes (CTLs) are essential for anti-tumour immunity, they are frequently dysfunctional

217 CAFs) have emerged as critical regulators of anti-tumour immunity, with both beneficial and detriment

218 heir cross-talk that is required for optimal anti-tumour immunity.

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

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

221 II molecules and provide anti-microbial and anti-tumour immunity.

222 e significantly augmented anti-PD-1-mediated anti-tumour immunity.

223 s delineate a mechanism of infection-induced anti-tumour immunity.

224 on CD4(+) or CD8(+) T cells-promotes strong anti-tumour immunity.

225 toxicity, cytokine production and subsequent anti-tumour immunity.

226 acrophages (TAMs) controls tumour growth and anti-tumour immunity.

227 the only mechanism leading to dysfunctional anti-tumour immunity.

228 blockade, AC484 monotherapy generates potent anti-tumour immunity.

229 h responses in anti-pathogen and potentially anti-tumour immunity.

230 mour antigens to CD8(+) T cells and triggers anti-tumour immunity.

231 e uptake via the transporter SLC38A2 to tune anti-tumour immunity.

232 ppressor by activating pyroptosis, enhancing anti-tumour immunity.

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

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

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

236 suggesting that IL-18 therapy could enhance anti-tumour immunity.

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

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

239 Anti-tumour inflammatory cytokines are highly toxic when

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

241 us, T cell-promoted tumour ferroptosis is an anti-tumour mechanism, and targeting this pathway in com

242 Anti tumour necrosis factor (anti-TNF) drugs increase th

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

244 rofiles, including biologics (in particular, anti-tumour necrosis factor (TNF) agents).

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

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

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

248 Since the early 2000s, anti-tumour necrosis factor (TNF) treatment has signific

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

250 is infection is routine before initiation of anti-tumour necrosis factor alpha (anti-TNFalpha) agents

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

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

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

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

255 Anti-tumour necrosis factor drugs were most commonly stu

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

257 Safety of anti-tumour necrosis factor-alpha (TNFalpha) therapy in

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

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

260 x (ECM) remodelling can induce pro-tumour or anti-tumour neutrophil polarization through biomechanica

261 phages with the ability to form an efficient anti-tumour niche, which could be harnessed for cell the

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

263 nished terminal differentiation and improved anti-tumour potency in five different mouse tumour model

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

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

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

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

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

269 icted neoantigens have a key function in the anti-tumour response that is nonoverlapping with that of

270 ed genes and, as a consequence, enhances the anti-tumour response to PD-1 blockade.

271 ere, to investigate and overcome this futile anti-tumour response within the leptomeninges, we develo

272 haracteristics consistent with a compromised anti-tumour response.

273 ' in the sentence starting "By contrast, the anti-tumour response...".

274 ' in the sentence starting "By contrast, the anti-tumour response...".

275 f CAR and T-SenSER in human T cells enhances anti-tumour responses in models of lung cancer and multi

276 an anti-PD-1 or anti-PD-L1 antibody promotes anti-tumour responses in multiple mouse tumour models th

277 heckpoint CD47-SIRPalpha may lead to durable anti-tumour responses in solid cancers.

278 692/29 showed good anti-tumour responses in vivo and is a strong therapeuti

279 within the tumour may greatly potentiate the anti-tumour responses of immune checkpoint inhibitors, s

280 w that spontaneous and immunotherapy-induced anti-tumour responses require the activity of both tumou

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

282 t of CheckMate 358, nivolumab showed durable anti-tumour responses, and the combination of nivolumab

283 tory T cells and induce T(H)17-cell-mediated anti-tumour responses.

284 of IRAP fail to develop efficient polyclonal anti-tumour responses.

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

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

287 IFNepsilon activated anti-tumour T and natural killer cells and prevented the

288 in cDC1s reduces tumour growth by enhancing anti-tumour T cell immunity, particularly increasing the

289 s to improved antigen presentation, enhanced anti-tumour T cell responses and reduced tumour growth i

290 to sense and respond to IFNgamma, preventing anti-tumour T cell responses.

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

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

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

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

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

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

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

298 copies SLC38A2 deficiency by eliminating the anti-tumour therapeutic effect of glutamine supplementat

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

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