ライフサイエンスコーパス: antitumor response

1 to R24L, R24C failed to induce an effective antitumor response.

2 both the priming and effector stages of the antitumor response.

3 nancies that may be sensitive to the NK cell antitumor response.

4 imulate a CD8(+) T cell-dependent protective antitumor response.

5 nable longer persistence and thereby improve antitumor response.

6 6 deficiency abrogated the Th9 cell-mediated antitumor response.

7 e to inhibit the development of an efficient antitumor response.

8 or cell-based vaccines led to no appreciable antitumor response.

9 ary treatment experiments showed a favorable antitumor response.

10 ance of immune tolerance and to insufficient antitumor response.

11 ed a naturally acquired CD8 T cell-dependent antitumor response.

12 ecific FcgammaR alleles were associated with antitumor response.

13 tinct functional activities that impair host antitumor response.

14 n why some immunotherapies fail to induce an antitumor response.

15 for cancer vaccines to trigger an effective antitumor response.

16 ved NK cells to mediate an effective in vivo antitumor response.

17 l tolerance that serve to limit an effective antitumor response.

18 of T- and natural killer (NK) cell-mediated antitumor response.

19 trategies aimed at enhancing immune-mediated antitumor response.

20 point inhibitor pathways, which suppress the antitumor response.

21 that macrophages were a major driver of the antitumor response.

22 d IFNgamma in MEKi-treated mice enhanced the antitumor response.

23 S specifications that may elicit the desired antitumor response.

24 L) but these cells do result in an effective antitumor response.

25 ation, and the ability to mount an effective antitumor response.

26 ntial for generating durable and synergistic antitumor response.

27 u-DOTATATE treatment and induces a prolonged antitumor response.

28 lymphocytes (TIL) are potent mediators of an antitumor response.

29 yclic dinucleotides elicit potent immune and antitumor response.

30 omotes stem cell memory T cells (T(SCM)) and antitumor responses.

31 cells to thwart the development of effective antitumor responses.

32 cells were required for gemcitabine-mediated antitumor responses.

33 ytes that are essential for antipathogen and antitumor responses.

34 ) T cells during chronic virus infection and antitumor responses.

35 ion of inflammatory responses and evasion of antitumor responses.

36 susceptibility to infections, and diminished antitumor responses.

37 ability to prime T cell function and induce antitumor responses.

38 nduction of spontaneous humoral and cellular antitumor responses.

39 is that CD4(+) T cells are involved in human antitumor responses.

40 cells act to promote effective T cell-based antitumor responses.

41 m in a manner that is sufficient to engender antitumor responses.

42 ne models was necessary for imatinib-induced antitumor responses.

43 valuable option to optimize iNKT cell-based antitumor responses.

44 rt the often tolerant immune response toward antitumor responses.

45 t immune effector cells capable of mediating antitumor responses.

46 a cytokine implicated in the enhancement of antitumor responses.

47 r-reactive gd T cells may result in enhanced antitumor responses.

48 r prodrugs are less toxic and induce durable antitumor responses.

49 une microenvironment to block effective host antitumor responses.

50 he native tumor antigen, resulting in potent antitumor responses.

51 by cytotoxic T lymphocytes, yet dampens the antitumor responses.

52 rd as potent activators of CD8(+) T cells in antitumor responses.

53 mmune system mark pDCs as inducers of potent antitumor responses.

54 ltration may be effective to further improve antitumor responses.

55 study is to examine the role of Fpr2 in host antitumor responses.

56 r cell NF-kappaB activity in T cell-mediated antitumor responses.

57 high level of Th1 polarization and superior antitumor responses.

58 s enhances DC activation and CXCR3-dependent antitumor responses.

59 mor antigen-specific CD4+ T cells, enhancing antitumor responses.

60 ther the ICOS/ICOSL pathway is necessary for antitumor responses.

61 een proposed to play a critical role in host antitumor responses.

62 IL-2 during adoptive cell transfer-mediated antitumor responses.

63 ur times fewer cells were needed to generate antitumor responses.

64 has been shown to be effective in enhancing antitumor responses.

65 of cancer due to its ability to drive strong antitumor responses.

66 strategy for cancer chemotherapy to increase antitumor responses.

67 tant role in the generation of antiviral and antitumor responses.

68 regulatory cells completely fails to enhance antitumor responses.

69 role in T(reg) cell-mediated suppression of antitumor responses.

70 y targeted APCs in vivo to induce protective antitumor responses.

71 nal CD4+ T (Tconv) cells, despite the marked antitumor responses.

72 er-2/neu(+) tumors, activate DCs, and induce antitumor responses.

73 CD47-deficient whole tumor cells can induce antitumor responses.

74 both T and natural killer (NK) cell-mediated antitumor responses.

75 T cell senescence and sustain CD8(+) T cell antitumor responses.

76 by increasing the frequency of long-lasting antitumor responses.

77 ly increased the frequency and durability of antitumor responses.

78 nce of CD137 in human immune homeostasis and antitumor responses.

79 sm and programming form the basis for potent antitumor responses.

80 metabolic reprogramming agent that supported antitumor responses.

81 an be manipulated therapeutically to enhance antitumor responses.

82 e the importance of T cell help in mediating antitumor responses.

83 CAR T-cell therapy would result in improved antitumor responses.

84 ligand fusion proteins, produced synergistic antitumor responses.

85 y during viral, intracellular bacterial, and antitumor responses.

86 an be activated to induce long-term, durable antitumor responses.

87 s, and blockade of these pathways attenuated antitumor responses.

88 ng AML-specific antibodies may contribute to antitumor responses.

89 8 with doxorubicin resulted in a significant antitumor response (22.6 d growth delay), which was supe

90 ur results showed that ICOS signaling during antitumor responses acts on both Teff and Treg cells, wh

91 tical ATF3-dependent genes that elicited the antitumor response after PDI and HDAC inhibition.

92 of memory cells capable of triggering robust antitumor responses after adoptive transfer.

93 these NKT-cell subsets in the host's innate antitumor response against a murine B-cell lymphoma mode

94 uses expressing Flagrp170 induces a superior antitumor response against B16 melanoma and its distant

95 rejection of donor cells leads to a specific antitumor response against recipient malignancies.

96 c in vitro but surprisingly elicited greater antitumor responses against advanced tumors in OT-I/B16-

97 unctional mechanisms behind NK cell-mediated antitumor responses against metastatic colorectal carcin

98 esults show how CD4 cells can mediate potent antitumor responses against modified self-epitopes prese

99 L-12 (SFV-IL-12) were shown to induce potent antitumor responses against s.c. MC38 colon adenocarcino

100 ic fitness and mediated robust, long-lasting antitumor responses against systemic acute lymphoblastic

101 In vivo blockade of B7-H1 restored antitumor responses against the B7-H1(-) BM-185-enhanced

102 otein can enhance innate and adaptive immune antitumor responses, also evoking additional nontargeted

103 ether, iMC expand independent of the type of antitumor response and are not immunosuppressive in a ce

104 adaptive immune system to mount an efficient antitumor response and frequently contributes to lessen

105 engineered T cells (CAR-Ts) provide a potent antitumor response and have become a promising treatment

106 d a drug-disease simulation model to predict antitumor response and overall survival in phase III stu

107 in patients with advanced melanoma improves antitumor response and progression-free survival but wit

108 dence for CD8(+) T cell-independent means of antitumor response and should lead to additional examina

109 The models were validated in simulation of antitumor response and survival in an independent phase

110 The patient experienced both a complete antitumor response and T cell-mediated allograft rejecti

111 that type I IFN is required to initiate the antitumor response and that its actions are temporally d

112 We evaluated the antitumor response and tolerability of sorafenib in pati

113 NKT cells mount strong antitumor responses and are a major focus in developing

114 TL could contribute to reduced antiviral and antitumor responses and autoimmunity reported in patient

115 rial dynamics and quality orchestrate T cell antitumor responses and commitment to the exhaustion pro

116 6 receptor that is essential for NK-mediated antitumor responses and immunity from infection.

117 ic tumors in mice activates NK cell-mediated antitumor responses and inhibits local recurrence of tum

118 of T(SCM) cells, resulting in more profound antitumor responses and prolonged host survival.

119 , alphaGalCer-pretreated iNKT cells impaired antitumor responses and reduced disease in experimental

120 cted with ICOS-based CARs mediated efficient antitumor responses and showed enhanced persistence comp

121 en human and mouse leukemias elicited potent antitumor responses and significantly prolonged survival

122 imultaneously stimulate cellular and humoral antitumor responses and the mechanisms involved have not

123 tion and lymphocyte infiltration, abolishing antitumor responses and therapeutic efficacy of the comb

124 our laboratory to be mediators in achieving antitumor responses and tumor protection through antibod

125 ceptor expressed by lymphocytes, in limiting antitumor responses and we review its mechanisms of acti

126 r NK-cell subsets have specific roles during antitumor responses and what the signals are that drive

127 s method could transform the manner in which antitumor responses and/or infectious events may be trac

128 Biochemical, radiographic, clinical antitumor response, and adverse events were analyzed.

129 tablished T cell dysfunction is a barrier to antitumor responses, and checkpoint blockade presumably

130 osuppressive myeloid populations, inhibiting antitumor responses, and enhancing angiogenesis, thus pr

131 (+) regulatory T cell induction, potentiated antitumor responses, and exacerbated experimental autoim

132 12 (IL-12), IL-15, and IL-18, exhibit potent antitumor responses, and safely induce complete remissio

133 modify inflammatory conditions or to promote antitumor responses, and situations where experimental a

134 o block negative signals and to maintain the antitumor response are particularly exciting.

135 e systematically demonstrated that effective antitumor responses are generated after vaccination with

136 Despite its immunogenicity, effective antitumor responses are limited, due, in part, to the pr

137 pon checkpoint blockade, leading to superior antitumor response as compared to SNP-SC in a therapeuti

138 ecruitment of T(reg) into the TME and elicit antitumor responses as a single agent or in combination

139 g modulation of ERAAP to generate protective antitumor responses as a strategy for cancer immunothera

140 ponse-assessable patients attained objective antitumor responses; best overall objective response was

141 er and Ag to CD8alpha(+) DCs promotes potent antitumor responses, both in prophylactic and in therape

142 tivation of IL10 in Treg did not elevate the antitumor response but instead further boosted tumor dev

143 approach is how to obtain the ideal initial antitumor response but still preserve antitumor immune m

144 ll types has been implicated in eliciting an antitumor response, but a direct role of MCPIP1 in apopt

145 okine therapy can activate potent, sustained antitumor responses, but collateral toxicity often limit

146 ells of the liver can inhibit autoimmune and antitumor responses by mechanisms that are poorly unders

147 R) ligands may be a valuable tool to promote antitumor responses by reinforcing antitumor immunity.

148 In cancer, Treg down-regulate antitumor responses by several distinct mechanisms.

149 ates that NK cell functions, and potentially antitumor responses, can be enhanced long term.

150 h possess superior immune reconstitution and antitumor response capabilities, can be identified by po

151 d (HA) nanoparticle (NP) induced synergistic antitumor response CD44 expressing tumors that are resis

152 s on the basis of the key player in adaptive antitumor response, CD8+ cells, and evaluates the immuno

153 nously expressed by SM1 resulted in superior antitumor responses compared with either therapy alone.

154 ADH-1 in combination with LPAM ILI improved antitumor responses compared with LPAM alone in both cel

155 nd that combined treatment produced superior antitumor responses compared with single treatments.

156 ty of GVHD and the strength of an alloimmune antitumor response could be manipulated by enhancing or

157 inistered to one tumor stimulated a systemic antitumor response, curing both tumors.

158 Antitumor responses depend on type 1 immunity, which is

159 The induction of antitumor responses depends on SIRPalpha(+)CD11c(+) DCs,

160 r setting, where the balance of protumor and antitumor responses dictates tumor initiation and progre

161 ereas in cancer, T cells are unable to mount antitumor responses due to the Treg-enriched suppressive

162 SPs; e.g., hsp110 and grp170), attenuated an antitumor response elicited by large HSP-based vaccines.

163 e inhibition in most tissues and elicited an antitumor response equivalent to intravenously administe

164 ved the SLAMF6 -/- T cells and expedited the antitumor response even further.

165 nt to overcome immune escape, led to durable antitumor responses even after drug withdrawal.

166 oral regulatory B cells and fails to improve antitumor responses, even while protecting against activ

167 Antitumor responses following chitosan/IL-12 treatments

168 In this study, we evaluated the mechanism of antitumor responses following IL-7 administration to mic

169 , but only elicits limited rates of systemic antitumor response for most cancers due to insufficient

170 fore, we examined the impact of SRA/CD204 on antitumor responses generated by DC vaccines and we also

171 immune-activating signals and maintains the antitumor response, has elicited a remarkable clinical r

172 n within human tumors is crucial for optimal antitumor responses; however, the regulation of IL-15 wi

173 o be important in allergy, autoimmunity, and antitumor responses; however, their role in human infect

174 g lymphocytes (TILs) indicates an endogenous antitumor response, immune regulatory pathways can subve

175 of KRAS status, cetuximab did not induce an antitumor response in a majority of patient tumors.

176 essing targets in vivo, and elicits a better antitumor response in a model of E7-expressing lung canc

177 tumor killing function, and exert a superior antitumor response in a mouse melanoma model.

178 ctivation in all tumors but failed to induce antitumor response in a subset.

179 herefore be an effective means to trigger an antitumor response in melanoma and other cancers.

180 onment (TME) has the potential to weaken the antitumor response in patients receiving treatment with

181 verexpressing CAR T cells elicit an impaired antitumor response in the absence of cDC1s.

182 re without toxicity but induced insufficient antitumor response in these high-tumor-burden patients.

183 s to chemotherapy and produced a synergistic antitumor response in vitro and in vivo.

184 enewal, expansion, persistence, and superior antitumor response in vivo.

185 ffects on downstream biomarkers and a robust antitumor response in xenograft models in which the phos

186 odeficient hosts, and they mediated superior antitumor responses in a humanized mouse model.

187 inhibitory drug AZD8055 elicited synergistic antitumor responses in a model of metastatic renal cell

188 Treatment with RS-1 promoted significant antitumor responses in a mouse model, providing proof-of

189 flow could augment drug delivery and improve antitumor responses in a regional model of melanoma.

190 feasible, directly observable, and augmented antitumor responses in a regional model of melanoma.

191 erapies, such as ipilimumab, induce dramatic antitumor responses in a subset of patients with advance

192 IT CMP-001 with systemic anti-PD-1 enhanced antitumor responses in both injected and noninjected tum

193 pecific Th9 cell treatment promoted stronger antitumor responses in both prophylactic and therapeutic

194 ous conditioning regimens to achieve optimal antitumor responses in cancer patients.

195 otherapy may be combined to achieve superior antitumor responses in cancer patients.

196 f IRES-J007 and PP242 to achieve synergistic antitumor responses in GBM.

197 (CARs) targeting CD19 have mediated dramatic antitumor responses in hematologic malignancies, but tum

198 that seek to improve DC function and elicit antitumor responses in hosts with cancer.

199 bacterial infections can produce efficacious antitumor responses in mice, rats, dogs, and humans.

200 CD8alpha:MyD88-expressing T cells improved antitumor responses in mice.

201 ccinia virus (Vv) has shown some encouraging antitumor responses in mouse models and patients, but th

202 ti-PD1, or adoptive T-cell transfer improved antitumor responses in multiple models, including cures

203 ould be possible to induce the activation of antitumor responses in neu mice.

204 We found that the 4BL cells increase antitumor responses in old mice, which may explain in pa

205 e been shown to increase T cell function and antitumor responses in patients with advanced metastatic

206 trials, PARP1/2 inhibitors elicit sustained antitumor responses in patients with germline BRCA gene

207 to reduce relapse risk and to induce durable antitumor responses in patients with Hodgkin's lymphoma

208 ever, the difficulties in the development of antitumor responses in patients with low tumor burden ra

209 dified (CAR) T cells has produced impressive antitumor responses in patients with refractory CD19(+)

210 mor cells, can mediate deep and long-lasting antitumor responses in patients with solid tumors.

211 entiated T effector cells can elicit durable antitumor responses in some patients with cancer, with t

212 ed mice and partially restored the defective antitumor responses in the middle-aged mice.

213 Given the ineffectual T cell antitumor responses in this mouse model of CLL, we sough

214 This in turn triggers antitumor responses in vitro and in vivo.

215 creasing phagocytosis in vitro and enhancing antitumor responses in vivo.

216 and induce immunogenic cancer cell death and antitumor responses in vivo.

217 NBP and gammadelta T cells yielded improved antitumor responses in vivo.

218 acute stimulation, resulting in impaired NK antitumor responses in vivo.

219 Calcium electroporation elicited dramatic antitumor responses in which 89% of treated tumors were

220 nslation of this strategy, and its impact on antitumor responses, in particular immune responses.See

221 ibitors in vivo to elicit potent and durable antitumor responses, including by a vaccine-like effect

222 ide inhibitory signaling might boost NK cell antitumor responses, independently of blockade of NK cel

223 r beta5 alone was insufficient to produce an antitumor response, inhibition of all proteasome subunit

224 agent 5-aza-cytidine distinctly enhanced the antitumor response, interestingly without inducing commo

225 e ability of post septic Tregs to impair the antitumor response mediated by CD8(+) T cells.

226 Furthermore, it did not impede antitumor responses mediated by anti-4-1BB-driven CD8(+)

227 Tag antibody response that led to successful antitumor responses not observed in animals treated only

228 ry genes that may contribute to the enhanced antitumor response observed in C3aR-deficient mice.

229 ated, with target engagement and preliminary antitumor responses observed.

230 ief priming with IL-15 markedly enhanced the antitumor response of CD56bright NK cells.

231 Finally, with the aim of increasing the antitumor response of perioperative RT, these agents may

232 ry type is more rapid than and dominates the antitumor response of tumor-specific effector T cells.

233 ressive capacity of T(reg) in inhibiting the antitumor responses of CD8(+) T cells, in the same way a

234 lymphopenic host can augment the therapeutic antitumor responses of the transferred cells.

235 depleting Foxp3(+) T(reg) cells can enhance antitumor responses provide proof of principle, these st

236 inhibits DNA methylation, produces variable antitumor response rates in patients with solid tumors t

237 the relationship of this differentiation to antitumor responses remains largely undefined.

238 s also increasing evidence that an effective antitumor response requires a systemic immune response i

239 synergizes with statins to produce a robust antitumor response.See related commentary by Cordes and

240 sufficient to dampen BRAF inhibitor-induced antitumor responses, suggesting that the impaired antitu

241 ers resulted in substantially more efficient antitumor responses than B cells or T cells alone (p < 0

242 nificantly decreased, resulting in a reduced antitumor response that allowed metastasis formation in

243 imulatory cells capable of triggering potent antitumor responses that abrogated the progression of es

244 nal; however, in nonpathogen settings (i.e., antitumor responses), the identity of the third signal i

245 ethyl pyruvate elicits a potent immune-based antitumor response through inhibition of indoleamine 2,3

246 xpression of effector molecules can initiate antitumor responses through engagement of specific recep

247 indicate that ERK inhibitors might influence antitumor responses through regulation of critical DC ef

248 Generating antitumor responses through the inhibition of tumor-deri

249 For antitumor responses, TNFSF14 was preferentially produced

250 reased Treg cells, resulting in a diminished antitumor response to a tissue-restricted, melanoma-asso

251 ffect of cediranib and might also reflect an antitumor response to antiangiogenic treatment during th

252 IF-2alpha, we recently demonstrated that the antitumor response to GM-CSF was dependent on HIF-2alpha

253 nd VEGF-neutralizing antibodies enhanced the antitumor response to IR.

254 Additionally, clinical antitumor response to monoclonal antibodies has been ass

255 bearing ER(+) xenografts displayed a durable antitumor response to palbociclib; however, over the cou

256 473)-Akt was insufficient to predict in vivo antitumor response to PX-866.

257 We observed a significant enhancement of antitumor response to radiation in squamous cell carcino

258 cells in thyroid cancer is critical for the antitumor response to radioactive iodide treatment, and

259 e residual tumor cells surviving the initial antitumor response to targeted therapies.

260 ent mice were more immunogenic in generating antitumor responses to B16 melanoma, compared with DCs f

261 inhibiting EphB2 signaling, and that optimal antitumor responses to EphB2 targeting may require concu

262 roliferation have been proposed as the major antitumor responses to histone deacetylase inhibitors (H

263 st that Skp2 levels are a key determinant of antitumor responses to mTOR inhibitors, highlighting a p

264 on, and reduced their fibrotic phenotype and antitumor responses to nintedanib in vitro and in vivo.

265 microtubules prior to therapy could enhance antitumor responses to paclitaxel treatment.

266 te a targeted agent in an attempt to augment antitumor responses to regional chemotherapy.

267 in BVE(Cyp24a1-null) cells, it strengthened antitumor responses to the BRAF(V600E) inhibitor PLX4720

268 induction of Ag-specific CD8(+) T cells and antitumor responses to whole Ag were independent of MHC

269 ions for CD40L and IFNgamma signaling in the antitumor responses triggered in vivo by B-Raf(V600E) in

270 s were impaired following successful initial antitumor responses using various immunotherapeutic appr

271 Notably, the AZD8055/alphaCD40-induced antitumor response was abolished in IFN-gamma(-/-) and C

272 The synergistic antitumor response was accompanied by a significant incr

273 Antitumor response was assessed according Response Evalu

274 This antitumor response was dependent on CD4 cells and not CD

275 Furthermore, a systemic antitumor response was observed in both bilateral and tu

276 The antitumor response was partially mediated by tumor-speci

277 The antitumor response was triggered by direct drug actions

278 As PD-1 can attenuate T-cell-mediated antitumor responses, we tested whether its blockade with

279 In this study, to evoke systemic antitumor responses, we utilized charge-altering releasa

280 Antitumor responses were elicited after U-Omp19 coadmini

281 reported that secondary CD8+ T cell-mediated antitumor responses were impaired following successful i

282 Accompanying the antitumor responses were increases in IFN-gamma, CXCL9,

283 crease in radioactivity uptake in the tumor, antitumor responses were not diminished significantly fo

284 However, antitumor responses were observed, identifying the vascu

285 rapy, whereas KRAS wild type demonstrated an antitumor response when treated with cetuximab.

286 inia virus (Vvdd) for its capacity to induce antitumor responses when combined with an agonist antibo

287 inity gamma9delta2TCRs that mediate improved antitumor responses when expressed in alphabetaT cells b

288 CD56dim NK cell subset is thought to mediate antitumor responses, whereas the CD56bright subset is in

289 mma are essential for the Flagrp170-elicited antitumor response, which also involves CD8(+) T cells a

290 both in aging and as a robust physiological antitumor response, which counteracts oncogenic insults.

291 ally providing an approach to achieve potent antitumor responses while minimizing ADC-induced toxicit

292 Because it is likely that an effective antitumor response will require high-avidity, PRAME-spec

293 ole of NK cells as helper cells in enhancing antitumor responses will reveal new strategies for clini

294 RP-1 and PARP-2-deficiency in modulating the antitumor response with an impact on tumor progression,

295 urthermore, CD36 targeting elicited additive antitumor responses with anti-programmed cell death prot

296 rrole-imidazole polyamides) has demonstrated antitumor responses with minimal side-effects.

297 SF play important roles in priming effective antitumor responses with these vaccines.

298 ective, transient ablation of Treg can evoke antitumor responses, with implications for immunotherape

299 expressing granulysin show markedly improved antitumor responses, with increased numbers of activated

300 T cells (T(conv)) is critical for productive antitumor responses yet their elicitation remains poorly