ライフサイエンスコーパス: antitumor response

1 6 deficiency abrogated the Th9 cell-mediated antitumor response.

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

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

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

5 ance of immune tolerance and to insufficient antitumor response.

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

7 ecific FcgammaR alleles were associated with antitumor response.

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

9 for cancer vaccines to trigger an effective antitumor response.

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

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

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

13 les of treatments were monitored for hepatic antitumor response.

14 environment was associated with a favorable antitumor response.

15 growth, suggesting it had little role in the antitumor response.

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

17 yclic dinucleotides elicit potent immune and antitumor response.

18 on signal, and IL-12/23 suggest partial host antitumor response.

19 immune network is regulated to achieve this antitumor response.

20 ate dendritic cells, nor induce an effective antitumor response.

21 n the Fas ligand pathway was involved in the antitumor response.

22 and may play a significant role in the host antitumor response.

23 particularly sensitive to a CCI-779-induced antitumor response.

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

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

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

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

28 ntial for generating durable and synergistic antitumor response.

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

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

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

32 une microenvironment to block effective host antitumor responses.

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

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

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

36 ltration may be effective to further improve antitumor responses.

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

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

39 high level of Th1 polarization and superior antitumor responses.

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

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

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

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

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

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

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

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

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

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

50 strategy for cancer chemotherapy to increase antitumor responses.

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

52 regulatory cells completely fails to enhance antitumor responses.

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

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

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

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

57 saline or cell lysate vaccines and showed no antitumor responses.

58 les provides a useful strategy for enhancing antitumor responses.

59 y may also impair the development of durable antitumor responses.

60 ficiently induced protective and therapeutic antitumor responses.

61 nt diseases leads to the suppression of host antitumor responses.

62 (+) regulatory T cells (Treg) suppressive to antitumor responses.

63 s) on effector cells is necessary to mediate antitumor responses.

64 ncers and a potential immunologic target for antitumor responses.

65 essed cell surface molecules and to maximize antitumor responses.

66 ligand fusion proteins, produced synergistic antitumor responses.

67 cells to thwart the development of effective antitumor responses.

68 cells were required for gemcitabine-mediated antitumor responses.

69 ytes that are essential for antipathogen and antitumor responses.

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

71 ion of inflammatory responses and evasion of antitumor responses.

72 susceptibility to infections, and diminished antitumor responses.

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

74 nduction of spontaneous humoral and cellular antitumor responses.

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

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

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

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

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

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

81 rt the often tolerant immune response toward antitumor responses.

82 t immune effector cells capable of mediating antitumor responses.

83 a cytokine implicated in the enhancement of antitumor responses.

84 8 with doxorubicin resulted in a significant antitumor response (22.6 d growth delay), which was supe

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

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

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

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

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

90 ogression, but could be modulated to enhance antitumor responses against autochthonous primary neopla

91 of all four molecules demonstrates stronger antitumor responses against established tumors.

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

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

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

95 by which immunity may be enhanced to elicit antitumor responses against selectively expressed cell s

96 ections plus Treg depletion could rescue the antitumor responses against self-tumor antigens in young

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

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

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

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

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

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

103 stinct mechanisms could significantly affect antitumor response and organ toxicity of these compounds

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

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

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

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

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

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

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

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

112 DC (PD-L2)-specific IgM Ab can induce strong antitumor responses and block inflammatory airway diseas

113 biologic changes that together cause strong antitumor responses and blockade of inflammatory airway

114 6 receptor that is essential for NK-mediated antitumor responses and immunity from infection.

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

116 clinical DC preparations may enhance type 1 antitumor responses and may thereby contribute to effect

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

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

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

120 t CD200 expression by tumor cells suppresses antitumor responses and suggest that anti-CD200 treatmen

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

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

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

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

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

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

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

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

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

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

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

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

133 These antitumor responses are maximized by the presence of hos

134 able activity against some cancers, although antitumor responses are often heterogeneous, and resista

135 qdx5 schedule resulted in the most effective antitumor response as compared with an equivalent total

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

137 e effective, there is a need to maximize the antitumor response at the tumor site as well as to elimi

138 The efficacy of SM16 was a result of a CD8+ antitumor response because (a) the antitumor effects wer

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

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

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

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

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

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

145 Thus, stimulation of an antitumor response by mimotopes may be optimal with pept

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 esults suggest that even though a productive antitumor response can be initiated by a DC vaccine, the

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

151 This suggested that CD8-mediated type 1 antitumor responses cannot only promote accumulation of

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

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

154 f Ag-specific CD8(+) T cells and an enhanced antitumor response compared with immunization with eithe

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

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

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

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

159 Antitumor responses depend on type 1 immunity, which is

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 Furthermore, we show that the antitumor responses elicited by transfer of all four mol

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

165 ocused on improving the effector limb of the antitumor response, few studies have addressed preventin

166 Antitumor responses following chitosan/IL-12 treatments

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

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

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

170 Finally, systemic antitumor responses generated upon therapeutic T reg cel

171 + Th1 cells during the effector phase of the antitumor response has been overshadowed by emphasis on

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

173 Partial antitumor responses have occurred in some of the subject

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

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

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

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

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 moral (i.t.) injections of CpG-ODN induce an antitumor response in neu mice.

181 The improved antitumor response in SR-A knockout mice is correlated w

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

183 CD8 T cell priming and lead to a functional antitumor response in vivo.

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

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

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

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

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

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

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

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

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

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

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

195 NKG2D ligand-positive tumor cells leading to antitumor responses in mice.

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

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

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

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

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

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

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

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

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

205 cell elimination may be required to bolster antitumor responses in patients with metastatic melanoma

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

207 nd interleukin-2 (IL-2) leads to synergistic antitumor responses in several models of advanced metast

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

209 murine EL4 or RMA tumor cells elicits potent antitumor responses in syngeneic C57BL/6 and SCID mice.

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

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

212 cells ex vivo with IL-12 and IL-18 enhanced antitumor responses in vivo and in vitro using a model o

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

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

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

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

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

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

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

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

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

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

223 icked efficiently into i.c. M05 and mediated antitumor responses more effectively than Tc2, and their

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

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

226 Immune-mediated antitumor responses occur in patients with metastatic me

227 Priming of antitumor responses occurs within 3 days of vaccination

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

229 These results indicate that the antitumor response of immune effector cells to exogenous

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

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

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

233 Endogenous antitumor responses of similar magnitude occurred in 22%

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 may, in part, underlie this failure of the antitumor response seen in most patients.

239 th innate natural killer and specific T-cell antitumor responses significantly increased following DC

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 n tumor xenograft models, PR-171 mediates an antitumor response that is both dose and schedule depend

244 Depletion of Tregs resulted in a persistent antitumor response that was maintained over a month afte

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

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

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

248 as now been shown that flavopiridol mediates antitumor responses through mechanism(s) yet to be defin

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

250 Generating antitumor responses through the inhibition of tumor-deri

251 For antitumor responses, TNFSF14 was preferentially produced

252 report the first comparative analysis of the antitumor response to 3'-methylcholanthrene-induced tumo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

271 The synergistic antitumor response was accompanied by a significant incr

272 Antitumor response was assessed according Response Evalu

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

274 The antitumor response was triggered by direct drug actions

275 n the endothelium was rate-limiting for this antitumor response, we engineered mouse mammary tumor vi

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

277 was expressed on primary human T cells, and antitumor responses were determined.

278 Antitumor responses were elicited after U-Omp19 coadmini

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

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

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

282 However, antitumor responses were observed, identifying the vascu

283 No major antitumor responses were observed.

284 No objective antitumor responses were seen.

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 olerance and possess the ability to suppress antitumor responses, which may in part explain the poor

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

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

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

295 in the repertoire and can be used to induce antitumor responses with higher avidity against native e

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 Ten of 15 patients showed significant antitumor responses, with 4 CRs and 6 PRs within one tre

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

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