ライフサイエンスコーパス: antitumor

1 at can become imprinted to stably reduce the antitumor ability of T cells.

2 s, MARCH E3 ligases can act as cofactors for antitumor Abs that target cell surface proteins, suggest

3 eptor, are potential targets for therapeutic antitumor Abs.

4 ts a promising approach in oncology, showing antitumor activities in various cancers.

5 We have reported the antitumor activities of phenformin to enhance the effica

6 GM-CSF-IRF5 axis as a critical driver of the antitumor activities of this versatile cell type.

7 It has antitumor activities, particularly against pancreatic ca

8 an TAMs immune suppression of NK- and T-cell antitumor activities.

9 e BTDs were characterized in vitro for their antitumor activity against A549, PC-3, and HCT-116 cance

10 is the first regimen to demonstrate improved antitumor activity against BMs in patients with HER2-pos

11 ulture condition (T9 CAR-T) have an enhanced antitumor activity against established tumors.

12 the ability of naive OT-1 T cells to develop antitumor activity against ovalbumin-expressing melanoma

13 HASPIN inhibition has direct antitumor activity and induces a favorable immune microe

14 -containing) CAR-T cells resulted in limited antitumor activity and persistence.

15 Although they can paradoxically exert antitumor activity and prime protective immunity, the pa

16 administered OxLys-SNAs exhibit significant antitumor activity and prolonged survival relative to al

17 The antitumor activity and safety of crizotinib were assesse

18 rating this Bicycle also demonstrated potent antitumor activity and was very well tolerated when comp

19 cgammaR-independent agonists with remarkable antitumor activity by isotype switching to hIgG2.

20 As a result, HR is inhibited and antitumor activity enhanced in otherwise HR-proficient s

21 The antitumor activity from Mertk inhibition was abrogated b

22 ared to ACT with IL-2, resulting in superior antitumor activity in a B16-F10 murine melanoma model.

23 e-2-carboxylic acid (43d), showing promising antitumor activity in breast cancer mice xenograft model

24 kinetic profile with encouraging preliminary antitumor activity in heavily pretreated patients with m

25 olecules that bind/inhibit Skp2 have in vivo antitumor activity in mouse tumors and human patient-der

26 nvatinib plus pembrolizumab showed promising antitumor activity in patients with advanced endometrial

27 I/T/DIN/GM-CSF has significant antitumor activity in patients with relapsed/refractory

28 ed a manageable safety profile and promising antitumor activity in patients with selected solid tumor

29 noma cell line SK-MEL-2 but showed only weak antitumor activity in the SK-MEL-2 human melanoma xenogr

30 This BTC demonstrated potent antitumor activity in vivo but was poorly tolerated, whi

31 expression (CVX-8) was used to test in vivo antitumor activity in xenografts models.

32 To investigate whether the antitumor activity is due to the predicted mechanism of

33 The antitumor activity of (67)Cu-CuSarTATE in the AR42J tumo

34 TR-214 may have the potential to improve the antitumor activity of ACT in humans through increased in

35 zation of IL1beta significantly enhanced the antitumor activity of alpha-PD-1 and was accompanied by

36 ion chimeric antigen receptor (CAR) improved antitumor activity of CAR-T cells.

37 ave been explored as a means of boosting the antitumor activity of chimeric antigen receptor (CAR) T

38 ignificantly and synergistically enhance the antitumor activity of HDACi in glioblastoma and pancreat

39 Taken together, our study reveals an antitumor activity of phenformin to promote keratinocyte

40 D-1/PD-L1 immunotherapy and demonstrates the antitumor activity of rimantadine.

41 f vancomycin-sensitive bacteria enhances the antitumor activity of RT, which has important clinical r

42 n tumors attenuate the metabolic fitness and antitumor activity of tumor-infiltrating T lymphocytes (

43 and refractory tumors, but the durability of antitumor activity requires in vivo persistence.

44 Intravenously injected monocytes displayed antitumor activity superior to DC vaccines in several ca

45 nsequently, T9 CAR-T cells mediate a greater antitumor activity than T1 CAR-T cells against establish

46 In vivo, 15 showed more efficacious antitumor activity than the corresponding drug combinati

47 of safety/tolerability and pharmacokinetics; antitumor activity was a secondary objective.

48 Using genetic and pharmacologic approaches, antitumor activity was seen with Skp2 loss or inhibition

49 aximum-tolerated dose (MTD), and preliminary antitumor activity were evaluated.

50 rofiles, high target specificity, and robust antitumor activity were observed in these models after a

51 Signs of single-agent antitumor activity were observed: 1 unconfirmed partial

52 b provided clinically meaningful and durable antitumor activity with a manageable safety profile.

53 Ipilimumab and nivolumab demonstrated antitumor activity with acceptable toxicity in patients

54 checkpoint or CSF1R blockade caused additive antitumor activity with complete tumor regressions in so

55 s, cancer cell line cytotoxicity and in vivo antitumor activity, structure-activity relationships, me

56 iations between hypoxia, neoangiogenesis and antitumor activity.

57 wed no significant effect on B7H3 CAR T-cell antitumor activity.

58 equiring dose deescalation, with only modest antitumor activity.

59 ks multiple oncogenic pathways, resulting in antitumor activity.

60 t (TME) contains ROS, which suppress NK cell antitumor activity.

61 d selectivity properties, and potent in vivo antitumor activity.

62 ntadine demonstrated remarkable single-agent antitumor activity.

63 as a novel therapeutic strategy to stimulate antitumor activity.

64 , which correlated with the earlier observed antitumor activity.

65 nducing chemotherapy resulted in synergistic antitumor activity.

66 ns, as well as for its antiproliferative and antitumor activity.

67 l without affecting CD19-specific CAR T-cell antitumor activity.

68 Pembrolizumab demonstrated effective antitumor activity; clinically meaningful, durable respo

69 SR-717 displayed antitumor activity; promoted the activation of CD8(+) T,

70 amplify innate immune response and activate antitumor adaptive responses, our finding indicates that

71 odomain-selective BET inhibitors that act as antitumor agents and demonstrates that these molecules h

72 to the identification of a number of potent antitumor agents and the first structure-activity relati

73 .e., azidothymidine) can represent promising antitumor agents, although showing high toxicity when ad

74 e used in the synthesis of the highly potent antitumor agents, spliceostatins, and their derivatives.

75 s become plausible targets for the design of antitumor agents.

76 The antioxidant, antitumor and alpha-amylase inhibitory activities of exo

77 n transplant recipients designed to uncouple antitumor and anti-allograft immunity.

78 + DACHPt)-loaded micelles displayed superior antitumor and antimetastatic activities without impairin

79 Natural killer (NK) cells have potent antitumor and antimetastatic activity.

80 his study has identified novel mechanisms of antitumor and antimigration function of miR-299-3p throu

81 molecular analysis and development of novel antitumor and antiviral drugs.

82 ractions of PD-1 with its ligands, enhancing antitumor and clinical responses.

83 eceptor 7 and 8 (TLR7/8) agonist with potent antitumor and immunostimulatory activity.

84 , anti-inflammatory, anti-HIV, antidiabetic, antitumor, and antimicrobial.

85 oselective synthesis of the ribosome-binding antitumor antibiotic (-)-bactobolin A is reported.

86 r cells whose functional plasticity leads to antitumor as well as protumor function in different sett

87 We examined urine's possible antitumor capability in response to medium-level, loadin

88 T cells, p40-Td CAR T cells showed improved antitumor capacity in vitro, with increased granzyme B a

89 The vaccination induced antitumor CD8 T cell immune responses in 40% of patients

90 response by directly or indirectly expanding antitumor CD8 T cells.

91 M2 macrophages and increased infiltration of antitumor CD8+ effector and memory T-cells.

92 n summary, this study presents a synergistic antitumor combination of PDI and HDAC inhibitors and dem

93 ptomyces species harbor BGCs known to encode antitumor compounds.

94 models, host LGP2 was essential for optimal antitumor control by ionizing radiation (IR).

95 o phenylalanine (CD28-YMFM) promoted durable antitumor control.

96 D2-selective agents are valid candidates for antitumor drug design for pediatric malignancies driven

97 ovaquone (ATO) recently was repurposed as an antitumor drug.

98 fy H1.0 as a major mediator of Quisinostat's antitumor effect and suggest that sequential administrat

99 Therefore, the antitumor effect associated to SHH deprivation, usually

100 AT using (225)Ac-PSMA-I&T showed a promising antitumor effect in advanced metastatic castration-resis

101 high molecular weight poly I:C improved the antitumor effect of IR.

102 notherapy, with an unanticipated cooperative antitumor effect of LDH inhibition and IL-21.

103 These data suggest that the long-lasting antitumor effect of the prodrug is due to a combination

104 t PD-1(FSY) exhibited strikingly more potent antitumor effect over the noncovalent wild-type PD-1, at

105 er is capable of inducing tumor immunity, an antitumor effect that results from enhanced function of

106 Finally, the antitumor effect was even more prominent when combined w

107 Molecular analysis revealed that the antitumor effect was linked to the reduction in molecula

108 nt with an anti-PD-L1 mAb had no significant antitumor effect, indicating that early, self-activating

109 mune cells from trained mice are more potent antitumor effector cells when transferred into tumor-bea

110 of Ldha prevented development of cells with antitumor effector function, transient LDH inhibition en

111 ntricularly or intratumorally mediate potent antitumor effects against cerebral ATRT xenografts in mi

112 Moreover, the antitumor effects against U251 were significantly greate

113 mmunosuppressive responses could augment the antitumor effects and induce an abscopal response.

114 l leaky tumor vascular system may have large antitumor effects at the tumor vascular level, and their

115 he Phoneutria nigriventer spider venom (PnV) antitumor effects by our group has shown that the venom

116 HLA-restricted T cell responses can induce antitumor effects in cancer patients.

117 e (to induce mitotic arrest) had synergistic antitumor effects in vitro, with minimal effect on norma

118 proliferation, induced apoptosis, and showed antitumor effects in vivo.

119 cisplatin/Nutlin-3 combination and enhanced antitumor effects more than either agent alone.

120 The antitumor effects of calcineurin inhibitors are associat

121 S-mediated inflammation is essential for the antitumor effects of immune checkpoint blockade.

122 In this study, we assessed the antitumor effects of synthetic LXR agonist TO901317 in a

123 response is essential for the antiviral and antitumor effects of TLR activation, these findings are

124 own pleiotropic effects in vitro, including: antitumor effects through inhibition of lipogenesis; dec

125 ed stimuli can offer improved, site-specific antitumor effects, and can improve the efficacy of conve

126 Of these, copanlisib exerts the most potent antitumor effects, markedly inhibiting cell proliferatio

127 ulatory CARs in an effort to improve durable antitumor effects.

128 ring mice also showed strong immune-mediated antitumor effects.

129 terial l-Met-degrading enzymes exerts potent antitumor effects.

130 ggers lethal replication stress and profound antitumor effects.

131 and clinical samples; we therefore examined antitumor efficacy across a panel of five PI3K inhibitor

132 nucleotide-bearing nanoparticles facilitate antitumor efficacy after systemic intravenous (i.v.) adm

133 the hybrid PeptiCRAd significantly enhanced antitumor efficacy and induced TT-specific, CD40 ligand-

134 owed that ibrutinib could improve CAR T cell-antitumor efficacy and reduce cytokine release syndrome

135 In vivo, the Prot-FOLR1-TCB mediates antitumor efficacy comparable to the parental FOLR1-TCB

136 its dose escalation over Taxol(R), enhancing antitumor efficacy in breast, lung and ovarian cancers.

137 mall cell lung cancer (SCLC) cell lines, and antitumor efficacy in patient-derived xenograft (PDX) SC

138 The antitumor efficacy of (212)Pb-L2 supports the correspond

139 This study aimed to explore the antitumor efficacy of (67)Cu-CuSarTATE in a preclinical

140 CD40, CD70, and CD80/CD86, in expansion and antitumor efficacy of adoptively transferred in vitro-pr

141 e found that TLR/CD40-mediated expansion and antitumor efficacy of adoptively transferred tumor-speci

142 of combination therapy to further boost the antitumor efficacy of ICB.

143 events intestinal toxicity and maintains the antitumor efficacy of irinotecan.

144 gs have been limited until recently, and the antitumor efficacy of most cancer immunotherapies still

145 sed several murine cancer models to test the antitumor efficacy of undifferentiated monocytes loaded

146 Methods: The antitumor efficacy of various doses of (67)Cu-CuSarTATE

147 ide, and hydroxyl radicals, to afford superb antitumor efficacy on mouse models of breast and colon c

148 ignificantly enhances its immunogenicity and antitumor efficacy when administered after chemotherapy.

149 r monoclonal antibodies to increase ADCC and antitumor efficacy, have been initiated.

150 ectives were to assess safety, tolerability, antitumor efficacy, pharmacokinetics, and pharmacodynami

151 ved pharmacokinetic properties and excellent antitumor efficacy, with significantly reduced tumor gro

152 MYCi with anti-PD-1/PD-L1 therapy to enhance antitumor efficacy.

153 th a controlled loading that achieved better antitumor efficacy.

154 -cell function but significantly compromised antitumor function.

155 a Th1 cytokine response resulting in potent antitumor function.

156 1-mTORC1 in mediating CD8(+) trafficking and antitumor function.

157 r cells into the tumors is crucial for their antitumor function.

158 ent (TME) exhibit a spectrum of protumor and antitumor functions, yet it is unclear how the TME regul

159 on of extracellular adenosine to (a) unleash antitumor immune cells from inhibition by intracellular

160 lso protects cancerous tissues by inhibiting antitumor immune cells in hypoxic and extracellular aden

161 biomaterial-based vaccines that will afford antitumor immune protection at mucosal surfaces, despite

162 tion in the TME has been shown to dampen the antitumor immune response and is thought to be an import

163 icted to the gut, potentiated the RT-induced antitumor immune response and tumor growth inhibition.

164 rrent immunotherapies focus on modulating an antitumor immune response by directly or indirectly expa

165 tested whether the gut microbiota modulates antitumor immune response following RT distal to the gut

166 n immune cell recognition and can trigger an antitumor immune response in cancer.

167 ired immunity to pathogens to convert a weak antitumor immune response into a much stronger one.

168 support the CTLs, converting a weak primary antitumor immune response into a stronger secondary one.

169 thways, along with evidence of activation of antitumor immune response signatures.

170 of using therapeutic ultrasound to elicit an antitumor immune response with examples that reveal spec

171 actors, rather than induction of an adaptive antitumor immune response, as the main mechanism of acti

172 uprastat and anti-PD1 immunotherapy enhances antitumor immune response, mediated by a decrease of pro

173 sive, T cell-deficient cancers can launch an antitumor immune response.

174 mor tissues, thereby dampening the resulting antitumor immune response.

175 oated with anti-CD47 antibodies, achieved an antitumor immune response.

176 ts, and expresses Ags that induce a specific antitumor immune response.

177 ile inducing a progressive depression of the antitumor immune response.

178 ent by alleviating hypoxia and improving the antitumor immune response.

179 onse in melanoma cells serves to amplify the antitumor immune response.

180 first time that HDAC6i can both improve ICB antitumor immune responses and diminish the invasiveness

181 erred to as M2-polarized) generally suppress antitumor immune responses and enhance the metastatic pr

182 ugh STING signaling is sufficient to promote antitumor immune responses in the B16-F0 melanoma model.

183 f immuno-radiotherapy for generating optimal antitumor immune responses in the clinical setting.

184 f various cancers, primary tumors can escape antitumor immune responses of their host and eventually

185 way-dependent tumor growth and liberation of antitumor immune responses.

186 e impaired immunosurveillance and/or trigger antitumor immune responses.

187 inhibition of Tregs that otherwise suppress antitumor immune responses.

188 t a major barrier to the induction of robust antitumor immune responses.

189 ia cellular cross-talk, NK cells orchestrate antitumor immune responses.

190 Tumor-infiltrating CD8+ T cells mediate antitumor immune responses.

191 opportunity to prompt or rewire a proficient antitumor immune surveillance.

192 ules as a valuable template for boosting the antitumor immune system.

193 eveal an essential role of LGP2 in promoting antitumor immunity after radiotherapy and provide a new

194 on of host-microbe interactions that curtail antitumor immunity also present opportunities for interv

195 h helical bodipy show efficient PDT-mediated antitumor immunity amplification with an ultra-low dose

196 uture cases may help elucidate mechanisms of antitumor immunity and allograft tolerance, and inform u

197 vironment is a key determinant for effective antitumor immunity and immunotherapy.

198 une checkpoint blockade effectively restores antitumor immunity and results in a significant survival

199 s of PD-1, which suggests potential roles in antitumor immunity and the response to immunotherapy.

200 nisms of exosome-mediated resistance against antitumor immunity and we discuss how this resistance co

201 at block PD-1 or PD-L1 facilitate endogenous antitumor immunity and, because of their broad activity

202 Additional approaches to mobilize antitumor immunity are required to overcome primary and

203 and inhibit immune cell activity can enhance antitumor immunity by reshaping the tumor microenvironme

204 CD73-neutralization synergistically enhances antitumor immunity in CAF-rich tumors.

205 ours, have reported that the virus can drive antitumor immunity in certain models.

206 The role of active antitumor immunity in hormone receptor-positive (HR(+))

207 n's sole contributions to local and systemic antitumor immunity in patients.

208 antagonists are also accompanied by enhanced antitumor immunity in PD-L1-expressing triple-negative b

209 ablation of eosinophils severely compromises antitumor immunity in syngeneic and genetic models of co

210 n by reducing vascular density and improving antitumor immunity in the lungs.

211 pathogen-specific "bystander" CD8 T cells to antitumor immunity remains largely unknown.

212 value of ERK5-targeted therapies to restore antitumor immunity through the blockade of protumorigeni

213 mmunity to biological processes ranging from antitumor immunity to microbiome homeostasis.

214 ired organ allograft tolerance and unleashed antitumor immunity via epigenetic activation of effector

215 gram the tumor microenvironment and activate antitumor immunity while reducing the incidence of immun

216 these molecules and their ability to enhance antitumor immunity will be discussed.

217 SYNB1891 treatment results in efficacious antitumor immunity with the formation of immunological m

218 umors, induced tumor regression with durable antitumor immunity, and synergized with anti-PD-1 therap

219 ate that DNA damage in cancer cells triggers antitumor immunity, but its intrinsic regulatory mechani

220 receptor (CAR) T cells are potent drivers of antitumor immunity, but promoting durable CAR T cell res

221 f protumorigenic M2 macrophages and promotes antitumor immunity, highlighting an investigational ther

222 of natural killer (NK) cell-mediated innate antitumor immunity, leading to increased lung metastases

223 50, an allosteric inhibitor of SHP2, induces antitumor immunity, with effects equivalent to or greate

224 ion by gammadelta and Th17 cells potentiates antitumor immunity.

225 h immunotherapy, promoting radiation-induced antitumor immunity.

226 eased from the MN patch further augments the antitumor immunity.

227 ll cycle activity in cancer cells suppresses antitumor immunity.

228 velopment of metastasis and further enhanced antitumor immunity.

229 ecific T(mem) that are essential for durable antitumor immunity.

230 dence of a pDC subset in the TME that favors antitumor immunity.

231 important regulator of T cell metabolism and antitumor immunity.

232 ed lipid metabolism is essential to maintain antitumor immunity.

233 ines offer a promising approach for inducing antitumor immunity.

234 acquire a dysfunctional state, which limits antitumor immunity.

235 mplicated in potential reinvigoration of the antitumor immunity.

236 in 1 (PD-1; PDCD1), was performed to improve antitumor immunity.

237 gen expression, which could be used to study antitumor immunity.

238 repurposing copper chelators as enhancers of antitumor immunity.

239 mulation in the tumor, resulting in enhanced antitumor immunity.

240 ram, which had crippling effects on adaptive antitumor immunity.

241 lls, and ZMYND8 may be a possible target for antitumor immunotherapy.

242 es in effectively activating macrophages for antitumor immunotherapy.

243 vity by DMXAA in MCC cells reactivates their antitumor inflammatory cytokine/chemokine production.

244 olarize tumor-associated macrophages from an antitumor M1 phenotype to a tumorigenic M2 phenotype.

245 s CD8(+) T cells are required for protective antitumor memory in this setting.

246 reprogram the TME towards a more immunogenic antitumor milieu, characterized by an influx of >20-fold

247 tic clocks were decelerated in SZ related to antitumor natural killer and CD8T cells, which may help

248 Taking advantage of the C(2)-symmetry of the antitumor naturally occurring disorazole B(1) molecule,

249 Most antitumor neoantigen-reactive TILs were found in the dif

250 therapeutic modulation of the TME to enhance antitumor NK cell function.

251 tantly, it skewed the cytokine profiles into antitumor one in the tumor microenvironment (TME).

252 y regulated target genes, and the associated antitumor phenotype.

253 scarcely available and urgently desired for antitumor photodynamic therapy (PDT).

254 s compound shows higher in vitro and in vivo antitumor potency than the BET inhibitor (+)-JQ1 and the

255 The clinical development harnessing the antitumor potential of recombinant IgE antibodies in can

256 t the lead candidate 11 exhibits significant antitumor properties as a single agent in these tumor mo

257 ts due to their molecular complexity, potent antitumor properties, and natural scarcity.

258 de (NO), whereas macrophages largely express antitumor properties.

259 likely contributing at least in part, to its antitumor properties.

260 e are distinct from TIL subsets enriched for antitumor reactivity.

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

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

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

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

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

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

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

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

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

270 nable longer persistence and thereby improve antitumor response.

271 ary treatment experiments showed a favorable antitumor response.

272 tinct functional activities that impair host antitumor response.

273 S specifications that may elicit the desired antitumor response.

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

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

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

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

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

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

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

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

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

283 12 (IL-12), IL-15, and IL-18, exhibit potent antitumor responses, and safely induce complete remissio

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

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

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

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

288 nd astrocytes, highlighting the protumor and antitumor roles of astrocytes in glioblastoma developmen

289 his death signaling could be activated as an antitumor strategy.

290 ical players in a broad range of infections, antitumor surveillance, autoimmune diseases, and tissue

291 tudies identified ATF3 as the driver of this antitumor synergy.

292 TIGIT inhibitory checkpoints in boosting the antitumor T cell activity of ICB nonresponders.

293 Ab-dependent manner and results in systemic antitumor T cell effects that are enhanced by anti-PD-1

294 Therefore, the magnitude of the antitumor T cell response and the corresponding downstre

295 We conclude IT CMP-001 induces a robust antitumor T cell response in an anti-Qbeta Ab-dependent

296 CD2 downregulation may attenuate antitumor T cell responses, with implications for checkp

297 ine platform targeting CD169(+) DCs to drive antitumor T cell responses.

298 1 (PD1) has emerged as a major inhibitor of antitumor T cells, and anti-PD1 therapies have demonstra

299 itor leads for the human AAA+ ATPase p97, an antitumor target.

300 describe the potential that combinations of antitumor targeted agents may offer in overcoming these