ライフサイエンスコーパス: anti-tumor

1 oversial debate whether MSCs exert a pro- or anti-tumor action, mathematical models such as this one

2 one modification profiles, and with specific anti-tumor activities.

3 ive anti-inflammatory, immunosuppressive and anti-tumor activities.

4 orated in DOPC nanoliposomes, we demonstrate anti-tumor activities.

5 Anti-tumor activity against breast cancer cell lines (MC

6 ST738), EC2629 showed significantly greater anti-tumor activity compared to their corresponding stan

7 A better understanding of how to uncouple anti-tumor activity from loss of self-tolerance is neces

8 TRuC-T cells demonstrate potent anti-tumor activity in both liquid and solid tumor xenog

9 al studies have demonstrated that EPA exerts anti-tumor activity in breast cancer.

10 nts targeting Her2 have not yet demonstrated anti-tumor activity in MIBC.

11 nd cancer-associated fibroblasts, had potent anti-tumor activity in primary short-term cultures and p

12 Selective anti-tumor activity in the absence of toxicity provides

13 + BET bromodomain inhibition led to additive anti-tumor activity in the most resistant cell lines.

14 cells/tissues, leading to a higher level of anti-tumor activity in vitro and in vivo.

15 On the basis of the potent preclinical anti-tumor activity of agonist anti-GITR antibodies, rep

16 a synthetic mimics significantly enhance the anti-tumor activity of all the above-mentioned anti-canc

17 In prostate cancer, specifically, the anti-tumor activity of BET bromodomain inhibition has be

18 Moreover, the anti-tumor activity of BET bromodomain inhibition in AR-

19 translational mechanisms, contributes to the anti-tumor activity of BET bromodomain inhibitors.

20 This regimen empowered the anti-tumor activity of CD8(+) T cells and possessed ther

21 microenvironment suggested that the in vivo anti-tumor activity of HDAC6i is mediated by its effect

22 lts demonstrated for the first time that the anti-tumor activity of megestrol acetate can be enhanced

23 cancer immune-checkpoint, and increases the anti-tumor activity of NK cell infusions.

24 was used to assess the BBB permeability and anti-tumor activity of the DOX-EDT-IONPs and DOX treatme

25 NKTR-214 shows superior anti-tumor activity over native IL-2 and systemically ex

26 ll depletion, which may underlie the lack of anti-tumor activity previously observed in pre-clinical

27 a novel mechanism(s) by which HNK exerts its anti-tumor activity through the inhibition of c-Met-Ras-

28 cells and offer a pathway to enhancement of anti-tumor activity through their manipulation.

29 n the TME to realize synergistic or additive anti-tumor activity.

30 cell metabolic activity and thereby modulate anti-tumor activity.

31 synergizes with carfilzomib and shows potent anti-tumor activity.

32 ion contributes to BET bromodomain inhibitor anti-tumor activity.

33 proteins, suggesting that TIMPs may possess anti-tumor activity.

34 elds highly aggressive tumors with decreased anti-tumor activity.

35 termine if molecular context associates with anti-tumor activity.

36 other mechanisms contribute to perifosine's anti-tumor activity.

37 ivo models have been used to investigate the anti-tumor and anti-angiogenic effect of SFN.

38 ation of netamine C, a member of a family of anti-tumor and anti-malarial natural products.

39 approved oral antibiotic, showed significant anti-tumor and anti-metastatic effects in mouse models o

40 including anti-diabetic, anti-inflammatory, anti-tumor, and anti-atherosclerotic effects.

41 ns, we consider the adaptive immune priming, anti-tumor, and autoimmune functions of IFNs.

42 ed that SPG-56 may have potential as a novel anti-tumor candidate for breast cancer.

43 We established the potent anti-tumor capabilities of our lead candidate MTP(10)-HD

44 tion has been transformative in promotion of anti-tumor CD8 T-cell responses in the treatment of cert

45 An improved understanding of the anti-tumor CD8(+) T cell response after checkpoint block

46 ISV induced anti-tumor CD8(+) T cell responses and systemic (abscopa

47 ty over native IL-2 and systemically expands anti-tumor CD8(+) T cells while inducing Treg depletion

48 hage iron deposits was associated with lower anti-tumor chelation therapy response.

49 a general pattern of prolonged increases in anti-tumor cytokines and relatively lower levels of pro-

50 oxically characterized by reduced markers of anti-tumor cytolytic activity and lower major histocompa

51 ogen atom transfer (HAT) pathways between an anti-tumor drug vitamin-K3 (MQ) and a nucleobase adenine

52 to paclitaxel, a microtubule stabilizer and anti-tumor drug.

53 Anti-tumor drugs of the di-2-pyridylketone thiosemicarba

54 STAT3 inhibitors significantly increases the anti-tumor effect compared to single-agent treatments.

55 rapeutic compounds) strongly potentiates the anti-tumor effect due to repression of DNA repair machin

56 se, sequential regimen that imparts a robust anti-tumor effect for non-small-cell lung cancer (NSCLC)

57 f human melanoma cells in vitro and a potent anti-tumor effect in vivo.

58 The anti-tumor effect induced by anti-MerTK treatment was lo

59 nce and immuno-response, we investigated the anti-tumor effect of a glutamine analog (6-diazo-5-oxo-L

60 Moreover, the anti-tumor effect of beta-glucan-induced trained granulo

61 The anti-tumor effect of beta-glucan-induced trained immunit

62 RANKL inhibition increases the anti-tumor effect of immunotherapies in breast cancer th

63 extracellular fluid translated into a strong anti-tumor effect prolonging survival of mice bearing GD

64 sults demonstrated enhanced cytotoxicity and anti-tumor effect with palbociclib plus taxanes at clini

65 s impairs TCR-driven activation, and thereby anti-tumor effector responses, tantamount to taking the

66 ith siRNA-loaded NPs may exhibit synergistic anti- tumor effects.

67 se-5 (PDE5) inhibitors are suggested to have anti-tumor effects and to inhibit surgery-induced immuno

68 BKM120 or LEE011 yielded more than additive anti-tumor effects both in vitro and in vivo in a melano

69 ound that gammaSI enhanced miR-34a-dependent anti-tumor effects by activating the extrinsic apoptotic

70 otent, reversible type I PRMT inhibitor with anti-tumor effects in human cancer models.

71 -molecule FTO inhibitors that exhibit strong anti-tumor effects in multiple types of cancers.

72 -1 pathway has consistently shown remarkable anti-tumor effects in patients with advanced cancers and

73 demethylase FTO that demonstrate significant anti-tumor effects in various models of acute myeloid le

74 to cancer initiation, our work demonstrates anti-tumor effects of 2HG in inhibiting proliferation/su

75 rationalize conflicting reports of pro- and anti-tumor effects of antioxidant treatment.

76 re, we investigated the in vitro and in vivo anti-tumor effects of the FDA-approved ETAR antagonist,

77 The anti-tumor effects of TMZ and DOX were mediated in part

78 We report potent anti-tumor effects of unacylated ghrelin, dependent on c

79 RAS signaling, thereby exerting synergistic anti-tumor effects on ovarian cancers with PTEN deficien

80 These anti-tumor effects result from trained immunity-induced

81 ession, however, has differing pro-tumor vs. anti-tumor effects, depending on the cancer types.

82 ex, with studies demonstrating both pro- and anti-tumor effects.

83 fications by biotin, which may affect RA16's anti-tumor effects.

84 ent in the microenvironment but have unclear anti-tumor effects.

85 yte infiltration of tumors and showed strong anti-tumor effects.

86 ta have been reported to have either pro- or anti-tumor effects.

87 Enhanced anti-tumor efficacy and great anti-metastatic effects we

88 r affinity CAR T cells demonstrated superior anti-tumor efficacy and safety compared to their nanomol

89 tion, there was a significant enhancement of anti-tumor efficacy and safety with PTX-nanotextiles.

90 ction and tumor progression but also greater anti-tumor efficacy and survival after checkpoint blocka

91 nmasked at the tumor site and have increased anti-tumor efficacy compared with unmasked antibodies in

92 ses anti-tumor immunity in vivo, and reduces anti-tumor efficacy in an immune-competent mouse model.

93 lacked endogenous TCR expression and showed anti-tumor efficacy in vitro and in vivo.

94 redesign the molecule in such a way that its anti-tumor efficacy is not compromised, but toxic effect

95 lation on mutant tumor cells, which improves anti-tumor efficacy of CD8(+) T cells.

96 a result, antioxidant treatment enhanced the anti-tumor efficacy of chronically stimulated T cells.

97 tumor growing and no negative effect on the anti-tumor efficacy of the platinum-containing nanodrug,

98 The anti-tumor efficacy of the PTX prodrug was greatly influ

99 hibitor AZD1208 shows significantly enhanced anti-tumor efficacy relative to single agents.

100 In vivo anti-tumor efficacy revealed that certain lipid nanostru

101 promising strategy for achieving synergistic anti-tumor efficacy with improved safety profiles.

102 ncer and melanoma mouse models show enhanced anti-tumor efficacy without any toxicity.

103 osed drugs or phytochemicals for an enhanced anti-tumor efficacy, along with the mechanisms involved

104 ed systemic cytokine expression and enhanced anti-tumor efficacy.

105 gs could be tested for target engagement and anti-tumor efficacy.

106 henotype switching of TAMs from pro- towards anti-tumor expression in vitro.

107 dentify a novel and therapeutically relevant anti-tumor facet of trained immunity involving appropria

108 APOE4 mice exhibited enhanced anti-tumor immune activation relative to APOE2 mice, and

109 In panCancer analyses anti-tumor immune activity was increased in EP300 mutate

110 misexpressed in tumors, where it suppresses anti-tumor immune activity.

111 ase cancer-suppressive cytokines and enhance anti-tumor immune cell populations.

112 ines that can directly and indirectly affect anti-tumor immune function and cancer cell growth.

113 to promote tumor growth via suppressing the anti-tumor immune response and that caveolin-2 could be

114 -FLuc and GL261-Luc2 murine models elicit an anti-tumor immune response by increasing pro-inflammator

115 cent studies have provided evidence that the anti-tumor immune response is reduced in both conditions

116 Antibody blockade of PD-L1 can activate an anti-tumor immune response leading to durable remissions

117 cent evidence also suggests that BAs promote anti-tumor immune response through activation and recrui

118 oter of glycolysis, which negatively affects anti-tumor immune response, we analyzed the association

119 age and systemic metabolic state affect the anti-tumor immune response, with an emphasis on CD8(+) T

120 p between the host microbiota and cancer and anti-tumor immune response, with implications for cancer

121 ytotoxic T cells, reflecting a vigorous host anti-tumor immune response.

122 across the BBB and activation of local brain anti-tumor immune response.

123 the impact of the tissue environment on the anti-tumor immune response.

124 ent, offers a unique approach to enhance the anti-tumor immune response.

125 fect of blocking apoptotic cell clearance on anti-tumor immune response.

126 Protective anti-tumor immune responses are mediated by effector mol

127 These agents may therefore modulate anti-tumor immune responses as a therapeutic modality fo

128 -intrinsic alterations that blunt productive anti-tumor immune responses by directly or indirectly ex

129 se immunosuppressive pathways may reactivate anti-tumor immune responses in ESCC.

130 enriched with CSCs and its ablation induces anti-tumor immune responses in mice.

131 Cancer immunotherapies enhance anti-tumor immune responses using checkpoint inhibitors,

132 ular evidence of improved, antigen-specific, anti-tumor immune responses which also depend upon T cel

133 90 inhibition can potentiate T-cell-mediated anti-tumor immune responses, and rationale to explore th

134 cancer neoantigens paradoxically attenuates anti-tumor immune responses, suggesting a need to quanti

135 se as a tool to enhance the understanding of anti-tumor immune responses.

136 onal caloric restriction and allows improved anti-tumor immune responses.

137 tes CD8(+) T-cell cross-priming and enhances anti-tumor immune responses.

138 CD8 T cells play essential roles in anti-tumor immune responses.

139 bolic checkpoint molecule - ARG1, mitigating anti-tumor immune responses.

140 ne checkpoint mediator" that interferes with anti-tumor immune responses.

141 s associated with the activation of adaptive anti-tumor immune responses.

142 some fs-indels escape degradation and elicit anti-tumor immune responses.

143 gs) play a pivotal role in the inhibition of anti-tumor immune responses.

144 cells within the lymph node in regulation of anti-tumor immune responses.

145 ns peripheral T cell quiescence and inhibits anti-tumor immune responses.

146 om annotated non-coding regions could elicit anti-tumor immune responses.

147 d modulating macrophages in order to promote anti-tumor immune responses.IMPORTANCE Cytomegalovirus (

148 enetic modulators DNMTi and HDAC6i increases anti-tumor immune signaling from cancer cells and has be

149 microenvironment, while enhancing effective anti-tumor immune-response.

150 the complexity of functions for IFN-gamma in anti-tumor immunity and demonstrate that intratumor hete

151 rtance of molecular diversity as a driver of anti-tumor immunity and discuss how these factors can be

152 stress responses to reinvigorate endogenous anti-tumor immunity and enhance the efficacy of various

153 in combination with FAK, can drive enhanced anti-tumor immunity and even complete regression of muri

154 correlate with the development of productive anti-tumor immunity and greater efficacy of PD1 immunoth

155 ustrate that the systemic context can impact anti-tumor immunity and immunotherapy responsiveness.

156 Tim-3(+)CD8(+) T cells can promote effective anti-tumor immunity and implicate PTPN2 in immune cells

157 increased CD226 surface expression, enhanced anti-tumor immunity and improved efficacy of immune chec

158 ification of parameters underlying effective anti-tumor immunity and is available to the research com

159 d reprogram them to a phenotype that induces anti-tumor immunity and promotes tumor regression.

160 stress increases innate sensing and adaptive anti-tumor immunity and provide strong rationales for co

161 ium, enriched in Rnf5(-/-) mice, establishes anti-tumor immunity and restricts melanoma growth in ger

162 using of Rnf5(-/-) and WT mice abolishes the anti-tumor immunity and tumor inhibition phenotype, wher

163 nisms by which PD-1/PD-L1 inhibition elicits anti-tumor immunity are not fully understood.

164 ndritic cells (cDC1s) control anti-viral and anti-tumor immunity by inducing antigen-specific cytotox

165 s, and may lead to a new strategy to restore anti-tumor immunity by inhibiting pathways of force-gene

166 T(reg) cells subvert beneficial anti-tumor immunity by modulating inhibitory receptor ex

167 Here, we investigated whether anti-tumor immunity can be enhanced through induction of

168 vivo, restoration of TTP expression enhances anti-tumor immunity dependent on degradation of PD-L1 mR

169 temness and invasion programs while inducing anti-tumor immunity genes and may therefore restrain mal

170 Breakthroughs in anti-tumor immunity have led to unprecedented advances i

171 0 gene expression was associated with higher anti-tumor immunity in most solid malignancies.

172 tilization in the tumor microenvironment and anti-tumor immunity in obese mice.

173 cytes, monocytes, and platelets and promotes anti-tumor immunity in pre-clinical models.

174 anisms may lead to novel therapies enhancing anti-tumor immunity in the context of aging or metabolic

175 blished tumors, this combination compromised anti-tumor immunity in the low tumor burden (LTB) state

176 or antibody blockade of Siglec-15 amplifies anti-tumor immunity in the TME and inhibits tumor growth

177 T cell activation, antibody production, and anti-tumor immunity in vivo, and m(6)A modification abro

178 tes cocultured T cells in vitro, compromises anti-tumor immunity in vivo, and reduces anti-tumor effi

179 Anti-tumor immunity is driven by self versus non-self di

180 the tumor microenvironment (TME) and impact anti-tumor immunity is not understood.

181 Understanding the mechanisms underlying anti-tumor immunity is pivotal for improving immune-base

182 that inhibit T-cell activation and influence anti-tumor immunity is unclear.

183 ss inflammation on the one hand, yet promote anti-tumor immunity on the other hand.

184 s-talk with dendritic cells (DCs) to support anti-tumor immunity remains unclear.

185 ade of MerTK-mediated phagocytosis mobilizes anti-tumor immunity through a mechanism that involves th

186 gation of additional therapies that modulate anti-tumor immunity through effects on T cells, myeloid

187 with altered gut microbiota composition and anti-tumor immunity to control melanoma growth.

188 liver X receptors, previously shown to boost anti-tumor immunity(4), exhibited therapeutic efficacy i

189 Steroidogenic T cells dysregulate anti-tumor immunity, and inhibition of the steroidogenes

190 inib and immune checkpoint blockade enhances anti-tumor immunity, and overcomes the resistance.

191 yte-derived cells, enhances T cell-dependent anti-tumor immunity, and synergizes with immune checkpoi

192 wart their pro-cancer activities and unleash anti-tumor immunity, but efforts to accomplish this are

193 ic blockade of PD-1 enhances T cell-mediated anti-tumor immunity, but many patients do not respond an

194 g host defense against microbial infections, anti-tumor immunity, cellular senescence, autophagy, and

195 altered intestinal microbiota contributes to anti-tumor immunity, limiting tumor expansion.

196 creases tumor immunogenicity and potentiates anti-tumor immunity, which has implications for cancer i

197 and the PD-L1 checkpoint inhibitor augments anti-tumor immunity.

198 tumor cells is essential for dMMR-triggered anti-tumor immunity.

199 n the breast TME and unleashes host adaptive anti-tumor immunity.

200 potent immunosuppressive functions hindering anti-tumor immunity.

201 linical success by blocking amplification of anti-tumor immunity.

202 able better strategies to restore protective anti-tumor immunity.

203 melanoma progression was mediated by altered anti-tumor immunity.

204 ides substantial room for engineering better anti-tumor immunity.

205 ng new insights into the regulation of human anti-tumor immunity.

206 responses through DCs, thereby strengthening anti-tumor immunity.

207 austion of CD8(+) TILs that limits effective anti-tumor immunity.

208 overlapping but non-redundant regulation of anti-tumor immunity.

209 g between cancer-associated inflammation and anti-tumor immunity.

210 an important role for the gut microbiome in anti-tumor immunity.

211 t to implanted tumors and displayed enhanced anti-tumor immunity.

212 ly replicates in cancer cells while inducing anti-tumor immunity.

213 -activating TLR4 agonist capable of inducing anti-tumor immunity.

214 (Th1) immune responses that are required for anti-tumor immunity.

215 ance promote T cell self-renewal and enhance anti-tumor immunity.

216 iggers Treg instability locally and restores anti-tumor immunity.

217 a pathophysiological context: suppression of anti-tumor immunity.

218 ntion of autoimmunity and the suppression of anti-tumor immunity.

219 r-infiltrating T cells results in diminished anti-tumor immunity.

220 Regulatory T cells (Tregs) are a barrier to anti-tumor immunity.

221 and are important targets of T cell-mediated anti-tumor immunity.

222 oidogenesis pathway is sufficient to restore anti-tumor immunity.

223 on CD8(+) T cells, which are key players in anti-tumor immunity.

224 effects in allergic airway inflammation and anti-tumor immunity.

225 vo steroidogenesis in T lymphocytes to evade anti-tumor immunity.

226 d CCL5 repression is critical for modulating anti-tumor immunity.

227 amming by tumor cells in obese mice improves anti-tumor immunity.

228 xpression, that is well known for triggering anti-tumor immunological response.

229 ll de novo steroidogenesis as a mechanism of anti-tumor immunosuppression and a potential druggable t

230 EPHA2-TGFbeta-PTGS2 pathway inhibitors with anti-tumor immunotherapy, and may change the treatment o

231 molecular characterization and incidence of anti-tumor lymphocytes present in patients with cancer.

232 The selective in vitro anti-tumor mechanisms of cold atmospheric plasma (CAP) a

233 Anti-tumor necrosis factor (anti-TNF) therapies are the

234 Anti-tumor necrosis factor (anti-TNF) therapy resistance

235 s fit in the 2 years before initiation of an anti-tumor necrosis factor (TNF) or immunomodulator ther

236 the stability of AVX-470, a bovine colostral anti-tumor necrosis factor (TNF) polyclonal antibody use

237 Conversely, anti-Tumor Necrosis Factor (TNF) therapies improve depre

238 laxis, comprising thiopurine in 69 (20%), or anti-tumor necrosis factor (TNF) therapy in 93 (27%).

239 icantly reduced after remission induction by anti-tumor necrosis factor (TNF) therapy.

240 of different trough drug concentrations for anti-tumor necrosis factor agents and thiopurines to inf

241 e newer biologics (e.g. vedolizumab) and the anti-tumor necrosis factor agents.

242 >10 mg/day, thiopurines, methotrexate); (2) anti-tumor necrosis factor agents; (3) combination thera

243 world effectiveness of vedolizumab (VDZ) and anti-tumor necrosis factor alpha (anti-TNFalpha) in UC a

244 nce for the long-term efficacy and safety of anti-tumor necrosis factor alpha agents (anti-TNF) in tr

245 We examined the outcome of anti-tumor necrosis factor and anti-interleukin-12/inter

246 sease and in patients subsequently requiring anti-tumor necrosis factor rescue therapy.

247 nd was the strongest in those initiated with anti-tumor necrosis factor therapy (beta = 0.79; 95% CI,

248 fractivity of patients with heart failure to anti-tumor necrosis factor therapy and cardiac toxicity

249 In adults, anti-tumor necrosis factor-alpha (TNF-alpha) therapy is

250 ion to immunomodulators (ie, thiopurines) or anti-tumor necrosis factor-alpha (TNFalpha) therapy.

251 er biopsy led to the targeted treatment with anti-tumor necrosis factor-alpha, which was highly effec

252 In adults, anti-tumor-necrosis-factor (TNF)-alpha therapy is associ

253 moting effect and reprogramming them into an anti-tumor phenotype is a potential therapeutic approach

254 iesis and neutrophil reprogramming toward an anti-tumor phenotype; this process required type I inter

255 se model allowing simultaneous monitoring of anti-tumor potency and systemic off-tumor toxicity, micr

256 tural killer T (NKT) cells have shown potent anti-tumor properties in murine tumor models and have be

257 ding Sudemycins and Spliceostatin A, display anti-tumor properties.

258 romote trained immunity and elicit a durable anti-tumor response either as a monotherapy or in combin

259 However, ICT fails to elicit an anti-tumor response in the bone CRPC model despite an in

260 cell activation of B cells to facilitate the anti-tumor response in these models.

261 we show that tumor-resection invigorates an anti-tumor response via increasing T cells, activated mi

262 The anti-PD-1-induced anti-tumor response was facilitated by CXCL9 production

263 We identified a rapid and potent anti-tumor response, with 8 of 27 patients experiencing

264 tic lethality between MK2 and p53, enhancing anti-tumor responses alone and in combination with cispl

265 demonstrate that TLR7/8 agonist R848 induces anti-tumor responses and attenuates cachexia in murine m

266 deletion in CD8(+) T cells enhanced Tim-3(+) anti-tumor responses and improved tumor control.

267 ssary and sufficient for eosinophil-mediated anti-tumor responses and that this mechanism contributed

268 nd the PD-1 ligand (PD-L1) exhibits superior anti-tumor responses compared with single-agent therapy.

269 (CAR) T-cell therapy has produced remarkable anti-tumor responses in patients with B-cell malignancie

270 Therapies that boost the anti-tumor responses of cytotoxic T lymphocytes (CTLs) h

271 death 1 (PD-1) may enhance the durability of anti-tumor responses that are induced by the combined in

272 condary objectives were to assess safety and anti-tumor responses, respectively, with immune response

273 LCs) that defend against viruses and mediate anti-tumor responses, yet mechanisms controlling their d

274 PD-1 ligands and preventing T cell-mediated anti-tumor responses.

275 chanism by which inhibition of DPP4 improves anti-tumor responses.

276 switching FGFR4's role from pro-oncogenic to anti-tumor signaling.

277 holesterol-lowering statins elicits superior anti-tumor synergy selectively in TNBC.

278 ate (CL) nanoparticles to facilitate priming anti- tumor T cells by tumor lysate-loaded DC vaccine.

279 nflammatory tumor microenvironment and boost anti-tumor T cell activity.

280 anti-4-1BB therapy associated with enhanced anti-tumor T cell immunity.

281 id cell (TIM) subsets that likely compromise anti-tumor T cell immunity.

282 ss-priming DCs is achievable and critical to anti-tumor T cell responses and PD1-blockade efficacy.

283 blockade can efficiently promote endogenous anti-tumor T cell responses(1-11).

284 ries on regulation of inflammation center on anti-tumor T cell responses.

285 bition of p38 improved the efficacy of mouse anti-tumor T cells and enhanced the functionalities of h

286 the proliferation, homing and persistence of anti-tumor T cells compared to ACT with IL-2, resulting

287 teristics defining therapeutically effective anti-tumor T cells have not been comprehensively elucida

288 rives generation of neoepitopes, which prime anti-tumor T cells.

289 neate four phenotypic qualities of effective anti-tumor T cells: cell expansion, differentiation, oxi

290 en investigated as adjuvants to conventional anti-tumor therapeutics, offering a safe and economic st

291 Telomerase is an attractive target for anti-tumor therapy as it is almost universally expressed

292 f-concept of a new algorithm of personalized anti-tumor therapy based on highly innovative APDC bioma

293 ines increases their immunogenicity to drive anti-tumor therapy in combination with immune checkpoint

294 targetable to induce lethal mitophagy as an anti-tumor therapy.

295 lead to dose reduction or even cessation of anti-tumor therapy.

296 nder intensive investigation as a target for anti-tumor therapy.

297 ional nanomedicines hold great potential for anti-tumor therapy.

298 ed CAP treatment is a potential non-invasive anti-tumor tool, which may have wide application for tum

299 consequently, STING-dependent expression of anti-tumor type I interferon.

300 Finally, in vivo anti-tumor xenograft studies demonstrated high anti-tumo