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1 nhibits MEK1/2 phosphorylation, and exhibits anti-tumor activities across multiple models carrying KR
2 how that apoptosis plays a key role in their anti-tumor activities in colon cancer cells and xenograf
3  which plays a mechanistic role in mediating anti-tumor activities of HER2-directed therapies.
4     Our results indicate that harnessing the anti-tumor activities of miR-182 via safe and robust del
5 proaches discovered recently can augment the anti-tumor activities of TNFR antibodies by enhancing th
6 dney tumor cell lines, with >250-fold higher anti-tumor activities than observed with the natural pro
7 ive anti-inflammatory, immunosuppressive and anti-tumor activities.
8 orated in DOPC nanoliposomes, we demonstrate anti-tumor activities.
9 cargos to immune recipient cells, inhibiting anti-tumor activities.
10 a topoisomerase I (TOP1) inhibitor, exhibits anti-tumor activity against a wide range of tumors.
11 nces oral absorption of DIM-14 and increased anti-tumor activity against lung tumor models.
12 of PA-L1-I207R and PA-U2-R200A showed potent anti-tumor activity and low toxicity, exceeding the perf
13                                              Anti-tumor activity and selectivity of Dp44mT in Pgp-exp
14 ase inhibitors is insufficient for effective anti-tumor activity because the reactivation of the ErbB
15    A better understanding of how to uncouple anti-tumor activity from loss of self-tolerance is neces
16  dose-dependent in vivo CARM1 inhibition and anti-tumor activity in an MM xenograft model.
17       A p53 rescue motif peptide exhibits an anti-tumor activity in cancer cell lines expressing wild
18             Consequently, Dp44mT has greater anti-tumor activity in drug-resistant relative to non-Pg
19 olecule inhibitors against EZH2 demonstrated anti-tumor activity in EZH2-mutated lymphomas and entere
20                          R-2HG also displays anti-tumor activity in glioma.
21 nts targeting Her2 have not yet demonstrated anti-tumor activity in MIBC.
22              To gain insight into perifosine anti-tumor activity in neuroblastoma we have studied cha
23 inds a unique CD38 epitope and showed strong anti-tumor activity in preclinical models.
24  available Notch-blocking agents are showing anti-tumor activity in preclinical studies, they are not
25  cells/tissues, leading to a higher level of anti-tumor activity in vitro and in vivo.
26 lly stable in liver microsomes and displayed anti-tumor activity in xenograft mouse cancer models.
27 a synthetic mimics significantly enhance the anti-tumor activity of all the above-mentioned anti-canc
28 lts demonstrated for the first time that the anti-tumor activity of megestrol acetate can be enhanced
29 ion and support that phenformin improves the anti-tumor activity of PD-1 blockade immunotherapy in me
30      Here, PHY906 is reported to enhance the anti-tumor activity of Sorafenib in nude mice bearing He
31 ge could counteract PHY906 to potentiate the anti-tumor activity of Sorafenib.
32 sing and novel approach for potentiating the anti-tumor activity of therapeutic mAb against EGFR and
33                                          The anti-tumor activity of TIR-199 was confirmed in hollow f
34          Long-term persistence and sustained anti-tumor activity of transferred CTL, as well as respo
35 r, the biparatopic ADC demonstrates superior anti-tumor activity over ado-trastuzumab emtansine (T-DM
36 ll depletion, which may underlie the lack of anti-tumor activity previously observed in pre-clinical
37  establish DMF as an NFkappaB inhibitor with anti-tumor activity that may add therapeutic value in th
38 -resistant metastatic melanoma patients show anti-tumor activity through B-cell depletion by anti-CD2
39 a novel mechanism(s) by which HNK exerts its anti-tumor activity through the inhibition of c-Met-Ras-
40                                              Anti-tumor activity was carried out in H1650 lung tumor
41  contrast, the anti-PD-L1 Abs show augmented anti-tumor activity when activating FcgammaR binding is
42  (HIF2A) is of central importance to miR-182 anti-tumor activity, as it results in enhanced therapy s
43 ble tool to simultaneously evaluate the drug anti-tumor activity, hepatotoxicity and pharmacokinetics
44 and tumor cell apoptosis and showed superior anti-tumor activity.
45 ibodies to OX40 and other TNFR with improved anti-tumor activity.
46  FcgammaR-binding capacity compromises their anti-tumor activity.
47 RF7/IFNbeta pathway was required for optimal anti-tumor activity.
48 idely used anti-diabetic drug with potential anti-tumor activity.
49  other mechanisms contribute to perifosine's anti-tumor activity.
50 al medicine and has been observed to contain anti-tumor activity.
51 is allowed the viral vectors to raise robust anti-tumor adaptive immune responses and sensitized esta
52 ta suggest that a viable strategy to improve anti-tumor adoptive cell therapy may be to engineer tumo
53 to DOX, lysosomal sequestration of the novel anti-tumor agent and P-glycoprotein (Pgp) substrate, di-
54         Herein, we investigate how the novel anti-tumor agent di-2-pyridylketone 4,4-dimethyl-3-thios
55 OA-inactivating group, making NMI a valuable anti-tumor agent.
56                            Several important anti-tumor agents form DNA interstrand crosslinks (ICLs)
57                              Moreover, novel anti-tumor agents of the di-2-pyridylketone class of thi
58 ivo models have been used to investigate the anti-tumor and anti-angiogenic effect of SFN.
59 3100 (IR780-AMD-Lip-NLCs) exhibited enhanced anti-tumor and anti-metastasis effects.
60 gamma) is a pleiotropic cytokine that exerts anti-tumor and anti-osteoclastogenic effects.
61 cinated animals displayed reduced protective anti-tumor and viral immunity.
62 hFcgammaRIIIA are now in clinical use, ideal anti-tumor antibodies must be optimized for both cytotox
63                  Thus, while next-generation anti-tumor antibodies with enhanced binding to only hFcg
64             We find that a combination of an anti-tumor antigen antibody and an untargeted IL-2 fusio
65  developed an ICAM-1 specific CAR with broad anti-tumor applicability that utilized a reduced affinit
66 e existence of a specialized TAN subset with anti-tumor capabilities in human cancer.
67 tion has been transformative in promotion of anti-tumor CD8 T-cell responses in the treatment of cert
68 IIA engagement on DCs to stimulate long-term anti-tumor cellular immunity.
69 hage iron deposits was associated with lower anti-tumor chelation therapy response.
70 lenged several years ago by the isolation of anti-tumor CTL that recognized spliced peptides, i.e. pe
71  immunotoxin (YP218 Fv-PE38) exhibits potent anti-tumor cytotoxicity towards primary mesothelioma cel
72 een the oncoprotein SRSF1 and members of the anti-tumor drug target SF3 complex.
73 t in vitro based in vivo prediction of novel anti-tumor drugs.
74 aintain genome stability and are targets for anti-tumor drugs.
75 ssays showed that Alox5 exhibited a moderate anti-tumor effect both in vitro and in vivo.
76 that DOX-HK-MPEG-PCL micelles improved Dox's anti-tumor effect by enhancing tumor cell apoptosis, sup
77 se, sequential regimen that imparts a robust anti-tumor effect for non-small-cell lung cancer (NSCLC)
78 myrcene- induced a statistically significant anti-tumor effect in mice but not alpha-pinene, myrcene
79 nce and immuno-response, we investigated the anti-tumor effect of a glutamine analog (6-diazo-5-oxo-L
80 ified two bacterial species potentiating the anti-tumor effect of cyclophosphamide that are kept in c
81  the critical role of FasL regulation in the anti-tumor effect of HDACIs.
82  uncovering a novel mechanism underlying the anti-tumor effect of HDACIs.
83           In this study, we investigated the anti-tumor effect of MLN4924 in human clear cell renal c
84 extracellular fluid translated into a strong anti-tumor effect prolonging survival of mice bearing GD
85 ivery and magnetic hyperthermia, the in vivo anti-tumor effect under a low-frequency magnetic field u
86  After irradiating with an NIR laser, a good anti-tumor effect was observed owing to the enhanced pho
87 , simvastatin has also been reported to have anti-tumor effect, but the underlying mechanism is large
88 ology wherein the CXCR3 axis drives both the anti-tumor effector cell chemoattraction and pro-tumor i
89 he evidence for DAMPs as tumor-promoting and anti-tumor effectors, as well as unsolved questions such
90 s not profound enough to achieve comparative anti-tumor effects as EE.
91  BKM120 or LEE011 yielded more than additive anti-tumor effects both in vitro and in vivo in a melano
92 ound that gammaSI enhanced miR-34a-dependent anti-tumor effects by activating the extrinsic apoptotic
93 ore, miR-497 exhibited anti-angiogenesis and anti-tumor effects in the VEGFR2-luc breast tumor model
94 nd human T cells, which results in augmented anti-tumor effects in vivo.
95  to cancer initiation, our work demonstrates anti-tumor effects of 2HG in inhibiting proliferation/su
96                      Herein, we characterize anti-tumor effects of a unique human CD4(+) helper T-cel
97 ibitor, has been demonstrated to enhance the anti-tumor effects of DNA damaging agents such as gemcit
98 ents a pharmacological target to enhance the anti-tumor effects of DNA damaging modalities in the tre
99 he signaling network thought to diminish the anti-tumor effects of mTORC1 inhibition.
100 ion and cancer growth but also abrogates the anti-tumor effects of PPARgamma and rosiglitazone.
101 and whose therapeutic targeting enhances the anti-tumor effects of radiotherapy.
102 nd its oncogenic activities and evaluate the anti-tumor effects of reducing IGF2 signaling.
103 mmary tumor development but also impairs the anti-tumor effects of rosiglitazone.
104 tivation of the STING pathway, enhancing the anti-tumor effects of STING agonists and radiotherapy.
105                   Therefore, the synergistic anti-tumor effects of type I IFNs and MSCs were achieved
106 larly evident in vivo and likely limited the anti-tumor effects, as confirmed by re-initiation of tum
107  acid (UA) has proved to have broad-spectrum anti-tumor effects, but its poor water solubility and in
108 ession, however, has differing pro-tumor vs. anti-tumor effects, depending on the cancer types.
109 yte infiltration of tumors and showed strong anti-tumor effects.
110 utically appealing, but has had very limited anti-tumor effects.
111 hat block TGFbeta signaling can increase the anti-tumor efficacies of trastuzumab and pertuzumab.
112 r affinity CAR T cells demonstrated superior anti-tumor efficacy and safety compared to their nanomol
113  verification revealed its markedly enhanced anti-tumor efficacy as compared to its bi- or mono-drug
114 to both PEG sizes significantly enhanced its anti-tumor efficacy following intratracheal instillation
115 o cancer metastasis and displayed remarkable anti-tumor efficacy in MDA-MB-436 xenograft model withou
116 re importantly, ixazomib demonstrated potent anti-tumor efficacy in vivo by enhancing dox-induced apo
117 compared to free Ce6, and exhibited improved anti-tumor efficacy in vivo in 4T1 tumor-bearing mice.
118 ment-mediated cytotoxicity in vitro, and for anti-tumor efficacy in xenografted humanized mice.
119 en achieved with the BH3 mimetic venetoclax, anti-tumor efficacy is limited by compensatory induction
120 redesign the molecule in such a way that its anti-tumor efficacy is not compromised, but toxic effect
121 of CDCP1 in vivo significantly increased the anti-tumor efficacy of carboplatin, the chemotherapy mos
122 NI-induced renal tumor growth and tested the anti-tumor efficacy of HNK.
123      Collectively, our study illustrates the anti-tumor efficacy of ixazomib in NB both alone and in
124 somal gemcitabine and significantly improved anti-tumor efficacy of liposomal gemcitabine.
125                                  The in vivo anti-tumor efficacy of SDT with IR-780 revealed signific
126  tumor growing and no negative effect on the anti-tumor efficacy of the platinum-containing nanodrug,
127 ogrammed death-1 antibody showed more potent anti-tumor efficacy than intraperitoneal injection in B1
128 DNA-demethylating agents have shown clinical anti-tumor efficacy via an unknown mechanism of action.
129  improve chemotherapy tolerance and increase anti-tumor efficacy, while also providing a novel diagno
130 ells overexpressing both antigens and potent anti-tumor efficacy.
131 DR1) and E1K (L-FR1) did not further improve anti-tumor efficacy.
132 tification of combination therapies to boost anti-tumor function of TIL specifically against tumor ce
133 d MDM2 inhibition, and stronger responses in anti-tumor growth and metastasis effects in vitro and in
134 FcgammaR-humanized mice, we demonstrate that anti-tumor human (h)IgG1 must engage hFcgammaRIIIA on ma
135 ber of a large family of anti-pathogenic and anti-tumor IFNs, induces T-bet, a lineage-defining trans
136         Focal adhesion kinase (FAK) promotes anti-tumor immune evasion.
137 role occurs during the effector phase of the anti-tumor immune response and is required for T cell an
138            Tumor cell senescence promoted an anti-tumor immune response by CD8(+) T cells in mice.
139             The poor efficacy of the in vivo anti-tumor immune response has been partially attributed
140 ctly, but whether it also regulates the host anti-tumor immune response is not known.
141 but because this vaccine can induce a potent anti-tumor immune response only during the early stages
142 n in NK cells, which is important in the HSP anti-tumor immune response, and leaves their cytotoxic c
143 ymphocytes (CTLs) play a critical role in an anti-tumor immune response.
144  immune response, as well as to dampening an anti-tumor immune response.
145 nergy crisis, cell death, senescence, and an anti-tumor immune response.
146 ion has been required to induce an effective anti-tumor immune response.
147  T cells within the tumor, thereby enhancing anti-tumor immune responses and suppressing melanoma gro
148 at approaches to utilize TR-CD4 will augment anti-tumor immune responses for durable therapeutic effi
149 tigate the role of NK cells in gp96-mediated anti-tumor immune responses given their propensity to ly
150 90 inhibition can potentiate T-cell-mediated anti-tumor immune responses, and rationale to explore th
151  Esophageal cancers develop systems to evade anti-tumor immune responses, but studies are needed to d
152 ting CD4(+) T cells using HDACIs can enhance anti-tumor immune responses, uncovering a novel mechanis
153 draining lymph nodes to identify patterns of anti-tumor immune responses.
154 y, leading to tumor destruction by enhancing anti-tumor immune responses.
155 ne checkpoint mediator" that interferes with anti-tumor immune responses.
156 s associated with the activation of adaptive anti-tumor immune responses.
157 gs) play a pivotal role in the inhibition of anti-tumor immune responses.
158 r features associated with the robustness of anti-tumor immune responses.
159 simultaneously inhibiting the development of anti-tumor immune responses.
160 e targeting of these receptors for improving anti-tumor immune responses.
161  cells (Tregs), a key mediator in regulating anti-tumor immune suppression, tumor immune escape, meta
162 or psoriasis, but pDCs are also involved in (anti-)tumor immunity.
163 ly unappreciated roles for IL-35 in limiting anti-tumor immunity and contributing to T cell dysfuncti
164 umor microenvironment lead to eradication of anti-tumor immunity and enhanced tumor cell survival.
165 and others in early development, can unleash anti-tumor immunity and mediate durable cancer regressio
166 3 with other check-point inhibitors enhances anti-tumor immunity and suppresses tumor growth in sever
167                   Our increased knowledge in anti-tumor immunity and the immunosuppressive tumor micr
168 ents with immunogenic properties may enhance anti-tumor immunity by inducing autophagic cell death.
169 ed peptide ligands in order to induce strong anti-tumor immunity capable of breaking tolerance toward
170 vivo, restoration of TTP expression enhances anti-tumor immunity dependent on degradation of PD-L1 mR
171 landscape of a tumor shapes and is shaped by anti-tumor immunity has not been systematically explored
172 ted control of TH9 differentiation regulated anti-tumor immunity in an experimental melanoma-bearing
173 r, its immunomodulatory activities to induce anti-tumor immunity predict the suppression of tumor gro
174  which melanoma and other cancer cells evade anti-tumor immunity remain incompletely understood.
175 role for tumor-derived HSP70 in facilitating anti-tumor immunity to limit tumor growth and highlight
176 ility of surrounding wild-type Tregs, boosts anti-tumor immunity, and facilitates tumor clearance.
177 nogenicity and its role in the activation of anti-tumor immunity.
178 une disease and graft rejection and promotes anti-tumor immunity.
179 austion ligands and thereby negated adaptive anti-tumor immunity.
180 ion of tumor antigens and thereby stimulates anti-tumor immunity.
181 -activating TLR4 agonist capable of inducing anti-tumor immunity.
182 (Th1) immune responses that are required for anti-tumor immunity.
183 ted role of the Hippo pathway in suppressing anti-tumor immunity.
184 modeling, and impairment of T cell-dependent anti-tumor immunity.
185 tes to reveal a role for zinc homeostasis in anti-tumor immunity.
186 iggers Treg instability locally and restores anti-tumor immunity.
187 reg) cells pose a major barrier to effective anti-tumor immunity.
188 ific alphabeta T cell receptor (TCR) mediate anti-tumor immunity.
189 astatic niche formation and the induction of anti-tumor immunity.
190 ved to be a major contributor to compromised anti-tumor immunity.
191 promoting T cell function, autoimmunity, and anti-tumor immunity.
192 a pathophysiological context: suppression of anti-tumor immunity.
193 ting T cell function during autoimmunity and anti-tumor immunity.
194 ntion of autoimmunity and the suppression of anti-tumor immunity.
195 glucose availability to T cells, suppressing anti-tumor immunity.
196 r-infiltrating T cells results in diminished anti-tumor immunity.
197 in tumor-infiltrating dendritic cells blunts anti-tumor immunity.
198 varian cancer (OvCa) progression by blunting anti-tumor immunity.
199 alignant melanoma, by impeding IgG1-mediated anti-tumor immunity.
200 ly replicates in cancer cells while inducing anti-tumor immunity.
201  Regulatory T cells (Tregs) are a barrier to anti-tumor immunity.
202 vitamin D signaling in humans could suppress anti-tumor immunity.
203 hibitory Siglecs that can potentially dampen anti-tumor immunity.
204 e attenuation as well as the facilitation of anti-tumor immunity.
205  cells and their ability to induce efficient anti-tumor immunity.
206 reprogrammed into indispensable mediators of anti-tumor immunity.
207 trated that Cu- and Zn-AMSs markedly induced anti-tumor-immunity and enhanced CD4(+) and CD8(+) T cel
208 xpression, that is well known for triggering anti-tumor immunological response.
209 emerged as one of the most potent agents for anti-tumor immunotherapy.
210  molecular characterization and incidence of anti-tumor lymphocytes present in patients with cancer.
211  targeting ligand with good selectivity over anti-tumor M1-like TAMs.
212 represent a major shift in understanding the anti-tumor mechanisms of DNA-demethylating agents and hi
213 es to the acquisition of a pro-inflammatory, anti-tumor microenvironment in mouse brain.
214                       Passively administered anti-tumor monoclonal antibodies (mAbs) rapidly kill tum
215                                              Anti-tumor monoclonal antibodies eliminate tumor cells t
216 utero exposure to and postnatal clearance of anti-tumor necrosis factor (anti-TNF) agents in neonates
217 bout the optimal duration of therapy with an anti-tumor necrosis factor (TNF) agent and/or an immunom
218         The risk of lymphoma associated with anti-tumor necrosis factor (TNF) agents either alone or
219 atory bowel disease (IBD) fail to respond to anti-tumor necrosis factor (TNF) agents such as inflixim
220 olitis (UC) do not respond to treatment with anti-tumor necrosis factor (TNF) agents, such as inflixi
221 nflammatory bowel disease (IBD) treated with anti-tumor necrosis factor (TNF) antibodies develop skin
222   In general, women on 5-ASA, thiopurine, or anti-tumor necrosis factor (TNF) monotherapy for mainten
223 5-ASA), corticosteroids, immunosuppressants, anti-tumor necrosis factor (TNF) therapies, and other th
224                Despite the increasing use of anti-tumor necrosis factor (TNF) therapy in ulcerative c
225 study was to examine differential effects of anti-tumor necrosis factor (TNF) treatment and CTLA4 imm
226                          The extent to which anti-tumor necrosis factor (TNF)-associated tuberculosis
227  of different trough drug concentrations for anti-tumor necrosis factor agents and thiopurines to inf
228             Patients previously treated with anti-tumor necrosis factor agents or those with more tha
229                  In pair-wise comparisons of anti-tumor necrosis factor agents, infliximab + azathiop
230 e newer biologics (e.g. vedolizumab) and the anti-tumor necrosis factor agents.
231                 No association was found for anti-tumor necrosis factor agents.
232 , antibiotics, budesonide, immunomodulators, anti-tumor necrosis factor alpha (anti-TNF) (started wit
233 equency of use of systemic corticosteroid or anti-tumor necrosis factor alpha (anti-TNFalpha) therapy
234 nce for the long-term efficacy and safety of anti-tumor necrosis factor alpha agents (anti-TNF) in tr
235                    Adalimumab, a fully human anti-tumor necrosis factor alpha monoclonal antibody, is
236 kin-23 therapy, as compared with established anti-tumor necrosis factor therapies, for the treatment
237 nd was the strongest in those initiated with anti-tumor necrosis factor therapy (beta = 0.79; 95% CI,
238                          Finally, initiating anti-tumor necrosis factor therapy (n=16) reduced psoria
239  and to characterize the impact of 1 year of anti-tumor necrosis factor therapy on vascular inflammat
240 ients who were nonresponsive to steroids and anti-tumor necrosis factor therapy.
241 erapy (60%), biological therapy (66%, mostly anti-tumor necrosis factor) and phototherapy (15%) (P <
242 eceive an anti-IL-12/23 (ustekinumab, n=50), anti-tumor necrosis factor-a (TNF-alpha; etanercept, n=5
243                                              Anti-tumor necrosis factor-alpha (TNF) antibodies are ma
244                                              Anti-tumor necrosis factor-alpha (TNF-alpha) therapy (5
245 on of TDM for biologic therapy, specifically anti-tumor necrosis factor-alpha agents, and for thiopur
246 -activated protein kinase activation and the anti-tumor necrosis factor-alpha effect of adiponectin w
247 the failure of these novel therapies such as anti-tumor necrosis factor-alpha has resulted in further
248 fection (14 treated with rituximab, 146 with anti-tumor necrosis factor-alpha, and 19 with other biol
249 er biopsy led to the targeted treatment with anti-tumor necrosis factor-alpha, which was highly effec
250  ulcerative colitis, to select candidates to anti-tumor necrosis factors [screening tests looking for
251 pectedly, a soluble NKG2D ligand can enhance anti-tumor NK cell activity.
252 se model allowing simultaneous monitoring of anti-tumor potency and systemic off-tumor toxicity, micr
253                               Currently, the anti-tumor properties of FGFR inhibitors are being teste
254 PEDF), a secreted glycoprotein known for its anti-tumor properties, blocked Wnt3a-directed induction
255 hat rely on ROS-induced cell death for their anti-tumor properties.
256 d to endow endothelial progenitor cells with anti-tumor properties.
257 ding Sudemycins and Spliceostatin A, display anti-tumor properties.
258 and these peptides confer anti-microbial and anti-tumor properties.
259 ouse model with LCL161 established long-term anti-tumor protection and induced regression in a fracti
260 ene homolog B) inhibitors elicit a transient anti-tumor response in approximately 80% of BRAF(V600)-m
261                  To overcome this suppressed anti-tumor response, we developed a protocol for combine
262  Tregs and promotes a CD8(+) T cell-mediated anti-tumor response.
263 ility to mount an effective CD4(+)-dependent anti-tumor response.
264 oint-blocking antibodies can generate potent anti-tumor responses by encouraging the immune system to
265 rcinoma and found that Treg cells suppressed anti-tumor responses in tumor-associated tertiary lympho
266  Modulation of the immune system can produce anti-tumor responses in various cancer types, including
267                     Therapies that boost the anti-tumor responses of cytotoxic T lymphocytes (CTLs) h
268 xicity, blunting of self-renewal, and strong anti-tumor responses, in vivo in unfavorable AML subtype
269 ssive phenotype and disabled T-cell-mediated anti-tumor responses.
270 been shown to facilitate macrophage-mediated anti-tumor responses.
271 tended survival by evoking protective type 1 anti-tumor responses.
272 ) cluster in lipid rafts and induce pro- and anti-tumor responses.
273 nsights into the induction of autoimmune and anti-tumor responses.
274 , our work shows that ALOX5 plays a moderate anti-tumor role and functions as a drug sensitizer, with
275 ever, the exact molecular mechanisms for the anti-tumor roles of DACH1 in breast carcinoma are still
276 ntroversial, with evidence for both pro- and anti-tumor roles.
277 le for the Norrin/Fzd4 axis as an endogenous anti-tumor signal in the preneoplastic niche.
278                                          New anti-tumor strategies could take advantage of the direct
279 id cell (TIM) subsets that likely compromise anti-tumor T cell immunity.
280                                              Anti-tumor T cell potency in vitro was directly proporti
281  dominantly resists the effector phase of an anti-tumor T cell response, contributing to immune escap
282 gen-presenting cells is required to generate anti-tumor T cell responses upon ADCC-mediated tumor cle
283 amming of tumor-reactive T cells can enhance anti-tumor T cell responses, illuminating new forms of i
284 l targeting of immune checkpoints to unleash anti-tumor T cell responses, resulting in durable long-l
285 y in the tumor microenvironment and enhances anti-tumor T cell responses.
286 ent antigens, as well as trigger and augment anti-tumor T cell responses.
287 ell cytotoxicity and generation of long-term anti-tumor T cell responses.
288                         Adoptive transfer of anti-tumor T cells together with this combination therap
289 equent inhibition of tDC capacity to support anti-tumor T cells.
290 ring is a powerful means to rapidly generate anti-tumor T cells.
291 ype of macrophages in tumors, increasing the anti-tumor T-cell response and slowing tumor growth.
292                                Resistance to anti-tumor therapeutics is an important clinical problem
293 e inhibitors of SFKs, which are conventional anti-tumor therapeutics, enhanced antiviral responses an
294 is known to limit the uptake and efficacy of anti-tumor therapeutics.
295 uld be a potential candidate or adjuvant for anti-tumor therapy in clinical settings.
296 as well as in the host response to cytotoxic anti-tumor therapy.
297 nder intensive investigation as a target for anti-tumor therapy.
298 ous cancers, AC might offer a new target for anti-tumor therapy.
299 d their potential to monitor the efficacy of anti-tumor treatments.
300  generated, we utilized a murine model of an anti-tumor vaccinal effect against a model neoantigen.

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