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1 1, thus inhibiting T-cell activation and the antitumor immune response.
2 d CD47 and PD-L1 expression and enhanced the antitumor immune response.
3 sive, T cell-deficient cancers can launch an antitumor immune response.
4 BLT1 and CXCR3 in mediating anti-PD-1 based antitumor immune response.
5 t is an important step for mounting a robust antitumor immune response.
6 that reflect the nature and magnitude of the antitumor immune response.
7 ing tumor first elicits and then inhibits an antitumor immune response.
8 or cell line harbors TAMAs that can drive an antitumor immune response.
9 ptor ligands can lead to a powerful systemic antitumor immune response.
10 L1) improve patient outcomes by promoting an antitumor immune response.
11 the malignant cells and/or depression of the antitumor immune response.
12 that it also exerts positive effects on the antitumor immune response.
13 mor tissues, thereby dampening the resulting antitumor immune response.
14 action of this therapy that elicits a potent antitumor immune response.
15 by activated PSCs could prevent an effective antitumor immune response.
16 bits proliferation and functions of cells of antitumor immune response.
17 depends on the presence of a T-cell-mediated antitumor immune response.
18 pressive GB microenvironment conducive to an antitumor immune response.
19 ent by alleviating hypoxia and improving the antitumor immune response.
20 re implicated as effectors of the vorinostat antitumor immune response.
21 r understanding of the full potential of the antitumor immune response.
22 mors, decreased MDSC frequency, and improved antitumor immune response.
23 ath in cancer cells that engages an adaptive antitumor immune response.
24 rk at multiple levels of the T-cell-mediated antitumor immune response.
25 the underlying mechanism that increased the antitumor immune response.
26 may modulate the development of an acquired antitumor immune response.
27 CD137(neg)CD44(hi) CD4 cells suppressed the antitumor immune response.
28 oated with anti-CD47 antibodies, achieved an antitumor immune response.
29 cells as a source of immunogens to induce an antitumor immune response.
30 spensable role in activation of the observed antitumor immune response.
31 ppression of T-effector cells and dampen the antitumor immune response.
32 ts, and expresses Ags that induce a specific antitumor immune response.
33 ranscription factor (FoxP3) and suppress the antitumor immune response.
34 ile inducing a progressive depression of the antitumor immune response.
35 phamide induced a marked augmentation of the antitumor immune response.
36 rcome tolerance and promote a more effective antitumor immune response.
37 l activation and downregulating the effector antitumor immune response.
38 onse in melanoma cells serves to amplify the antitumor immune response.
39 are also exhausted, preventing an effective antitumor immune response.
40 e, yet RT alone rarely results in a systemic antitumor immune response.
41 antigens results in the absence of a de novo antitumor immune response.
42 ting immune infiltrate and a highly specific antitumor immune response.
43 hibitors (CPIs), antibodies that unleash the antitumor immune response.
44 fer cells and endothelial cells inhibits the antitumor immune response.
45 way-dependent tumor growth and liberation of antitumor immune responses.
46 ivation of cytotoxic lymphocytes and impairs antitumor immune responses.
47 umor cell growth and indirectly by dampening antitumor immune responses.
48 own that photodynamic therapy (PDT) elevates antitumor immune responses.
49 ing preexisting immunity and thereby evoking antitumor immune responses.
50 mulating factor (GM-CSF) to enhance systemic antitumor immune responses.
51 terpiece of immunodominance in antiviral and antitumor immune responses.
52 associated antigens (TAAs) that can activate antitumor immune responses.
53 ic mutations may clarify what drives natural antitumor immune responses.
54 e impaired immunosurveillance and/or trigger antitumor immune responses.
55 PD-1) enables tumor progression by dampening antitumor immune responses.
56 ntibodies to Tim-3 can enhance antiviral and antitumor immune responses.
57 Th1 and Th2 T cells and potentially enhance antitumor immune responses.
58 ed in low glucose conditions and may inhibit antitumor immune responses.
59 , and TIM-3 and TIGIT synergized to suppress antitumor immune responses.
60 at ROS inhibitors may be useful in promoting antitumor immune responses.
61 esenting Ags, in the induction of protective antitumor immune responses.
62 nteresting target cells for the induction of antitumor immune responses.
63 les that prevent the generation of effective antitumor immune responses.
64 lopment of spontaneous and therapy-inducible antitumor immune responses.
65 e NKG2D ligands on myeloid cells, subverting antitumor immune responses.
66 inhibition of Tregs that otherwise suppress antitumor immune responses.
67 when virus replication stimulates sustained antitumor immune responses.
68 re they may contribute to the suppression of antitumor immune responses.
69 voring neoangiogenesis and/or by suppressing antitumor immune responses.
70 influence their capacity to mount efficient antitumor immune responses.
71 s (DCs), thereby supporting the induction of antitumor immune responses.
72 of Tregs, with the aim of eliciting enhanced antitumor immune responses.
73 of eliciting potent specific and nonspecific antitumor immune responses.
74 t a major barrier to the induction of robust antitumor immune responses.
75 umors due largely to effector failure of the antitumor immune responses.
76 nt microenvironmental factor that suppresses antitumor immune responses.
77 ty of designing therapies to induce targeted antitumor immune responses.
78 Tregs and allow more effective induction of antitumor immune responses.
79 on of activated T(regs) that greatly limited antitumor immune responses.
80 adjuvant strategy to improve stimulation of antitumor immune responses.
81 ) share important roles in the antiviral and antitumor immune responses.
82 ing the importance of CCR5 in the control of antitumor immune responses.
83 ancers and is equally capable of suppressing antitumor immune responses.
84 a potential therapeutic target for enhancing antitumor immune responses.
85 r mouse model, suggesting the elicitation of antitumor immune responses.
86 ells has a critical impact on the outcome of antitumor immune responses.
87 ia cellular cross-talk, NK cells orchestrate antitumor immune responses.
88 o induce therapeutically relevant endogenous antitumor immune responses.
89 t to be an important factor in antiviral and antitumor immune responses.
90 mes resulted in profound defects in adaptive antitumor immune responses.
91 lls is an attractive approach for generating antitumor immune responses.
92 type immunity, dampening natural and induced antitumor immune responses.
93 -reactive T cells and contribute to impaired antitumor immune responses.
94 jor role in cancer by suppressing protective antitumor immune responses.
95 of multiple epitopes that may elicit memory antitumor immune responses.
96 th by promoting angiogenesis and suppressing antitumor immune responses.
97 , but also for protecting tumor tissues from antitumor immune responses.
98 for IDO in the regulation of IL-12-mediated antitumor immune responses.
99 on regulatory T cells that negatively impact antitumor immune responses.
100 ciated immune cells and ultimately to potent antitumor immune responses.
101 tant for T(reg) cell-mediated suppression of antitumor immune responses.
102 lities in cancer and leads to suppression of antitumor immune responses.
103 Lymphocytes play a critical role in antitumor immune responses.
104 roles in various immune responses, including antitumor immune responses.
105 promising target structures to elicit potent antitumor immune responses.
106 ) is crucial for the generation of effective antitumor immune responses.
107 (CD8+) T lymphocytes play a central role in antitumor immune responses.
108 s to be harnessed for better invigoration of antitumor immune responses.
109 emerged as a critical impediment to adaptive antitumor immune responses.
110 on the context, pDCs can promote or suppress antitumor immune responses.
111 y tilt the tumor microenvironment to promote antitumor immune responses.
112 in vivo and if deletion of host xCT impacted antitumor immune responses.
113 r T cells (T(eff)) in the TME can potentiate antitumor immune responses.
114 specific CD8(+) T cells and raise subsequent antitumor immune responses.
115 ls into a therapeutic vaccine and stimulates antitumor immune responses.
116 an conventional Tregs and may play a role in antitumor immune responses.
117 ation of tumor antigens, leading to dramatic antitumor immune responses.
118 Tumor-infiltrating CD8+ T cells mediate antitumor immune responses.
119 -derived suppressor cells (MDSC), inhibiting antitumor immune responses.
120 n of the chemokine CXCL14 and suppression of antitumor immune responses.
121 n is necessary for successful antiviral, and antitumor immune responses.
122 envisaging strategies aimed at facilitating antitumor immune responses.
123 lishment of premetastatic niches and inhibit antitumor immune responses.
124 MicroRNA-155 (miR-155) regulates antitumor immune responses.
125 e immune surveillance is required to enhance antitumor immune responses.
126 negative regulator of NK-cell maturation and antitumor immune responses.
127 to use oncolytic viruses to induce secondary antitumor immune responses.
128 sor cells (MDSCs), which actively suppressed antitumor immune responses.
129 NF-kappaB) that mediates innate and adaptive antitumor immune responses.
130 cancer in part by effects on DNA repair and antitumor immune responses.
131 and cancer cells, where it can downregulate antitumor immune responses.
132 hocyte proliferation and tumor cell-specific antitumor immune responses.
133 nvasive modality capable of imaging the host antitumor immune response against intracranial tumors.
134 y directly kill cancer cells but also induce antitumor immune responses against a broad spectrum of s
135 ld further assist in the induction of potent antitumor immune responses against primary and metastati
136 um stress and apoptosis, toxic autophagy, an antitumor immune response, an antiangiogenic effect, and
137 t decade with promising results in enhancing antitumor immune response and cancer vaccine efficacy.
139 discuss the ways in which Tregs suppress the antitumor immune response and elaborate on our recent di
140 We postulated that pDC may interfere with antitumor immune response and favor tolerance in breast
141 tumor microenvironment inhibits an effective antitumor immune response and highlights early Treg recr
142 t role of the 15-PGDH in regulation of local antitumor immune response and highlights the potential t
143 tion in the TME has been shown to dampen the antitumor immune response and is thought to be an import
144 lockade enhances both the local and systemic antitumor immune response and may represent a more effic
145 ponse; however, Tregs eventually inhibit the antitumor immune response and thereby limit the power of
146 icted to the gut, potentiated the RT-induced antitumor immune response and tumor growth inhibition.
147 in including peptides that may be targets of antitumor immune responses and 2) it is a tyrosine kinas
148 TNFalpha promotes both vessel remodeling and antitumor immune responses and acts as a potent adjuvant
150 s induced by chemotherapeutic agents promote antitumor immune responses and contribute to their full
151 a such as bacillus Calmette-Guerin increases antitumor immune responses and delays tumor growth.
152 first time that HDAC6i can both improve ICB antitumor immune responses and diminish the invasiveness
153 feasible and well tolerated and resulted in antitumor immune responses and disease stabilization in
154 ived particulate beta-glucan elicited potent antitumor immune responses and drastically down-regulate
155 erred to as M2-polarized) generally suppress antitumor immune responses and enhance the metastatic pr
156 reclinical investigations of tissue-specific antitumor immune responses and how they influence the tu
158 the unique ability to shape immunity during antitumor immune responses and other forms of sterile an
159 stigated whether an ENO1 DNA vaccine elicits antitumor immune responses and prolongs survival of mice
161 d immune cell effector functions to suppress antitumor immune responses and promote tumor growth thro
162 ized by chronic inflammation that suppresses antitumor immune responses and promotes tumor growth and
163 uence melanoma development through dampening antitumor immune responses and promoting angiogenesis.
164 g Fc fusion protein induced higher levels of antitumor immune responses and protection than the 47-LD
165 mically administered TLR7 agonist to improve antitumor immune responses and provide durable remission
166 Mice lacking this protein mounted potent antitumor immune responses and rejected implanted tumors
167 vestigated the role of GITR agonism in human antitumor immune responses and report here the preclinic
168 ockade of CD73 enhanced doxorubicin-mediated antitumor immune responses and significantly prolonged t
169 dritic cells (DCs) required for induction of antitumor immune responses and success of cancer immunot
170 stablishes a role of IL-36gamma in promoting antitumor immune responses and suggests its potential cl
171 however, the impact of CD4(+) Tregs on human antitumor immune responses and their influence on cancer
173 P2X7R expression was critical to support an antitumor immune response, and to restrict tumor growth
174 vaccines despite small tumor size, an intact antitumor immune response, and unaltered cancer cells.
175 Clinically, PD-1 blockade elicits potent antitumor immune responses, and antibodies blocking PD-1
176 nists are in clinical development to enhance antitumor immune responses, and one proposed mechanism o
179 T-cell defects, immune suppression, and poor antitumor immune responses are hallmarks of chronic lymp
180 of tumors can limit cancer development, but antitumor immune responses are often blocked by tumor-me
181 y in animals mounting a strong and effective antitumor immune response as compared with those experie
182 us be possible to use immuno-PET and monitor antitumor immune responses as a prognostic tool to predi
183 actors, rather than induction of an adaptive antitumor immune response, as the main mechanism of acti
184 AP1), a key regulator of innate and adaptive antitumor immune responses, as a previously unknown play
185 require combinations that generate effective antitumor immune responses, as well as overcome immune e
186 hosphamide administration activates a potent antitumor immune response associated with brain tumor re
187 outside the bone marrow, thus weakening the antitumor immune response at the primary site of tumor g
191 rrent immunotherapies focus on modulating an antitumor immune response by directly or indirectly expa
192 eneration of endostatin, AdMMP-9 promoted an antitumor immune response by inducing massive neutrophil
193 pomethylation agents (HMAs), can enhance the antitumor immune response by inducing TAA expression.
194 e inhibitors (HDACis) may induce a favorable antitumor immune response by regulating the expression o
195 ith trastuzumab may experience a more robust antitumor immune response by restimulation of T cells wi
197 une-based cancer treatment strive to augment antitumor immune responses by expanding tumor-reactive T
198 Tumor cells counteract innate and adaptive antitumor immune responses by recruiting regulatory T ce
199 y-based strategies have focused on enhancing antitumor immune responses by targeting immune cells, ir
200 Thus, tumor-associated MAIT cells may affect antitumor immune responses by their secreted cytokines.
201 umor cells directly, (b) orchestrate diverse antitumor immune responses, (c) manifest long-lasting me
203 4 blockade greatly increased T-cell-mediated antitumor immune responses, conferring a significant sur
204 esent in animals that developed an effective antitumor immune response could be correlated with a spe
205 ponses to dead cells and to induce effective antitumor immune responses during anti-PD-1 treatment in
206 he complex control involved in antiviral and antitumor immune responses during these infections can b
207 iR-146a could be a novel strategy to enhance antitumor immune response elicited by checkpoint therapy
208 ivo visualized the IFN-beta required for the antitumor immune response elicited in a therapeutic mode
209 TOR inhibition in abolishing T-cell-mediated antitumor immune responses essential for the therapeutic
210 tested whether the gut microbiota modulates antitumor immune response following RT distal to the gut
211 apeutics in tumor tissue and induce a potent antitumor immune response for an extended time period vi
214 ts regulatory pathways in T cells to enhance antitumor immune responses, has led to important clinica
216 therapies, as well as to the suppression of antitumor immune response, highlights the critical need
218 ymphocytes, in addition to polarizing type-1 antitumor immune responses, impair tumor-induced CD4(+)C
219 under endogenous as well as vaccine-induced antitumor immune response in a syngeneic murine model of
221 ioxide (As(2)O(3)) was shown to increase the antitumor immune response in CT26 colon tumor-bearing mi
222 aluated how autophagy inhibition impacts the antitumor immune response in immune-competent mouse mode
225 nce of cancer and lead to a natural adaptive antitumor immune response in the absence of exogenous in
227 mmune aggregates would generate a productive antitumor immune response in the peritoneal cavity.
228 t stimulated a strong CD8(+) T cell-mediated antitumor immune response in vivo that regressed establi
229 ell (DC)/breast carcinoma fusions stimulated antitumor immune responses in a majority of patients wit
230 n several cancer histologies, reinvigorating antitumor immune responses in a subset of patients.
231 s engineered to express ICOS ligand enhanced antitumor immune responses in both quantity and quality
239 a novel combination of this type to augment antitumor immune responses in preclinical murine models
240 and interleukin (IL)-2 have elicited potent antitumor immune responses in preclinical studies, but t
241 ugh STING signaling is sufficient to promote antitumor immune responses in the B16-F0 melanoma model.
242 f immuno-radiotherapy for generating optimal antitumor immune responses in the clinical setting.
244 Interestingly, frequent vaccinations restore antitumor immune responses in the presence of establishe
245 e cell transfer and resulted in induction of antitumor immune responses in the setting of established
246 er, the molecular factors that could empower antitumor immune responses in this setting remain to be
249 tic executioner caspase 3 (CASP3) attenuates antitumor immune responses induced by radiation therapy
250 that 15-PGDH expression by OSVP enhanced the antitumor immune response initiated by viral infection o
251 ired immunity to pathogens to convert a weak antitumor immune response into a much stronger one.
252 support the CTLs, converting a weak primary antitumor immune response into a stronger secondary one.
253 n vivo assays of C4HD tumors showed that the antitumor immune response involves the participation of
256 s indicated that the major DAMP driving host antitumor immune responses is tumor-derived DNA, sensed
258 ells (DCs) in the expansion of antiviral and antitumor immune responses is well-documented; however,
259 the hematologic compartment that may enhance antitumor immune responses, mainly by activation of dend
260 s study, we demonstrate that rapamycin harms antitumor immune responses mediated by T cells in the se
261 uprastat and anti-PD1 immunotherapy enhances antitumor immune response, mediated by a decrease of pro
262 e capable of directly facilitating effective antitumor immune responses, mice bearing established sub
263 actual contribution of cross-presentation to antitumor immune responses nor the intracellular pathway
264 eg) population in the TME can potentiate the antitumor immune response of checkpoint inhibitors.
266 ation provides new opportunities to evaluate antitumor immune responses of immunotherapies currently
267 f various cancers, primary tumors can escape antitumor immune responses of their host and eventually
268 nment may have clinical benefit, stimulating antitumor immune responses or enhancing immunotherapeuti
269 7, whose pathogenic effects can override the antitumor immune response orchestrated by IFNgamma.
272 d by NPM-ALK are also involved in evasion of antitumor immune response, protection from hypoxia, angi
274 VA-5T4 each independently induced beneficial antitumor immune responses, resulting in prolonged survi
275 livery and activation of innate and adaptive antitumor immune responses results in a potent cyto-immu
276 ells and molecules associated with effective antitumor immune responses, reverse transcription-PCR ar
278 ies reveal a novel role for TNF-alpha in the antitumor immune response, specifically in stimulating h
279 perspective on KP dysregulation in defeating antitumor immune responses, specifically bringing light
280 ish an unexpected role for Nlrp3 in impeding antitumor immune responses, suggesting novel approaches
281 dies in a single tumor, generated a systemic antitumor immune response that eradicated disseminated d
282 that some patients with cancer can mount an antitumor immune response that has the potential to cont
283 of antitumor potency and induced a systemic antitumor immune response that was greater than that ind
284 leased within the microenvironment to thwart antitumor immune responses, thereby facilitating tumor g
286 e metastasizing cancer cells to escape local antitumor immune responses through interactions with the
287 al killer cells, and CD8 T cells to mount an antitumor immune response, thus explaining the remarkabl
290 specific immunotherapeutic target to improve antitumor immune responses to immune checkpoint therapy
291 Despite the appreciation of CD8(+) T-cell antitumor immune responses toward improvement in patient
292 developing therapeutic approaches to enhance antitumor immune responses using novel immunomodulatory
293 used anthracycline, by suppressing adaptive antitumor immune responses via activation of A2A adenosi
294 he genetic basis and mechanisms of disparate antitumor immune response was investigated in Diversity
295 umor-secreted GRP94 has been shown to elicit antitumor immune responses when used as antitumor vaccin
296 bsets is not sufficient for the induction of antitumor immune responses, whereas early induction of T
297 of using therapeutic ultrasound to elicit an antitumor immune response with examples that reveal spec
298 elivered to tumor sites to generate powerful antitumor immune responses with minimal off-target disse
300 deficiency was associated with a suppressed antitumor immune response, with both increased infiltrat