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1 by activated PSCs could prevent an effective antitumor immune response.
2 bits proliferation and functions of cells of antitumor immune response.
3 depends on the presence of a T-cell-mediated antitumor immune response.
4 pressive GB microenvironment conducive to an antitumor immune response.
5 re implicated as effectors of the vorinostat antitumor immune response.
6 r understanding of the full potential of the antitumor immune response.
7 mors, decreased MDSC frequency, and improved antitumor immune response.
8 ath in cancer cells that engages an adaptive antitumor immune response.
9 rk at multiple levels of the T-cell-mediated antitumor immune response.
10 the underlying mechanism that increased the antitumor immune response.
11 may modulate the development of an acquired antitumor immune response.
12 CD137(neg)CD44(hi) CD4 cells suppressed the antitumor immune response.
13 cells as a source of immunogens to induce an antitumor immune response.
14 spensable role in activation of the observed antitumor immune response.
15 ppression of T-effector cells and dampen the antitumor immune response.
16 ranscription factor (FoxP3) and suppress the antitumor immune response.
17 phamide induced a marked augmentation of the antitumor immune response.
18 rcome tolerance and promote a more effective antitumor immune response.
19 l activation and downregulating the effector antitumor immune response.
20 growth and metastasis and in suppressing the antitumor immune response.
21 amplification of the subsequent destructive antitumor immune response.
22 ls by A(133)Gmono-crePV may lead to a robust antitumor immune response.
23 otherapy in vivo without changes in systemic antitumor immune response.
24 use of PDE5 inhibitors as modulators of the antitumor immune response.
25 enic JMML cells, may serve as a target of an antitumor immune response.
26 ms of gp96 in tumor cells would stimulate an antitumor immune response.
27 ased from tumor cells and stimulate a potent antitumor immune response.
28 id receptors by specifically suppressing the antitumor immune response.
29 riming rather than the effector phase of the antitumor immune response.
30 ect the development of an effective cellular antitumor immune response.
31 aker" autoimmune response into a more potent antitumor immune response.
32 fer cells and endothelial cells inhibits the antitumor immune response.
33 actor (GM-CSF) expression induces a systemic antitumor immune response.
34 ly transferred T cells to induce an enhanced antitumor immune response.
35 ting factor (GM-CSF) can generate a systemic antitumor immune response.
36 1, thus inhibiting T-cell activation and the antitumor immune response.
37 d CD47 and PD-L1 expression and enhanced the antitumor immune response.
38 BLT1 and CXCR3 in mediating anti-PD-1 based antitumor immune response.
39 t is an important step for mounting a robust antitumor immune response.
40 that reflect the nature and magnitude of the antitumor immune response.
41 ing tumor first elicits and then inhibits an antitumor immune response.
42 or cell line harbors TAMAs that can drive an antitumor immune response.
43 hibitors (CPIs), antibodies that unleash the antitumor immune response.
44 ptor ligands can lead to a powerful systemic antitumor immune response.
45 L1) improve patient outcomes by promoting an antitumor immune response.
46 the malignant cells and/or depression of the antitumor immune response.
47 that it also exerts positive effects on the antitumor immune response.
48 action of this therapy that elicits a potent antitumor immune response.
49 n of the chemokine CXCL14 and suppression of antitumor immune responses.
50 n is necessary for successful antiviral, and antitumor immune responses.
51 lopment of spontaneous and therapy-inducible antitumor immune responses.
52 e NKG2D ligands on myeloid cells, subverting antitumor immune responses.
53 when virus replication stimulates sustained antitumor immune responses.
54 re they may contribute to the suppression of antitumor immune responses.
55 e immune surveillance is required to enhance antitumor immune responses.
56 voring neoangiogenesis and/or by suppressing antitumor immune responses.
57 influence their capacity to mount efficient antitumor immune responses.
58 s (DCs), thereby supporting the induction of antitumor immune responses.
59 negative regulator of NK-cell maturation and antitumor immune responses.
60 of Tregs, with the aim of eliciting enhanced antitumor immune responses.
61 of eliciting potent specific and nonspecific antitumor immune responses.
62 umors due largely to effector failure of the antitumor immune responses.
63 nt microenvironmental factor that suppresses antitumor immune responses.
64 ty of designing therapies to induce targeted antitumor immune responses.
65 Tregs and allow more effective induction of antitumor immune responses.
66 on of activated T(regs) that greatly limited antitumor immune responses.
67 adjuvant strategy to improve stimulation of antitumor immune responses.
68 ) share important roles in the antiviral and antitumor immune responses.
69 ing the importance of CCR5 in the control of antitumor immune responses.
70 ancers and is equally capable of suppressing antitumor immune responses.
71 a potential therapeutic target for enhancing antitumor immune responses.
72 to use oncolytic viruses to induce secondary antitumor immune responses.
73 r mouse model, suggesting the elicitation of antitumor immune responses.
74 sor cells (MDSCs), which actively suppressed antitumor immune responses.
75 ells has a critical impact on the outcome of antitumor immune responses.
76 o induce therapeutically relevant endogenous antitumor immune responses.
77 t to be an important factor in antiviral and antitumor immune responses.
78 NF-kappaB) that mediates innate and adaptive antitumor immune responses.
79 mes resulted in profound defects in adaptive antitumor immune responses.
80 lls is an attractive approach for generating antitumor immune responses.
81 type immunity, dampening natural and induced antitumor immune responses.
82 -reactive T cells and contribute to impaired antitumor immune responses.
83 envisaging strategies aimed at facilitating antitumor immune responses.
84 jor role in cancer by suppressing protective antitumor immune responses.
85 of multiple epitopes that may elicit memory antitumor immune responses.
86 th by promoting angiogenesis and suppressing antitumor immune responses.
87 , but also for protecting tumor tissues from antitumor immune responses.
88 for IDO in the regulation of IL-12-mediated antitumor immune responses.
89 on regulatory T cells that negatively impact antitumor immune responses.
90 ciated immune cells and ultimately to potent antitumor immune responses.
91 tant for T(reg) cell-mediated suppression of antitumor immune responses.
92 lities in cancer and leads to suppression of antitumor immune responses.
93 roles in various immune responses, including antitumor immune responses.
94 paid to the role of virotherapy in promoting antitumor immune responses.
95 cancer in part by effects on DNA repair and antitumor immune responses.
96 r-beta, however, which could suppress T-cell antitumor immune responses.
97 reg) cells control immunologic tolerance and antitumor immune responses.
98 and cancer cells, where it can downregulate antitumor immune responses.
99 roles in the development and maintenance of antitumor immune responses.
100 d gp96 can induce protective and therapeutic antitumor immune responses.
101 es, tumor-derived stress proteins can elicit antitumor immune responses.
102 pitopes in immunogenic form, could stimulate antitumor immune responses.
103 hocyte proliferation and tumor cell-specific antitumor immune responses.
104 une effector cells in tumors is critical for antitumor immune responses.
105 CD4+ T cells and macrophages in DC1-induced antitumor immune responses.
106 cer and appear to play a role in suppressing antitumor immune responses.
107 our understanding of limitation of the host antitumor immune responses.
108 end retrovirus is associated with suppressed antitumor immune responses.
109 of tolerance and play a role in the lack of antitumor immune responses.
110 more versatile effector cell population for antitumor immune responses.
111 ivation of cytotoxic lymphocytes and impairs antitumor immune responses.
112 lishment of premetastatic niches and inhibit antitumor immune responses.
113 umor cell growth and indirectly by dampening antitumor immune responses.
114 own that photodynamic therapy (PDT) elevates antitumor immune responses.
115 MicroRNA-155 (miR-155) regulates antitumor immune responses.
116 ing preexisting immunity and thereby evoking antitumor immune responses.
117 mulating factor (GM-CSF) to enhance systemic antitumor immune responses.
118 terpiece of immunodominance in antiviral and antitumor immune responses.
119 associated antigens (TAAs) that can activate antitumor immune responses.
120 ic mutations may clarify what drives natural antitumor immune responses.
121 PD-1) enables tumor progression by dampening antitumor immune responses.
122 ntibodies to Tim-3 can enhance antiviral and antitumor immune responses.
123 Th1 and Th2 T cells and potentially enhance antitumor immune responses.
124 ed in low glucose conditions and may inhibit antitumor immune responses.
125 , and TIM-3 and TIGIT synergized to suppress antitumor immune responses.
126 at ROS inhibitors may be useful in promoting antitumor immune responses.
127 esenting Ags, in the induction of protective antitumor immune responses.
128 nteresting target cells for the induction of antitumor immune responses.
129 les that prevent the generation of effective antitumor immune responses.
130 t the first demonstration of a potent innate antitumor immune response against CNS tumors in the abse
131 nvasive modality capable of imaging the host antitumor immune response against intracranial tumors.
133 young mice, restoring the primary and memory antitumor immune responses against BM-185-EGFP tumors.
134 ld further assist in the induction of potent antitumor immune responses against primary and metastati
135 um stress and apoptosis, toxic autophagy, an antitumor immune response, an antiangiogenic effect, and
136 t decade with promising results in enhancing antitumor immune response and cancer vaccine efficacy.
138 discuss the ways in which Tregs suppress the antitumor immune response and elaborate on our recent di
139 We postulated that pDC may interfere with antitumor immune response and favor tolerance in breast
140 tumor microenvironment inhibits an effective antitumor immune response and highlights early Treg recr
141 t role of the 15-PGDH in regulation of local antitumor immune response and highlights the potential t
142 rcome obstacles at the effector phase of the antitumor immune response and improve the therapeutic ef
143 osen for its ability to induce a strong host antitumor immune response and its potential antiangiogen
144 ponse; however, Tregs eventually inhibit the antitumor immune response and thereby limit the power of
145 in including peptides that may be targets of antitumor immune responses and 2) it is a tyrosine kinas
146 TNFalpha promotes both vessel remodeling and antitumor immune responses and acts as a potent adjuvant
148 s induced by chemotherapeutic agents promote antitumor immune responses and contribute to their full
149 a such as bacillus Calmette-Guerin increases antitumor immune responses and delays tumor growth.
150 feasible and well tolerated and resulted in antitumor immune responses and disease stabilization in
151 ived particulate beta-glucan elicited potent antitumor immune responses and drastically down-regulate
153 stigated whether an ENO1 DNA vaccine elicits antitumor immune responses and prolongs survival of mice
155 d immune cell effector functions to suppress antitumor immune responses and promote tumor growth thro
156 ized by chronic inflammation that suppresses antitumor immune responses and promotes tumor growth and
157 uence melanoma development through dampening antitumor immune responses and promoting angiogenesis.
158 g Fc fusion protein induced higher levels of antitumor immune responses and protection than the 47-LD
159 mically administered TLR7 agonist to improve antitumor immune responses and provide durable remission
160 Mice lacking this protein mounted potent antitumor immune responses and rejected implanted tumors
161 vestigated the role of GITR agonism in human antitumor immune responses and report here the preclinic
162 ockade of CD73 enhanced doxorubicin-mediated antitumor immune responses and significantly prolonged t
163 dritic cells (DCs) required for induction of antitumor immune responses and success of cancer immunot
164 stablishes a role of IL-36gamma in promoting antitumor immune responses and suggests its potential cl
165 egulation of CD200 on tumor cells suppresses antitumor immune responses and that antagonistic anti-hu
166 however, the impact of CD4(+) Tregs on human antitumor immune responses and their influence on cancer
168 P2X7R expression was critical to support an antitumor immune response, and to restrict tumor growth
169 vaccines despite small tumor size, an intact antitumor immune response, and unaltered cancer cells.
170 Clinically, PD-1 blockade elicits potent antitumor immune responses, and antibodies blocking PD-1
171 apy, as direct cytotoxic agents, inducers of antitumor immune responses, and as expressers of antican
174 T-cell defects, immune suppression, and poor antitumor immune responses are hallmarks of chronic lymp
175 of tumors can limit cancer development, but antitumor immune responses are often blocked by tumor-me
176 y in animals mounting a strong and effective antitumor immune response as compared with those experie
177 us be possible to use immuno-PET and monitor antitumor immune responses as a prognostic tool to predi
178 the growing emphasis on enhancement of host antitumor immune responses as the key to successful ther
179 require combinations that generate effective antitumor immune responses, as well as overcome immune e
180 hosphamide administration activates a potent antitumor immune response associated with brain tumor re
181 outside the bone marrow, thus weakening the antitumor immune response at the primary site of tumor g
182 r direct targeting tumor tissues to generate antitumor immune response before surgical excision produ
185 eneration of endostatin, AdMMP-9 promoted an antitumor immune response by inducing massive neutrophil
186 e inhibitors (HDACis) may induce a favorable antitumor immune response by regulating the expression o
187 ith trastuzumab may experience a more robust antitumor immune response by restimulation of T cells wi
189 at cyclophosphamide augments the efficacy of antitumor immune responses by depleting CD4+ CD25+ T reg
190 une-based cancer treatment strive to augment antitumor immune responses by expanding tumor-reactive T
191 Tumor cells counteract innate and adaptive antitumor immune responses by recruiting regulatory T ce
192 y-based strategies have focused on enhancing antitumor immune responses by targeting immune cells, ir
193 Thus, tumor-associated MAIT cells may affect antitumor immune responses by their secreted cytokines.
194 umor cells directly, (b) orchestrate diverse antitumor immune responses, (c) manifest long-lasting me
196 4 blockade greatly increased T-cell-mediated antitumor immune responses, conferring a significant sur
197 esent in animals that developed an effective antitumor immune response could be correlated with a spe
198 ponses to dead cells and to induce effective antitumor immune responses during anti-PD-1 treatment in
199 ntigen presentation attenuator in control of antitumor immune responses during both the priming and t
200 he complex control involved in antiviral and antitumor immune responses during these infections can b
201 ivo visualized the IFN-beta required for the antitumor immune response elicited in a therapeutic mode
202 TOR inhibition in abolishing T-cell-mediated antitumor immune responses essential for the therapeutic
203 nt way to generate a CD8(+) T-cell-dependent antitumor immune response even in animals with relativel
204 apeutics in tumor tissue and induce a potent antitumor immune response for an extended time period vi
207 ts regulatory pathways in T cells to enhance antitumor immune responses, has led to important clinica
209 therapies, as well as to the suppression of antitumor immune response, highlights the critical need
211 ymphocytes, in addition to polarizing type-1 antitumor immune responses, impair tumor-induced CD4(+)C
212 lity, ERK activation in MM attenuates a host antitumor immune response, implicating CD200 and its int
213 y-stimulating factor (GM-CSF) would activate antitumor immune response in a syngeneic murine model of
214 under endogenous as well as vaccine-induced antitumor immune response in a syngeneic murine model of
215 differences might be associated with a host antitumor immune response in asmase(+/+) mice that is no
216 ioxide (As(2)O(3)) was shown to increase the antitumor immune response in CT26 colon tumor-bearing mi
217 aluated how autophagy inhibition impacts the antitumor immune response in immune-competent mouse mode
219 nce of cancer and lead to a natural adaptive antitumor immune response in the absence of exogenous in
220 mmune aggregates would generate a productive antitumor immune response in the peritoneal cavity.
221 t stimulated a strong CD8(+) T cell-mediated antitumor immune response in vivo that regressed establi
224 ell (DC)/breast carcinoma fusions stimulated antitumor immune responses in a majority of patients wit
225 n several cancer histologies, reinvigorating antitumor immune responses in a subset of patients.
227 s engineered to express ICOS ligand enhanced antitumor immune responses in both quantity and quality
237 a novel combination of this type to augment antitumor immune responses in preclinical murine models
238 and interleukin (IL)-2 have elicited potent antitumor immune responses in preclinical studies, but t
241 Interestingly, frequent vaccinations restore antitumor immune responses in the presence of establishe
242 e cell transfer and resulted in induction of antitumor immune responses in the setting of established
243 er, the molecular factors that could empower antitumor immune responses in this setting remain to be
247 that 15-PGDH expression by OSVP enhanced the antitumor immune response initiated by viral infection o
249 n vivo assays of C4HD tumors showed that the antitumor immune response involves the participation of
251 lenge to efforts aimed at inducing effective antitumor immune responses is that CD8(+) T cells, which
253 s indicated that the major DAMP driving host antitumor immune responses is tumor-derived DNA, sensed
255 ells (DCs) in the expansion of antiviral and antitumor immune responses is well-documented; however,
256 the hematologic compartment that may enhance antitumor immune responses, mainly by activation of dend
257 s study, we demonstrate that rapamycin harms antitumor immune responses mediated by T cells in the se
258 e capable of directly facilitating effective antitumor immune responses, mice bearing established sub
259 actual contribution of cross-presentation to antitumor immune responses nor the intracellular pathway
261 ation provides new opportunities to evaluate antitumor immune responses of immunotherapies currently
262 , but the consequences of a highly effective antitumor immune response on self-tissue have not been f
263 nment may have clinical benefit, stimulating antitumor immune responses or enhancing immunotherapeuti
264 7, whose pathogenic effects can override the antitumor immune response orchestrated by IFNgamma.
267 d by NPM-ALK are also involved in evasion of antitumor immune response, protection from hypoxia, angi
269 VA-5T4 each independently induced beneficial antitumor immune responses, resulting in prolonged survi
270 ells and molecules associated with effective antitumor immune responses, reverse transcription-PCR ar
271 ies reveal a novel role for TNF-alpha in the antitumor immune response, specifically in stimulating h
272 perspective on KP dysregulation in defeating antitumor immune responses, specifically bringing light
273 infiltrate and the lack of an effective host antitumor immune response suggest that RS cells use pote
274 ish an unexpected role for Nlrp3 in impeding antitumor immune responses, suggesting novel approaches
275 dies in a single tumor, generated a systemic antitumor immune response that eradicated disseminated d
276 that some patients with cancer can mount an antitumor immune response that has the potential to cont
277 of antitumor potency and induced a systemic antitumor immune response that was greater than that ind
278 id dendritic cells (mDC) in the induction of antitumor immune responses, the role of pDC in antitumor
279 leased within the microenvironment to thwart antitumor immune responses, thereby facilitating tumor g
281 e metastasizing cancer cells to escape local antitumor immune responses through interactions with the
282 al killer cells, and CD8 T cells to mount an antitumor immune response, thus explaining the remarkabl
283 pressive mechanisms and enables a measurable antitumor immune response to be generated that substanti
285 cell depletion could therapeutically enhance antitumor immune responses to certain tumors by decreasi
286 re, imatinib mesylate significantly enhanced antitumor immune responses to dendritic cell-based immun
288 cumulate dendritic cells in tumors and evoke antitumor immune responses to inhibit tumor growth.
289 rate that when trying to elicit an effective antitumor immune response, two obstacles must be conside
290 developing therapeutic approaches to enhance antitumor immune responses using novel immunomodulatory
291 used anthracycline, by suppressing adaptive antitumor immune responses via activation of A2A adenosi
293 ognate helper CD4+ T cells would enhance the antitumor immune response, we conducted a phase I clinic
294 immature naive dendritic cells to induce an antitumor immune response when injected directly into a
295 umor-secreted GRP94 has been shown to elicit antitumor immune responses when used as antitumor vaccin
296 ce in the setting of autoimmune diseases and antitumor immune responses where NK cells play key regul
297 bsets is not sufficient for the induction of antitumor immune responses, whereas early induction of T
299 deficiency was associated with a suppressed antitumor immune response, with both increased infiltrat
300 etically deficient mice, can induce dramatic antitumor immune responses within the CNS that surpass t
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