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1 infiltrated by CD8+ T cells, contributing to tumor escape.
2 ffects, including autoimmune pathogenesis or tumor escape.
3 essarily ends in either tumor elimination or tumor escape.
4 ced immune suppression that likely underlies tumor escape.
5 ic T cell tolerance plays a critical role in tumor escape.
6 D8(+) effector T cells, thus contributing to tumor escape.
7  sensitization is a predominant mechanism of tumor escape.
8  single epitope, there is always the risk of tumor escape.
9 nto the model altered the timing and mode of tumor escape.
10 ls (MDSCs), is one of the main mechanisms of tumor escape.
11 ells (ImC) is one of the major mechanisms of tumor escape.
12 nce is a result of lymphocyte dysfunction or tumor escape.
13    T cell tolerance is a critical element of tumor escape.
14  antigen presentation may play a key role in tumor escape.
15 paration and may minimize the risk of clonal tumor escape.
16 tions in tumor-specific antigens may lead to tumor escape.
17 viding a potential molecular explanation for tumor escape.
18 ys can subvert the effector phase and enable tumor escape.
19 cers and provides a mechanism for inhibiting tumor escape.
20 y vaccination against CSDE1(P5S), preventing tumor escape.
21 immune system to circumvent antigen-negative tumor escape.
22 fibroblasts to investigate the mechanisms of tumor escape after VEGF inactivation.
23 in defective T cell priming, also leading to tumor escape and growth.
24 t result in complete tumor regression versus tumor escape and progression.
25                                              Tumor escape and recurrence are major impediments for su
26          Thus, SMG impaired the mechanism of tumor escape and rendered the cancer cells more suscepti
27 ntenance and growth, loss of p53 facilitates tumor escape and the acquisition of oncogene independenc
28                                              Tumors escape antiangiogenic therapy by activation of pr
29 ere are 2 prevailing hypotheses on how these tumors escape antiangiogenic therapy: switch to VEGF-ind
30 hen stromal cells are not destroyed, and the tumor escapes as Ag loss variants.
31                                              Tumor escape associated with low target antigen expressi
32 t work has suggested two broad categories of tumor escape based on cellular and molecular characteris
33 c heterogeneity of solid cancers and prevent tumor escape by engineering T lymphocytes to produce a b
34 essor cells (MDSC) play an important role in tumor escape by suppressing T-cell responses.
35           We identified a novel mechanism of tumor escape by which VEGF-A directly triggers Treg prol
36                         The ability to block tumor escape depends on a better understanding of cellul
37 city in vivo was an important determinant of tumor escape following CTL-based immunotherapy.
38 r suppressor p53 remain a vital mechanism of tumor escape from apoptosis and senescence.
39 d with BRAFi/MEKi, unveil genetic drivers of tumor escape from C1a, and identify a combinatorial trea
40 differentiation is an important mechanism of tumor escape from immune control.
41 t protection against cancer and facilitating tumor escape from immune destruction.
42 umor T cells has been hypothesized to permit tumor escape from immune destruction.
43 mor-induced immunosuppression and subsequent tumor escape from immune recognition and elimination.
44                           This suggests that tumor escape from immune surveillance may have occurred
45 ing immune infiltrate, and (3) mechanisms of tumor escape from immune surveillance.
46           This mechanism could contribute to tumor escape from immune surveillance.
47  of these cells is an important mechanism of tumor escape from immune system control.
48  PD-1(+) T lymphocytes plays a major role in tumor escape from immune system during cancer progressio
49                       Therefore, in general, tumor escape from immune-mediated clearance is not attri
50 cient in cytolysis, a defect that may permit tumor escape from immune-mediated destruction.
51 proposed by several groups as a mechanism of tumor escape from immunological detection.
52  is frequently associated with mechanisms of tumor escape from immunosurveillance.
53 develop strategies to override mechanisms of tumor escape from oncogene dependence.
54 mmune-checkpoint regulator implicated in the tumor escape from the host immune system.
55 s important contributors to tumor growth and tumor escape from the host immune system.
56                                The result is tumor escape from the host immune system.
57  of suppression that TEX use, thus promoting tumor escape from the host immune system.
58                            Significantly, no tumors escaped from dormancy without HSP27 expression.
59 t mechanisms by which PD1hi TST cells permit tumor escape; high signal strength drives dysfunction, w
60 however, a better understanding of how these tumors escape immune surveillance is required to enhance
61 flammatory infiltrate, suggesting that these tumors escape immune surveillance.
62 focal, nonmetastatic Stat3-deficient mammary tumors escaped immune surveillance after a long latency
63                                           In tumors escaping immunologic rejection, the expression of
64 y its soluble receptor may explain how CD30+ tumors escape immunosurveillance and may be related to t
65 e elucidated genetic determinants underlying tumor escape in a transgenic mouse model of Wnt pathway-
66 s, and its interaction with PD-1 resulted in tumor escape in experimental models.
67 on and the design of inhibitors that prevent tumor escape in quiescence.
68 sponses, we found that IFN-gamma can promote tumor escape in the CT26 colon carcinoma by down-regulat
69                                              Tumor escape is accomplished through the activation of o
70                One approach to overcome this tumor escape is by utilizing a tandem CAR recognizing tw
71                      These epidermal-derived tumors escape local immune surveillance and infiltrate t
72 tion may represent a previously unrecognized tumor escape mechanism that facilitates tumor progressio
73 than one target specific inhibitors based on tumor escape mechanism, genetic, epigenetic and molecula
74 ne and are therefore considered an important tumor escape mechanism.
75          Altogether our data propose a novel tumor escape-mechanism based on the modulation of chemok
76 d clinical efficacy to date, possibly due to tumor escape mechanisms that inhibit NK cell function.
77                            By removing these tumor escape mechanisms, sildenafil enhances intratumora
78                         The establishment of tumor escape mutants, which can be driven by innate and/
79                                Nevertheless, tumor escape occurs after several months in most patient
80 ; core or rim injections alone may result in tumor escape, particularly in a well-vascularized tumor;
81 une-privileged site within the eye develop a tumor escape phenotype in the absence of selective T cel
82 vileged environment within the eye induces a tumor escape phenotype that is not driven by selective T
83                           We show that brain tumors escape pro-inflammatory M1 conversion of microgli
84 rsistence strikingly parallels mechanisms of tumor escape, prompting investigations into the generati
85 ce of these molecules and their relevance in tumor escape remain unknown.
86                                              Tumors escaping reversion maintained c-Myc and c-Myc tar
87 suppressed in vivo and how MITF-low cells in tumors escape senescence are poorly understood.
88           Nevertheless, Tag-expressing solid tumors escape the immune surveillance and are devoid of
89              Finally, in an in vivo model of tumor escape, there was complete ACAR-mediated tumor cle
90 mited by levels of natural antibodies and by tumor escape through elimination of antigen-positive cel
91 reted by tumor-infiltrating T cells promotes tumor escape through the down-regulation of the endogeno
92                                              Tumor escape variants (TEV) recovered from the lungs of
93 ry disease and the emergence of antigen-loss tumor escape variants after treatment demonstrate the ne
94                        However, antigen-loss tumor escape variants and the absence of currently targe
95                                              Tumor escape variants are likely to emerge after treatme
96             To avoid severe side effects and tumor escape variants observed for conventional CAR-T ce
97                 Although our data regarding "tumor escape" were inconclusive, some patients had growi
98  both promoted rapid, EMT-associated mammary tumor escape, whereas isolated p16 Ink4a deficiency fail
99             Simply put, there is no need for tumor escape without immunological pressure.