戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 to escape immunosurveillance (known as tumor immunoediting).
2 nes influence somatic evolution by mediating immunoediting.
3 ify genes that impact early phases of cancer immunoediting.
4 sms leading to cancer immunosurveillance and immunoediting.
5 issue identification, resulting from epitope immunoediting.
6 pport of the likelihood of NK-mediated tumor immunoediting.
7  related to immune equilibrium during cancer immunoediting.
8  whether innate immunity alone is capable of immunoediting.
9 ich act as important effectors during cancer immunoediting.
10 n process represents one mechanism of cancer immunoediting.
11 genesis to investigate the process of cancer immunoediting.
12 ctions of immunity are referred to as cancer immunoediting.
13 orally distinct from IFN-gamma during cancer immunoediting.
14 pe mechanisms of tumor cells selected during immunoediting.
15 enic mutations as an epigenetic mechanism of immunoediting.
16 anisms, including induction of tolerance and immunoediting.
17 etastatic progression, suggesting neoantigen immunoediting.
18 ening of this concept into one termed cancer immunoediting.
19 omponent of a more general process of cancer immunoediting.
20 ent AML immune evasion by proteasome-related immunoediting.
21 of immune response and immune escape through immunoediting.
22                                       Cancer immunoediting(1) is a hallmark of cancer(2) that predict
23 ity of tumours defines the process of cancer immunoediting(1).
24 at innate immune cells could manifest cancer immunoediting activity in the absence of adaptive immuni
25 ific antigens by lymphocytes is critical for immunoediting against sarcomas.
26 y players in the elimination phase of cancer immunoediting, also referred to as cancer immunosurveill
27 echanisms by which CD1e contributes to lipid immunoediting and CD1-restricted presentation to T cells
28  historical and experimental basis of cancer immunoediting and discuss its dual roles in promoting ho
29 opening new avenues for comprehending cancer immunoediting and enhancing the conversion of cold tumor
30 s a lipid transfer protein influencing lipid immunoediting and membrane transfer of PIM lipids.
31 res endogenous versus therapy-induced cancer immunoediting and outlines the molecular and cellular ch
32 nherent epigenetic mechanisms rather than by immunoediting and the consequent Darwinian selection of
33 w evidence supporting immunotherapy-mediated immunoediting and the dual opposing roles of IFNs that l
34 ent of stochastic models that explain cancer immunoediting and tumor-immune co-evolution.
35 mmune system and how these mechanisms impact immunoediting and tumour evolution.
36 ncing of immunodominant neoantigens (antigen immunoediting) and promoting an immunosuppressive tumor
37 es a deeper understanding of cancer biology, immunoediting, and evolution during ICI and promise to e
38 sociated effects of immunotherapy, including immunoediting; and allowed exploration of treatment of t
39 , there were no differences in the levels of immunoediting between initial and recurrent gliomas.
40 tory tumors obtained following the course of immunoediting by PD-1 blockade and adoptive T cell thera
41 ' that characterises each of the three Es of immunoediting, by combining wPCF measurements with the c
42                                During cancer immunoediting, cancer cells deregulate cell death execut
43 ntly been attributed to clonal selection and immunoediting, comparisons of paired primary and relapse
44 nd to differentiate between phases of cancer immunoediting concept (odds ratio: 1.17 [95% CI: 1.1-1.2
45 in autochthonous sarcomas, which demonstrate immunoediting, decreased neoantigen expression, and tumo
46                    Quantification of genetic immunoediting, defined as a lower number of neoantigens
47                                       Cancer immunoediting describes the process whereby highly immun
48 enesis or in the elimination phase of cancer immunoediting, did not play critical roles in maintainin
49              Somatic mutations together with immunoediting drive extensive heterogeneity within non-s
50        Previously, we have demonstrated that immunoediting driven by cytotoxic T lymphocytes (CTLs) e
51                                   Neoantigen immunoediting drives immune checkpoint blockade efficacy
52                                       Cancer immunoediting drives the adaptation of tumor cells to ho
53 these models cannot simulate early phases of immunoediting during initial tumorigenesis.
54 sults support that MHC-I genotype-restricted immunoediting during tumor formation shapes the landscap
55 mmunotherapy can be limited by induced tumor immunoediting (e.g., antigen loss) or through failure to
56 on and evolution into the three Es of cancer immunoediting--elimination, equilibrium, and escape.
57 cient mice recapitulated the three phases of immunoediting: elimination, equilibrium, and escape.
58 iours which resemble the 'three Es of cancer immunoediting': Equilibrium, Escape, and Elimination.
59                                       Cancer immunoediting explains the dual role by which the immune
60 idual DCIS, suggesting an active process of "immunoediting" for HER-2/neu-expressing tumor cells foll
61 or cells interact in a process called cancer immunoediting, giving rise to changes in gene expression
62 eshift mutations, showed genetic evidence of immunoediting, had higher densities of Th1, effector-mem
63                                       Cancer immunoediting has been postulated to contribute to the e
64 ar, the importance of CD8+ T cells in cancer immunoediting has been shown, and more broadly in those
65                     The principles of cancer immunoediting have set the foundations for understanding
66    Furthermore, we developed an index of the immunoediting history of each tumor sample based on the
67 ic regions and pseudogenes and evaluated the immunoediting history of each tumor.
68 ways associated with their immune status and immunoediting history.
69  provide experimental support for the cancer immunoediting hypothesis, but we also show that aggressi
70 so discuss the temporal occurrence of cancer immunoediting in metastases and whether it differs from
71                                              Immunoediting in NKC(KD) mice was restricted to MHC-I mo
72                  In this study, we evaluated immunoediting in the neu-transgenic mouse model of breas
73                            However, impaired immunoediting in the obese environment enhances tumor im
74 ng in metastases and whether it differs from immunoediting in the primary tumor of origin.
75 imination or the equilibrium phase of cancer immunoediting in the small intestine in this model.
76 r progression, independently of any need for immunoediting in the tumor microenvironment.
77 r genetic findings thus provide evidence for immunoediting in tumors and uncover mechanisms of tumor-
78 illance constitutes the first step of cancer immunoediting in which developing malignant lesions are
79 or landscape is associated with differential immunoediting, in which minor clones are marked by an in
80     This occurs through a novel mechanism of immunoediting, in which modulation of the quaternary str
81 veillance hypothesis into one termed "cancer immunoediting." In this review, we summarize the history
82                     Integration of a genetic immunoediting index with an adaptive immunity signature
83                                       Cancer immunoediting is a process by which immune cells, partic
84                                       Cancer immunoediting is a process consisting of three phases: e
85                    A central tenet of cancer immunoediting is that T-cell recognition of tumour antig
86                                       Cancer immunoediting is the process whereby immune cells protec
87                                       Cancer immunoediting is the process whereby the immune system s
88                                      'Cancer immunoediting' is a process wherein the immune system pr
89 to control and shape cancer, that is, cancer immunoediting, is the result of three processes that fun
90 mmune function that accumulate during cancer immunoediting lead to a progressive escape from host imm
91                  We conclude that epigenetic immunoediting may drive an acquired immune evasion progr
92 ating in the tumor microenvironment as a new immunoediting mechanism has not been addressed.
93                 We revealed a new neoantigen immunoediting mechanism regulated by immune forces (IL-6
94        Although proven in mice(1,3), whether immunoediting occurs naturally in human cancers remains
95 ntation, and recognition of pathogens by the immunoediting of cancer cells is, in large part, made po
96  CD8(+) T cell-mediated immune surveillance, immunoediting of chemotherapy-induced neoantigens, and d
97              We also demonstrate that cancer immunoediting of d42m1 occurs via a T-cell-dependent imm
98 rocesses(2), phenotypic differences(3-6) and immunoediting of neoantigens(7,8); however, to our knowl
99                   These results suggest that immunoediting of tumor results in cellular reprogramming
100                                              Immunoediting of tumor-associated antigens occurs in res
101 ild-type mice, suggesting an NKG2D-dependent immunoediting of tumors in this model.
102 r genome-immune interactions and the role of immunoediting or immune escape mechanisms in cancer deve
103 ng the existence of each of the three cancer immunoediting phases.
104 erons are important components of the cancer immunoediting process and function in a way that does no
105  and human clinical data supporting a cancer immunoediting process that provide the fundamental basis
106 plex I was necessary and sufficient for this immunoediting process to occur.
107 f tumor subclones, but through an epigenetic immunoediting process wherein stable transcriptional and
108 ur understanding of each phase of the cancer immunoediting process, summarizes the discovery of new p
109 dress the role of IFN-gamma in mediating the immunoediting process.
110 r dampen the immune system during the cancer immunoediting process.
111 arboured inflammatory signalling and ongoing immunoediting, reflected in loss of HLA diversity and tu
112 , many questions about the process of cancer immunoediting remain unanswered, in part because of the
113                                              Immunoediting results in reshaping the immunogenicity of
114                                During cancer immunoediting, the ability of the tumor to escape immune
115                                During cancer immunoediting, the host immune system shapes tumour fate
116                                       Cancer immunoediting, the process by which the immune system co
117                                       Cancer immunoediting, the process by which the immune system co
118                                 Thus, during immunoediting, tumor cell populations evolve strategies
119                          To quantify whether immunoediting underlies these observations, we infer tha
120                              Although cancer immunoediting was first demonstrated using mouse models
121 he stresses of innate and adaptive immunity (immunoediting), which provoke epigenetic changes in the
122 itumour T cell responses (a process known as immunoediting), which results in a clonally selected tum
123           Other cancer cells arise to resist immunoediting, which leads to a tumour that includes sev
124 unifying conceptual framework called "cancer immunoediting," which integrates the immune system's dua
125 munobiology of cancer immunosurveillance and immunoediting will hopefully stimulate development of mo
126 nding of this dynamic process, called cancer immunoediting, will provide important insights into the
127  These results suggest that coupling genetic immunoediting with activation of adaptive immunity is a
128 infiltrated tumour regions exhibited ongoing immunoediting, with either loss of heterozygosity in hum

 
Page Top