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1 in tumor cells results in their destruction (oncolysis).
2  recent attention as an anticancer strategy (oncolysis).
3  within tumors can mediate tumor regression (oncolysis).
4 ancer cells can result in their destruction (oncolysis).
5 ations in cell lines relatively resistant to oncolysis.
6 ctious particle production, and cytotoxicity/oncolysis.
7 ity of human melanoma types for VSV-mediated oncolysis.
8 interferon application, indicating selective oncolysis.
9 6 interactions to sensitize gliomas to viral oncolysis.
10 ide insight into the complex nature of viral oncolysis.
11 ial ovarian cancer cells and cause efficient oncolysis.
12 ring sites of HSV-TK expression during viral oncolysis.
13  other viruses in ongoing clinical trials of oncolysis.
14 n cancer cells for efficient replication and oncolysis.
15 on that may help explain mechanisms of viral oncolysis.
16 s and thus play a large role in facilitating oncolysis.
17 y for development of HSV-1 mutants for viral oncolysis.
18 roy tumors in a process referred to as viral oncolysis.
19 e, which can be cytokine-enhanced to improve oncolysis.
20 ne expression, de novo virus production, and oncolysis.
21  which was shown to enhance viral spread and oncolysis.
22 eny virion in a process referred to as viral oncolysis.
23 significantly reducing viral replication and oncolysis.
24 tiviral immunity, limiting viral replication/oncolysis.
25 to prevent virus neutralization and maximize oncolysis.
26 developed to exploit the unique mechanism of oncolysis afforded by tumor-specific viral replication.
27  and improved overall survival compared with oncolysis alone.
28 its increased efficacy over that mediated by oncolysis alone.
29 ped for gene therapy, vaccination, and viral oncolysis and are extensively used for gene transduction
30  to induce significant tumor control through oncolysis and immune repolarization.
31 ally altering the kinetics of virus-mediated oncolysis and may be useful in the treatment of malignan
32 mune-incompetent mice, suggesting that viral oncolysis and not the host immune response is the primar
33 immune responses by NDV results in selective oncolysis and offer a novel and safe virotherapy platfor
34 of the dual therapeutic benefit of selective oncolysis and P450 transgene delivery.
35                                  Combination oncolysis and prodrug bioactivation leads to significant
36 atment with CPA enhances HSV replication and oncolysis and reduces an HSV-mediated increase in CD68+
37 ts in a series of sequential events, such as oncolysis and release of tumor and viral antigens, dendr
38                              We imaged viral oncolysis and tumor response to oncolysis sequentially w
39  MV may have utility as vectors for targeted oncolysis and vaccination.
40 static burden was initially reduced by viral oncolysis and was then eradicated, as tumor cell killing
41 ous in their susceptibility to virus-induced oncolysis, and several cell lines were resistant to all
42 mune recognition, favoring oHSV replication, oncolysis, and spread.
43 mediate multiple antitumor effects including oncolysis, apoptosis, induction of T-cell responses, and
44 imally invasive focal therapies for nonviral oncolysis are a cornerstone of cancer therapeutics.
45 py has brought the old concept of adenovirus oncolysis back into the spotlight.
46 ression of hsp 70i also enhanced Ad-mediated oncolysis but did not decrease intracellular Ad DNA leve
47                                              Oncolysis by a replicating HSV-1 mutant combined with th
48 t into the basis for susceptibility to viral oncolysis by agents such as HSV1.
49                                    Selective oncolysis by Ar6pAE2fF was dependent on the presence of
50  be the use of local hyperthermia to augment oncolysis by increasing the burst of replication-compete
51 NF-alpha signalling pathway is implicated in oncolysis by reducing the viability of ZIKV-infected bra
52 k squamous cell carcinoma (HNSCC) lines from oncolysis by vesicular stomatitis virus (VSV).
53 lls were less sensitive or even resistant to oncolysis by wild-type virus.
54  and that unusually strong resistance to VSV oncolysis can be overcome with interferon attenuators.
55 multimodal treatment allowed by rRp450 viral oncolysis combined with CPA/CYP2B1 and GCV/HSV-TK gene t
56               One barrier to effective viral oncolysis, consisting of the interferon (IFN) response i
57  enabled both efficient Ad gene transfer and oncolysis for otherwise resistant RMS cells, suggesting
58 lore the utility of adenovirus (Ad)-mediated oncolysis for rhabdomyosarcoma (RMS), we tested RMS cell
59       The RGD modification enabled increased oncolysis for RMS cells by a conditionally replicative A
60 by oncolytic viruses (OVs), including direct oncolysis, immune activation, and tumor microenvironment
61 or I) strongly stimulate VSV replication and oncolysis in all resistant cell lines but only partially
62 of mice with C3L5 cells that underwent viral oncolysis in combination with Flt3L or granulocyte-macro
63 emonstrate that M51R VSV efficiently induces oncolysis in GBM tumor cells despite deregulation of apo
64 II capsid enhanced efficient replication and oncolysis in MO59J gliomas cells; other gliomas tested r
65 n, we found a strong susceptibility to viral oncolysis in over 70% of melanomas.
66 1, enhanced the efficacy of reovirus-induced oncolysis in vitro and in vivo.
67 inhibition compromises viral infectivity and oncolysis in vitro or anticancer efficacy in vivo.
68  ad5/IFN was the result of two events: viral oncolysis in which tumor cells are being selectively lys
69  tumor cell degradation resulting from viral oncolysis increases over time, which limits intracellula
70                              rRp450-mediated oncolysis is enhanced in the presence of cyclophosphamid
71 host cell factors needed for infectivity and oncolysis, is lacking.
72 FN-alpha and -beta differentially affect VSV oncolysis, justifying the evaluation and comparison of I
73  Concurrently, oncolytic virotherapy-induced oncolysis leads to further release of neoantigens and su
74 tive expression of ICP34.5 in the context of oncolysis may be useful.
75       Alternatively, susceptibility to viral oncolysis may change during cancer progression.
76                                              Oncolysis of cell lines was similar to that of a wild-ty
77                                HSV1-mediated oncolysis of diffuse liver metastases is effective in mi
78 l targeted agents for gene therapy and viral oncolysis of metastatic melanoma.
79 d throughout the tumor mass and cause direct oncolysis of tumor cells.
80 ers and HSV-TK protein in the tumor as viral oncolysis proceeds, tumor cell degradation resulting fro
81                                     Although oncolysis releases tumor epitopes and provides costimula
82 fects, and (Ad5/3-hTERT-E1A-hCD40L)-mediated oncolysis resulted in enhanced calreticulin exposure and
83  coculture assays, ICOVIR-15K-cBiTE-mediated oncolysis resulted in robust T-cell activation, prolifer
84 imaged viral oncolysis and tumor response to oncolysis sequentially with bioluminescence and positron
85               The role of hsp in Ad-mediated oncolysis should be additionally explored.
86 d14P1 showed more efficient viral spread and oncolysis than Ad14.
87 effective at protecting HNSCC cells from VSV oncolysis than was IFN-alpha2a.
88                                        Viral oncolysis, the destruction of cancer cells by replicatin
89                                        Viral oncolysis, the destruction of cancer cells by replicatin
90 h has potential utility for monitoring viral oncolysis therapy in patients.
91  significantly increase the potency of viral oncolysis; this may lead to an enhanced clinical perform
92 hat immune activation may combine with viral oncolysis to induce tumor eradication in this model, pro
93 emonstrate that the addition of direct viral oncolysis to the HSV-tk/GCV suicide gene system resulted
94 lls either resistant or susceptible to viral oncolysis, we discovered that the epithelial phenotype o
95 ected pancreatic cancer cells were killed by oncolysis, whereas infection of stellate cells reduced f
96 ock resulted in augmentation of Ad burst and oncolysis while decreasing total intracellular Ad DNA.
97 cate in tumor cells, where they kill through oncolysis while sparing normal cells.
98    Preclinical and clinical studies of viral oncolysis will benefit significantly from development of
99 results indicate that a combination of viral oncolysis with a virus of low pathogenicity, itself resi