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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 ctious particle production, and cytotoxicity/oncolysis.
6 ity of human melanoma types for VSV-mediated oncolysis.
7 interferon application, indicating selective oncolysis.
8 6 interactions to sensitize gliomas to viral oncolysis.
9 ide insight into the complex nature of viral oncolysis.
10 ial ovarian cancer cells and cause efficient oncolysis.
11 ring sites of HSV-TK expression during viral oncolysis.
12 other viruses in ongoing clinical trials of oncolysis.
13 n cancer cells for efficient replication and oncolysis.
14 on that may help explain mechanisms of viral oncolysis.
15 s and thus play a large role in facilitating oncolysis.
16 y for development of HSV-1 mutants for viral oncolysis.
17 roy tumors in a process referred to as viral oncolysis.
18 e, which can be cytokine-enhanced to improve oncolysis.
19 ne expression, de novo virus production, and oncolysis.
20 which was shown to enhance viral spread and oncolysis.
21 eny virion in a process referred to as viral oncolysis.
22 significantly reducing viral replication and oncolysis.
23 developed to exploit the unique mechanism of oncolysis afforded by tumor-specific viral replication.
26 ped for gene therapy, vaccination, and viral oncolysis and are extensively used for gene transduction
27 ally altering the kinetics of virus-mediated oncolysis and may be useful in the treatment of malignan
28 mune-incompetent mice, suggesting that viral oncolysis and not the host immune response is the primar
29 immune responses by NDV results in selective oncolysis and offer a novel and safe virotherapy platfor
32 atment with CPA enhances HSV replication and oncolysis and reduces an HSV-mediated increase in CD68+
35 static burden was initially reduced by viral oncolysis and was then eradicated, as tumor cell killing
36 ous in their susceptibility to virus-induced oncolysis, and several cell lines were resistant to all
37 mediate multiple antitumor effects including oncolysis, apoptosis, induction of T-cell responses, and
39 ression of hsp 70i also enhanced Ad-mediated oncolysis but did not decrease intracellular Ad DNA leve
43 be the use of local hyperthermia to augment oncolysis by increasing the burst of replication-compete
46 and that unusually strong resistance to VSV oncolysis can be overcome with interferon attenuators.
47 multimodal treatment allowed by rRp450 viral oncolysis combined with CPA/CYP2B1 and GCV/HSV-TK gene t
49 enabled both efficient Ad gene transfer and oncolysis for otherwise resistant RMS cells, suggesting
50 lore the utility of adenovirus (Ad)-mediated oncolysis for rhabdomyosarcoma (RMS), we tested RMS cell
52 or I) strongly stimulate VSV replication and oncolysis in all resistant cell lines but only partially
53 of mice with C3L5 cells that underwent viral oncolysis in combination with Flt3L or granulocyte-macro
54 emonstrate that M51R VSV efficiently induces oncolysis in GBM tumor cells despite deregulation of apo
55 II capsid enhanced efficient replication and oncolysis in MO59J gliomas cells; other gliomas tested r
58 ad5/IFN was the result of two events: viral oncolysis in which tumor cells are being selectively lys
59 tumor cell degradation resulting from viral oncolysis increases over time, which limits intracellula
61 FN-alpha and -beta differentially affect VSV oncolysis, justifying the evaluation and comparison of I
68 ers and HSV-TK protein in the tumor as viral oncolysis proceeds, tumor cell degradation resulting fro
70 fects, and (Ad5/3-hTERT-E1A-hCD40L)-mediated oncolysis resulted in enhanced calreticulin exposure and
71 coculture assays, ICOVIR-15K-cBiTE-mediated oncolysis resulted in robust T-cell activation, prolifer
72 imaged viral oncolysis and tumor response to oncolysis sequentially with bioluminescence and positron
79 significantly increase the potency of viral oncolysis; this may lead to an enhanced clinical perform
80 hat immune activation may combine with viral oncolysis to induce tumor eradication in this model, pro
81 emonstrate that the addition of direct viral oncolysis to the HSV-tk/GCV suicide gene system resulted
82 lls either resistant or susceptible to viral oncolysis, we discovered that the epithelial phenotype o
83 ock resulted in augmentation of Ad burst and oncolysis while decreasing total intracellular Ad DNA.
85 Preclinical and clinical studies of viral oncolysis will benefit significantly from development of
86 results indicate that a combination of viral oncolysis with a virus of low pathogenicity, itself resi
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