Clinical trials: The sensitizing side of Onyx-015
نویسندگان
چکیده
منابع مشابه
Evaluation of Clinical Trials
In a number of important clinical issues such as evaluation of the efficacy or effectiveness of therapeutic or preventive interventions as well as for comparing the harms of interventions, randomized controlled trials (RCTs) provide the highest levels of evidence, either directly or indirectly. It is obvious that critical appraisal of these studies to assess their validity and precision is of p...
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ONYX-015 has been reported to kill selectively tumor cells lacking functional p53. Genetic alterations of INK4a/ARF locus, which is a predominant event in malignant pleural mesothelioma, may result in loss of p14(ARF) and subsequent disruption of p53 pathway in cancer cells. In the present study, ONYX-015 was able to kill three mesothelioma cell lines (H28, H513, and 211H) with wild-type p53 bu...
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Increased knowledge of how normal cell growth is altered during tumorigenesis has led to the development of novel approaches to killing cancer cells. However, the application of novel tumor therapies, like conventional therapies, still depends on there being an effective means of selectively targeting tumors. One new approach uses an attenuated adenovirus (Ad) that has been designated ONYX-015 ...
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The 55-kDa E1B protein of adenovirus, which binds to and inactivates the tumor suppressor protein p53, is not expressed in the adenoviral mutant termed ONYX-015 (i.e., dl1520). It was reported that the mutant virus due to a deletion in E1B is able to replicate only in cells deficient for wild-type p53. Accordingly, dl1520 is currently being evaluated as a potential tool in the therapy of p53 de...
متن کاملLate viral RNA export, rather than p53 inactivation, determines ONYX-015 tumor selectivity.
ONYX-015 is an adenovirus that lacks the E1B-55K gene product for p53 degradation. Thus, ONYX-015 was conceived as an oncolytic virus that would selectively replicate in p53-defective tumor cells. Here we show that loss of E1B-55K leads to the induction, but not the activation, of p53 in ONYX-015-infected primary cells. We use a novel adenovirus mutant, ONYX-053, to demonstrate that loss of E1B...
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ژورنال
عنوان ژورنال: Gene Therapy
سال: 2005
ISSN: 0969-7128,1476-5462
DOI: 10.1038/sj.gt.3302429