ArticleCancer biology & therapy2017
Adenovirus-based strategies enhance antitumor capability through p53-mediated downregulation of MGMT in uveal melanoma.
Article in Cancer biology & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Ubiquitination and degradation of MGMT by TRIM72 increases the sensitivity of uveal melanoma cells to Dacarbazine treatment.Cancer biomarkers : section A of Disease markers · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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Abstract
Uveal melanoma (UM) is an intractable disease with a low survival rates, despite adequate local treatment, as a result of its metastatic characteristics. Thus, new therapeutic strategies, including combinations of novel gene therapy and traditional chemotherapy, are under investigation to improve long-term prognosis. Dacarbazine or DTIC, an alkylating agent which results in DNA methylation, is most commonly used to treat melanoma but the response is very limited. The O6-methylguanine DNA methyl transferase (MGMT), a DNA repair protein, is involved in chemoresistance in DTIC treatment. We previously investigated a combination of oncolytic adenovirus H101 and the alkylating agent DTIC in the treatment of UM cells in vitro and observed a synergistic antitumor effect. In this study, we validated this result and report an enhanced therapeutic effect in vivo. Our findings also demonstrated that the oncolytic adenovirus H101 decreased MGMT levels via accumulation of p53 overcoming DTIC chemoresistance. Therefore, the clinical therapeutic efficacy of DTIC in the treatment of UM might be improved using this adenovirus-based combination therapy.
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