ArticleComputational and mathematical methods in medicine2014
Systematic analysis of time-series gene expression data on tumor cell-selective apoptotic responses to HDAC inhibitors.
Article in Computational and mathematical methods in medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 4 citations in OpenAlex.
- Uncovering Effective Explanations for Interactive Genomic Data Analysis.Patterns (New York, N.Y.) · 2020Article
- HEDD: the human epigenetic drug database.Database : the journal of biological databases and curation · 2016Article
- The role of epigenetics in kidney malignancies.Central European journal of urology · 2015Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
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Abstract
SAHA (suberoylanilide hydroxamic acid or vorinostat) is the first nonselective histone deacetylase (HDAC) inhibitor approved by the US Food and Drug Administration (FDA). SAHA affects histone acetylation in chromatin and a variety of nonhistone substrates, thus influencing many cellular processes. In particularly, SAHA induces selective apoptosis of tumor cells, although the mechanism is not well understood. A series of microarray experiments was recently conducted to investigate tumor cell-selective proapoptotic transcriptional responses induced by SAHA. Based on that gene expression time series, we propose a novel framework for detailed analysis of the mechanism of tumor cell apoptosis selectively induced by SAHA. Our analyses indicated that SAHA selectively disrupted the DNA damage response, cell cycle, p53 expression, and mitochondrial integrity of tumor samples to induce selective tumor cell apoptosis. Our results suggest a possible regulation network. Our research extends the existing research.
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