The histone deacetylase (HDAC) inhibitor vorinostat has received significant attention in recent years as an ‘epigenetic’ drug used to treat solid tumors. However, its mechanisms of action are not entirely understood, particularly with regard to its interaction with the aberrations in 3D nuclear structure that accompany neoplastic progression.
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- Nandakumar, Vivek (Author)
- Hansen Katdare, Nanna (Author)
- Glenn, Honor (Author)
- Han, Jessica (Author)
- Helland, Stephanie (Author)
- Hernandez, Kathryn (Author)
- Senechal, Patti (Author)
- Johnson, Roger (Author)
- Bussey, Kimberly J. (Author)
- Meldrum, Deirdre (Author)
- Ira A. Fulton Schools of Engineering (Contributor)
- Digital object identifier: 10.1038/srep30593
- Identifier TypeInternational standard serial numberIdentifier Value2045-2322
- The final version of this article, as published in Scientific Reports, can be viewed online at: http://www.nature.com/articles/srep30593, opens in a new window
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Nandakumar, V., Hansen, N., Glenn, H. L., Han, J. H., Helland, S., Hernandez, K., . . . Meldrum, D. R. (2016). Vorinostat differentially alters 3D nuclear structure of cancer and non-cancerous esophageal cells. Scientific Reports, 6(1). doi:10.1038/srep30593