Abstract
Background: Glioblastoma is the most common primary adult brain tumor. Surgery followed by radiation therapy in combination with temozolomide (Tmz) produces a median survival of 14.6 months. Tmz is a DNA akylating agent that leads to the mispairing of guanine residues with thymine. An intact mismatch-repair mechanism (MMR) converts the mispaired thymine into a lethal double-strand DNA break. Vorinostat (SAHA), an HDAC inhibitor, has been shown to act as a radiosensitizer, possibly through inhibition of DNA repair. SAHA has successfully been combined with a number of cytotoxic agents. We hypothesized that SAHA would further potentiate the radiosensitizing properties of Tmz in glioblastoma.
American Association for Cancer Research (AACR) 101st Annual Meeting April 17-21, Washington, DC
Recommended Citation
Lawrence, Y. R.; Liu, Y.; Andersen, B.; Xia, X.; Dicker, A. P.; and Wachsberger, P.
(2010)
"Functional Antagonism Between Vorinostat and Temozolomide when Combined with Ionizing Radiation (IR) in Glioblastoma,"
Bodine Journal: Vol. 3:
Iss.
1, Article 2.
DOI: https://doi.org/10.29046/TBJ.003.1.001
Available at:
https://jdc.jefferson.edu/bodinejournal/vol3/iss1/2