作者: David Cerna , Kevin Camphausen , Philip J. Tofilon
DOI: 10.1016/S0070-2153(05)73006-4
关键词:
摘要: Due to an increase in the understanding of molecular radiobiology, strategies for enhancing tumor radiosensitivity have begun focus on targeting molecules and processes that regulate cellular radioresponse. Toward this end, histone acetylation has receive considerable attention as a potential target radiosensitization. Histone acetylation, which is determined by competing actions acetylases (HATs) deacetylases (HDACs), plays role regulating chromatin structure gene expression--two parameters long been considered determinants As means modifying status, effort put into development inhibitors HDAC activity, often aberrant cells. This led generation relatively large number structurally diverse compounds inhibit activity result hyperacetylation, importantly, are applicable patient treatment. Whereas these antitumor preclinical cancer models when delivered single agents, recent studies indicated also significantly enhance cell radiosensitivity. A set shown vitro human lines generated from spectrum solid tumors. Moreover, increased xenografts. Although mechanism responsible radiosensitization not definitely elucidated, data suggest inhibiting repair radiation-induced DNA damage may be involved. currently clinical trials modalities combination with chemotherapeutic results effectiveness radiotherapy.