EPIGENIC TOXICITY OF POLYCYCLIC AROMATIC HYDROCARBONS

点击翻译按钮获取中文摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Polycyclic aromatic hydrocarbons (PAHs) are abundant components of tobacco smoke that have been implicated in cancer formation. A large body of work indicates that these compounds induce genetic damage and this results cancer. However, cancer is not solely the consequence of non-reversible mutagenic events but also involves reversible, epigenetic events. Thus, there is a need to reassess the toxicity of PAHs at the epigenetic level. Gap junctional intercellular communication (GJIC) centrally modulates signal transduction pathways that epigenetically alters gene expression. There is considerable evidence linking abnormal regulation of GJIC with the non-genotoxic steps of tumor promotion. We have worked with the Upham laboratory to devise a proteomics approach to detect early changes in protein abundance and post-translational modification due to PAHs.