Cancer arises from a progression of acquired genomic mutations, with significant portions corresponding to point mutations, insertions and deletions in critical cell growth regulating genes.  Chemical alkylating agents from endogenous metabolic processes and chemical exposures can result in the alkylation and oxidation of DNA and formation of highly pro-mutagenic types of DNA damage.  Additionally, small molecule-induced DNA damage is amongst the most commonly used strategies for treating cancer, whereby replication and transcription are stalled.  However, problems related with adverse toxicities and drug resistance can arise, including from the cell’s programmed response to remove chemically-induced DNA damage. In order to advance precision prevention and therapeutic strategies, there is a need to better understand the basis of toxic selectivity of DNA damage, how the distribution of damage on a genomic scale relates with the acquisition of mutations, and to create new strategies for stratifying responsive cancer patients.  The talk will concern studies focusing on relationships between the chemical structures and biochemical effects of chemical and drug-induced DNA damage, and how DNA damage response pathways impact genomic damage patterns and cellular responses. In the results, we have identified non-canonical nucleic acid structures and genome alterations relevant for diagnostic purposes in the prevention and treatment of cancer.

Striking at cancer genomes with chemistry arrows

ACS Spring Meeting 2021

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.