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What We Study:

How cancer genomes arise and how cancer cells tolerate DNA damage.

Why We Study These Problems:

Mutagenesis and DNA damage tolerance drive carcinogenesis and enable cancer cells to adapt, evolve and resist therapy.  Understanding mechanisms of mutagenesis and DNA damage tolerance will help explain how cancer arises and identify molecular vulnerabilities that can be exploited to prevent and treat cancer.

Our Approach:

Trans-Lesion Synthesis (TLS) is a specialized mode of DNA replication that is both error-prone and DNA damage-tolerant.

We have found that cancer cells specifically activate TLS.  Therefore, TLS provides potential ways for cancer cells to mutate their genomes and resist intrinsic and therapeutic stress.  We are using diverse approaches to elucidate regulatory mechanisms and roles of TLS in normal cells and cancer cells.

Key words: 

Cell Cycle, DNA Replication, DNA Repair, Mutagenesis, Cancer, Chemotherapy, Biochemistry, Molecular Biology, Genetics & Genomics