Research

Multiple processes contribute to somatic mutations in cancer genomes, these mutations mainly arise from three sources: 1) Dysfunctions of DNA polymerases, including mutations in replicative polymerase or the activity of translesion synthesis polymerase; 2) Environmental exposures and drug treatment, such as UV radiation and tobacco smoking; 3) Endogenous metabolism. Understanding the origin of these mutational signatures will help us prevent and intervene the cancer initiation, progression, and drug resistance. Tang lab focuses on leveraging mass spectrometry, gene editing and next-generation sequencing techniques to study how DNA damage induced by environmental exposure and endogenous metabolism contributes to cancer and other aging-related diseases. By developing a series of cutting-edge techniques to analyze the genome-wide distributions and proteome-wide interactions of DNA damage and repair proteins, we aim to achieve our goals of studying the fundamental mechanisms of DNA repair, understanding disease etiology, and monitoring treatment efficacy.