Li Lan, MD, PhD

Associate Professor

Dr. Li Lan


Fax: 412-623-7761

2.6 Hillman Cancer Center

5117 Centre Avenue

Pittsburgh, PA 15213-1862


MD, Tohuku University, Sendai (Japan)

PhD, Tohuku University, Sendai (Japan)

Research Summary

The long-term goal of my lab is to understand the mechanisms by which cells maintain genome stability against oxidative stress and its impact on aging and cancer, employing various aspects of basic cell biology, state-of-the-art live cell imaging techniques and animal models. We are now focusing on two major directions.

(1). Transcription-coupled oxidative DNA damage response and human diseases: My group has aimed to reveal how transcription-coupled DNA repair mechanisms contribute to genome stability. We developed the DNA Damage at RNA Transcribed sites (DART) system (Mol Cell 2010, NAR 2014), which is a unique and precise approach that allows oxidative DNA damage to be introduced at a specific transcribed region in a dose-dependent manner. Recently, our research led to the discovery of a novel RNA-templated HR mechanism of DSB repair at active transcription sites in G0/G1 cell populations (PNAS 2015). (2). The telomere’s response to oxidative DNA damage and cancer: Our group has made a breakthrough with a novel technique for introducing oxidative damage specifically at the telomeres in a highly controlled manner and discovered the mechanisms for telomere maintenance in cancer cells (NAR 2015, Mol Cell 2017). Given the importance of telomeres in stem cell self-renewal, pursuing the regulating mechanisms of telomere maintenance will also have a broad impact on advancing research on organogenesis, tissue regeneration, and aging, as well as providing a potential drug discovery platform to develop new chemo- and radio-sensitizing agents.

Click here for a full listing of publications

Research Lab Affiliation


Tan R, Nakajima S, Zeng X, Yates N, Smithgall TE, Lei M, Jiang Y, Levine AS, Su B and Lan L. (2017) Nek7 protects telomeres from oxidative DNA damage by phosphorylation and stabilization of TRF1. Mol Cell. [in press] |  

Sun L, Nakajima S, Teng Y, Chen H, Yang L, Chen X, Gao B, Levine AS, Lan L. (2017) WRN is recruited to damaged telomeres via its RQC domain and tankyrase1-mediated poly-ADP-ribosylation of TRF1. Nucleic Acids Res. |  View Abstract

Yang L, Sun L, Teng Y, Chen H, Gao Y, Levine AS, Nakajima S, Lan L. (2017) Tankyrase1-mediated poly(ADP-ribosyl)ation of TRF1 maintains cell survival after telomeric DNA damage. Nucleic Acids Res. |  View Abstract

Gao Y, Li C, Wei L, Teng Y, Nakajima S, Ma H, Spagnol ST, Leger B, Wan Y, Dahl KN, Liu Y, Levine AS, Lan L. (2017) SSRP1 cooperates with PARP and XRCC1, facilitating single strand break repair through chromatin priming. Cancer Res. (In press) |  

Wei L, Nakajima S, Bohm S, Bernstein KA, Shen Z, Tsang M, Levine AS and Lan L. (2015) DNA damage during the G0/G1 phase triggers RNA-templated, Cockayne syndrome B-dependent homologous recombination. Proc Natl Acad Sci USA. 112: E3495-E3504. |  View Abstract