Li Lan

About

Li Lan is an Associate Professor of Molecular Genetics and Microbiology, as well as in Pharmacology and Cancer Biology, and a member of the Duke Cancer Institute. Her lab is dedicated to researching how cancer cells respond to DNA damage through DNA repair mechanisms and developing innovative strategies to target these pathways in cancer therapy. Her significant contributions include uncovering the critical role of PARP in DNA repair, leading to successful applications of PARP inhibitors in the treatment of breast, ovarian, and other types of cancer. Her research studies how DNA responds to oxidative damage at specific chromosomal locations, advancing understanding of DNA damage response in different chromosomal environments. Recently, her investigations have revealed a novel mRNA and R-loop-dependent DNA repair pathway that acts as a protective mechanism for transcribed regions of the genome, introducing a new paradigm in DNA repair research. Her research interests encompass unraveling the mechanisms of mRNA and R-loop-dependent DNA repair (RDDR) in cancer, developing targeted therapies, and exploring the molecular regulation of the RDDR pathway, including its interaction with DNA replication and chromatin remodeling. She employs screening platforms to monitor RDDR and aims to develop inhibitors that disrupt RDDR in cancer cells, as well as identify biomarkers for patient stratification and therapy response prediction. Her work also explores the potential applications of…

Research topics

• Biology
• Cell biology
• Genetics
• Molecular biology

Selected publications

• Transcription‐coupled <scp>DNA</scp> repair protects genome stability upon oxidative stress‐derived <scp>DNA</scp> strand breaks

  FEBS Letters · 2024-05-30 · 7 citations

  reviewOpen accessSenior authorCorresponding

  Elevated oxidative stress, which threatens genome stability, has been detected in almost all types of cancers. Cells employ various DNA repair pathways to cope with DNA damage induced by oxidative stress. Recently, a lot of studies have provided insights into DNA damage response upon oxidative stress, specifically in the context of transcriptionally active genomes. Here, we summarize recent studies to help understand how the transcription is regulated upon DNA double strand breaks (DSB) and how…

  PublisherOA PDFDOI

• Abstract B010: Exploring the synthetic lethal interactions between mRNA methyl-5-cytocine at sites of R-loops and mismatch repair deficiency in solid tumor

  Cancer Research · 2025-03-11

  article1st authorCorresponding

  Abstract The RNA methyltransferase TRDMT1 generates 5-methyl Cytosine (m5C) at R-loops which promotes transcription coupled homologous recombination (TC-HR) and thus impedes cellular sensitivity to R-loop induced DNA double-strand breaks (DSBs) at transcribing regions of the genome. We performed TRDMT1 inhibitor based drug screening approach in 300 cancer cell lines and identifies key factors associated with DNA mismatch repair (MMR) pathway especially in solid tumors. The R-loop accumulation co…

  PublisherDOI

• 1928 Previous use of chemotherapy or multikinase inhibitor decreases efficacy of Pralsetinib in RET fusionpositive non-small-cell lung cancer

  Radiotherapy and Oncology · 2025-05-01

  article
  PublisherDOI

• cGAS restricts PARP1-mediated microhomology-mediated end joining by suppressing poly-ADP-ribosylation

  Cell Death and Differentiation · 2025-12-17

  articleSenior author
  PublisherDOI

• Abstract PR001: Targeting mRNA methyltransferase in RNA-dependent DNA repair in cancer therapy

  Molecular Cancer Therapeutics · 2024-11-14

  article1st authorCorresponding

  Abstract The treatment of many solid tumors presents significant challenges with chemotherapy, radiation therapy, and the limited effectiveness of immunotherapy. Targeted therapy offers a promising approach, yet the lack of validated targets limits its applicability across the spectrum of solid tumors. Our past studies have revealed that an R-loop and mRNA-dependent DNA repair (RDDR) pathway, induced by damage at the transcribed regions of the genome, contributes to cell survival and drug resist…

  PublisherDOI

Recent grants

• NIH Grant R21AG045545

  NIH · $422k · 2016

• NIH Grant R01GM118833

  NIH · $1.6M · 2022

Frequent coauthors

• Lee Zou

  Harvard University

  75 shared

• Satoshi Nakajima

  62 shared

• Arthur S. Levine

  University of Miami

  51 shared

• Yaqun Teng

  Peking Union Medical College Hospital

  46 shared

• Akira Yasui

  SPring-8

  39 shared

• Jian Ouyang

  MUSC Hollings Cancer Center

  38 shared

• Haibo Yang

  Shenyang University of Technology

  38 shared

• Leizhen Wei

  38 shared

Labs

• Lan LabPI

Similar researchers at Duke University

• Douglas Alan Marchukh-110
• Jack Donald Keeneh-100
• Hiroaki Matsunamih-86