A photo of Qing Richard Lu.

Qing Richard Lu, PhD

  • Beatrice C. Lampkin Endowed Chair in Cancer Epigenetics
  • Scientific Director, Brain Tumor Center
  • Professor, UC Department of Pediatrics



I have been interested in neuroscience and cancer biology to uncover the mechanisms and pathways that interconnect the nervous system with diseases and cancer. Our current research activities focus on 1) how distinct glial cell types such as myelinating oligodendrocytes and their stem/progenitor cells contribute to neurological diseases, and 2) how dysregulated developmental programs and tumor microenvironment cross-communications contribute to tumorigenesis, recurrence and metastasis both in the central and peripheral nervous systems.

As a developmental and cancer biologist, I have been studying gliogenesis, myelination and tumor biology, spanning brain and nerve sheath tumors. During my postdoctoral work in Dr. Charles Stiles’ lab at the Dana-Farber Cancer Institute, Harvard Medical School, I sought the lineage-specific factors that control glial cell fate specification from multipotent neural stem/progenitor cells. I discovered a pair of bHLH transcription factors, Olig1 and Olig2, which are critical for oligodendrocyte lineage development. These findings have set a key milestone in understanding the molecular mechanisms of gliogenesis and brain tumorigenesis.

My work as an independent investigator, starting at UT Southwestern and now at Cincinnati Children’s, where I am the Scientific Director of the Brain Tumor Center, has used a combination of state-of-the-art molecular genetic approaches and adopted novel concepts to address the mechanisms underlying neural tumorigenesis and demyelinating neurological disorders, such as multiple sclerosis, as well as autism spectrum disorders. My lab has a strong translational theme with two major directions: 1) development of targeted therapy, radiotherapy, and immunotherapy to treat brain tumors such as medulloblastoma and malignant gliomas, including glioblastoma and diffuse midline gliomas (DMG / DIPG); 2) development of novel therapeutics for promoting myelin repair to treat neurodegenerative disorders, such as the devastating demyelinating disease multiple sclerosis. Our research goals include dissecting the etiological mechanisms of these neurological diseases and cancers to develop effective therapies by promoting functional regeneration while blocking brain tumorigenesis and recurrence. Our studies have contributed to an understanding of critical genetic and epigenetic mechanisms that regulate myelin repair, brain tumorigenesis and therapeutic efficacy.

I am honored to be the recipient of several awards, including:

  • Best Research Award, Cincinnati Children’s (2018)
  • Beatrice C. Lampkin Endowed Chair in Cancer Epigenetics (2018)
  • Javits Neuroscience Award from the National Institutes of Health / National Institute of Neurological Disorders and Stroke (2016)
  • Best Team Award, Brain Tumor Center, Cincinnati Children’s (2015)
  • Harry Weaver Neuroscience Award from the National Multiple Sclerosis Society (2003–2008)
  • Basil O’Connor Scholarship from the March of Dimes Birth Defect Foundation (2004–2006)

I’ve been a researcher for over 20 years, and I began my work at Cincinnati Children’s in 2013. I have supported young researchers who wish to pursue a career in biomedical science. More than a dozen of my past trainees have become independent principal investigators with academic ranks from assistant to full professor in educational research institutions.

BS: Peking Normal University, Beijing, China, 1988.

MS: Rutgers University, Piscataway, NJ, 1993.

PhD: Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ, 1997.

Postdoctoral Fellow: Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, 1997-2002.


Neuro-oncology; neurology


Neoplastic stem cells; malignant glioma; pediatric brain tumors such as medulloblastoma, ependymoma, and diffuse midline gliomas (DMG / DIPG); tumor microenvironment and immunotherapy; myelinogenesis and myelin repair in neurodegenerative disorders such as devastating multiple sclerosis; epigenetics and chromatin remodeling control

Research Areas

Experimental Hematology and Cancer Biology, Cancer and Blood Diseases, Developmental Biology



Loss of phosphatase CTDNEP1 potentiates aggressive medulloblastoma by triggering MYC amplification and genomic instability. Luo, Z; Xin, D; Liao, Y; Berry, K; Ogurek, S; Zhang, F; Zhang, L; Zhao, C; Rao, R; Dong, X; et al. Nature Communications. 2023; 14:762.


Nuclear condensates of YAP fusion proteins alter transcription to drive ependymoma tumourigenesis. Hu, X; Wu, X; Berry, K; Zhao, C; Xin, D; Ogurek, S; Liu, X; Zhang, L; Luo, Z; Sakabe, M; et al. Nature Cell Biology. 2023; 25:323-336.


Human fetal cerebellar cell atlas informs medulloblastoma origin and oncogenesis. Luo, Z; Xia, M; Shi, W; Zhao, C; Wang, J; Xin, D; Dong, X; Xiong, Y; Zhang, F; Berry, K; et al. Nature. 2022; 612:787-794.


EED-mediated histone methylation is critical for CNS myelination and remyelination by inhibiting WNT, BMP, and senescence pathways. Wang, J; Yang, L; Dong, C; Wang, J; Xu, L; Qiu, Y; Weng, Q; Zhao, C; Xin, M; Lu, QR. Science Advances. 2020; 6:eaaz6477.


Single-Cell Transcriptomics in Medulloblastoma Reveals Tumor-Initiating Progenitors and Oncogenic Cascades during Tumorigenesis and Relapse. Zhang, L; He, X; Liu, X; Zhang, F; Huang, LF; Potter, AS; Xu, L; Zhou, W; Zheng, T; Luo, Z; et al. Cancer Cell. 2019; 36:302-318.e7.


Single-Cell Transcriptomics Uncovers Glial Progenitor Diversity and Cell Fate Determinants during Development and Gliomagenesis. Weng, Q; Wang, J; Wang, J; He, D; Cheng, Z; Zhang, F; Verma, R; Xu, L; Dong, X; Liao, Y; et al. Cell Stem Cell. 2019; 24:707-723.e8.


A histone deacetylase 3-dependent pathway delimits peripheral myelin growth and functional regeneration. He, X; Zhang, L; Queme, LF; Liu, X; Lu, A; Waclaw, RR; Dong, X; Zhou, W; Kidd, G; Yoon, S; et al. Nature Medicine. 2018; 24:338-351.


Olig2-Dependent Reciprocal Shift in PDGF and EGF Receptor Signaling Regulates Tumor Phenotype and Mitotic Growth in Malignant Glioma. Lu, F; Chen, Y; Zhao, C; Wang, H; He, D; Xu, L; Wang, J; He, X; Deng, Y; Lu, EE; et al. Cancer Cell. 2016; 29:669-683.


The G protein α subunit Gαs is a tumor suppressor in Sonic hedgehog-driven medulloblastoma. He, X; Zhang, L; Chen, Y; Remke, M; Shih, D; Lu, F; Wang, H; Deng, Y; Yu, Y; Xia, Y; et al. Nature Medicine. 2014; 20:1035-1042.


Olig2 targets chromatin remodelers to enhancers to initiate oligodendrocyte differentiation. Yu, Y; Chen, Y; Kim, B; Wang, H; Zhao, C; He, X; Liu, L; Liu, W; Wu, LM N; Mao, M; et al. Cell. 2013; 152:248-261.