Dr. Qing Richard Lu, Ph.D., is an internationally recognized neurobiologist whose work has advanced our understanding of glial development, myelination, and brain tumor biology. His research focuses on how dysregulation of glial cells, including oligodendrocyte lineage cells, contributes to neurological disease and cancer, and how aberrant cellular programs and the tumor microenvironment drive brain tumor initiation, progression, recurrence, and metastasis. He joins the Department of Pediatrics at the University of Alabama at Birmingham Heersink School of Medicine as a tenured Professor, Director of Basic and Translational Research, and the Olivia Turlington Miller Endowed Chair of Cancer Genetics.
Dr. Lu received his B.S. from Beijing Normal University and his Ph.D. from Rutgers University–Robert Wood Johnson Medical School. He completed his postdoctoral training at Dana-Farber Cancer Institute/Harvard Medical School under the guidance of Dr. Charles Stiles and Dr. David Rowitch. During his postdoctoral work, Dr. Lu discovered a pair of the bHLH transcription factors OLIG1 and OLIG2, which are critical regulators of glial lineage development and myelination. These landmark findings established important principles for understanding the molecular mechanisms of gliogenesis and brain tumorigenesis.
Dr. Lu began his independent career at UT Southwestern Medical Center and later moved to Cincinnati Children’s Hospital Medical Center, where he served as Scientific Director of the Brain Tumor Center and held the Beatrice C. Lampkin Endowed Chair in Cancer Epigenetics in the Division of Experimental Hematology and Cancer Biology. He joined UAB in April of 2026.
Dr. Lu’s laboratory integrates state-of-the-art molecular, cellular, genetic, epigenetic, genomic, and computational approaches to define mechanisms underlying neurological diseases, including multiple sclerosis and autism, as well as brain tumorigenesis and recurrence. His research program emphasizes translating basic discoveries into therapeutic strategies, particularly for brain cancers and neurological diseases. His work spans two major areas: developing precision therapies, radiotherapy strategies, and immunotherapies for brain tumors, including malignant gliomas, DIPG/DMG, and medulloblastoma; and advancing novel approaches to promote myelin repair in neurodegenerative diseases and following brain injury.
Dr. Lu’s work has advanced our understanding of the genetic and epigenetic mechanisms that regulate oligodendrocyte lineage specification, survival, differentiation, myelination, and remyelination in the CNS. His studies have identified multiple key transcription factors, signaling receptors, microRNAs, histone modifiers, and chromatin remodelers that control myelinogenesis. More recently, his laboratory has uncovered new epigenetic mechanisms that govern myelin production and regeneration.
Dr. Lu’s laboratory has also made significant contributions to cancer biology, including identifying GNAS as a tumor suppressor in medulloblastoma through its regulation of Sonic hedgehog signaling and ciliary trafficking, and demonstrating a central role for OLIG2 in tumor growth and phenotypic plasticity in glioma and medulloblastoma. Using multi-omics approaches, his group has identified intermediate glial progenitor populations and key determinants of cell fate and gliomagenesis. His work has further revealed critical roles for HIPPO signaling in malignant transformation during peripheral tumorigenesis and for the tumor suppressor CTDNEP1 in regulating MYC-driven medulloblastoma.
Dr. Lu’s research has been supported by multiple NIH R01 grants and philanthropic foundation awards. His work has been published in leading journals, including Cell, Cancer Cell, Nature Medicine, Nature Neuroscience, Nature Cell Biology, Neuron, Developmental Cell, Science Advances, and Nature Communications. He is the recipient of several prestigious honors, including the NIH/NINDS Javits Neuroscience Investigator Award and the Harry Weaver Neuroscience Scholar Award from the National Multiple Sclerosis Society.