Lu Le, M.D., Ph.D.
Graduate Programs: Integrative Biology
Graduate Programs: Integrative Biology
Dr. Le received his Ph.D. degree in Microbiology, Immunology and Molecular Genetics (with Owen N. Witte), and a medical degree (M.D.) from the Medical Scientist Training Program at the University of California, Los Angeles (UCLA). He completed an Internship in Internal Medicine at UCLA/St. Mary Medical Center, residency training in Dermatology and a postdoctoral fellowship in Cancer Biology (with Luis F. Parada) from University of Texas Southwestern Medical Center. He is board certified by the American Board of Dermatology. Dr. Le sees patients in the Dermatology clinic and at the UTSW Comprehensive Neurofibromatosis clinic.
As a principal investigator in cancer biology, his laboratory investigates early, initiating genetic and microenvironmental events that regulate tumorigenesis. His research group focuses on: (1) identifying the cells of origin of tumorigenesis (how do certain type of cancers originate and develop from adult stem/progenitor cells?); and (2) elucidating the roles of tumor microenvironment in cancer development (how do neighboring non-cancerous cells dictate cancer development and progression?). His laboratory dissects these cellular and molecular mechanisms of tumorigenesis from the developmental perspective. They utilize Neurofibromatosis Type I (NF1), a common tumor predisposition human genetic disorder, as a model to address these two fundamental issues of cancer biology as well as elucidating cutaneous nervous system development and regeneration. His major research goals are to understand mechanisms that initiate Neurofibroma genesis and drive their malignant transformation as well as to develop novel therapeutic targets for Neurofibroma. Research in Dr. Le's laboratory is supported by R01 grant from the National Cancer Institute of the National Institutes of Health as well as grants from the U.S. Department of Defense and the Burroughs Wellcome Fund.
|Graduate School||University of California - Los Angeles (2002)|
|Medical School||University of California, Los Angeles (2003)|
|Internship||Saint Mary's Medical Center-Long Beach (2004), Internal Medicine|
|Residency||University of Texas Southwestern Medical School at Dallas (2007), Dermatology|
|Fellowship||UT Southwestern Graduate School of Biomed Sciences (2009), Cancer Biology|
CXCR4/CXCL12 mediate autocrine cell cycle progression in NF1-associated malignant peripheral nerve sheath tumors
Mo, W., Chen, J., Patel, A., Zhang, L., Chau, V., Li, Y, Cho, W., Lim, K., McKay, R., Lev, D., Le, L.Q. (Co-corresponding author) and Parada, L. (Co-corresponding author) Cell 2013 152 (5)1077-1090
Skin-derived precursors as a source of progenitors for cutaneous nerve regeneration
Chen, Z., Pradhan, S., Liu, C. and Le, L.Q. Stem Cells 2012 30 (10) 2261-2270.
Susceptible Stages in Schwann cells for NF1-Associated Plexiform Neurofibroma Development
Le, L.Q. (Corresponding author), Liu, C., Shipman, T., Chen, Z., Suter, U., Parada, L.F. Cancer Research 2011 71(13) 4686-95
Cutaneous features predict paraspinal neurofibromas in Neurofibromatosis type 1
Brown, R., Klesse, L., Le, L.Q. Journal of Investigative Dermatology 2010 130 (9) 2167-9
Cell of origin and microenvironment contribution for NF1-associated dermal neurofibromas.
Le, L.Q., Shipman, T., Burns, D.K., Parada, L.F. Cell Stem Cell May 2009 4 (5) 453-463
Tumor Microenvironment and Neurofibromatosis Type I: Connecting the GAPs
Le, L.Q., Parada, L.F. Oncogene 2007 26(32) 4609-4616
Positron Emission Tomography Imaging Analysis of G2A as a Negative Modifier of Lymphoid Leukemogenesis Initiated by the BCR-ABL Oncogene
Le, L.Q., Kabarowski, J., Wong, S., Nguyen, K., Gambhir, S., Witte, O.N. Cancer Cell 2002 1(4) 381-391
Mice lacking the orphan G protein-coupled receptor, G2A, develop a late-onset autoimmune syndrome
Le, L.Q., Kabarowski, J., Weng, Z., Satterthwaite, A., Harvill, E., Jensen, E., Miller, J.F. and Witte, O.N. Immunity 2001 14(5) 561 - 571
The transcriptionally regulated orphan G protein-coupled receptor (G2A) elicits RhoA dependent actin rearrangement via G-alpha13
Kabarowski, J.H.S., Feramisco, J.D., Le, L.Q., Gu, J.L., Luoh, S-W., Simon, M.I., and Wite, O.N. Proc. Natil. Acad. Sci. USA 2000 97 12109 - 12114