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Lyuba Varticovski, M.D.

Portait Photo of Lyuba Varticovski
Laboratory of Receptor Biology and Gene Expression
Hormone Action and Oncogenesis Section
Associate Scientist
Center for Cancer Research
National Cancer Institute
Building 41, Room B301
Bethesda, MD 20892-5505


Dr. Varticovski was born in Siberia, Russia, where she completed undergraduate and first-year medical school. She received her M.D. degree from the University of Valle, Colombia. After a 2-year research fellowship with Max Wintrobe and James Kushner at the Univeristy of Utah and training in internal medicine at Albany Medical College, NY, she completed a fellowship in hematology and oncology at the New England Medical Center in Boston, MA. She joined the laboratory of Lewis C. Cantley in 1985 where she shared in discovery and biochemistry of phosphatidylinositol 3-kinase (PI 3-Kinase). She held a clinical staff position in hematology and oncology at a Tufts University-affiliated hospital in Boston, MA, from 1989 to 2001. She studied the role of PI 3-kinase in protein-tyrosine kinase-mediated signal transduction in cell growth and vesicular trafficking at Tufts Medical School where she rose to the rank of Associate Professor. Dr. Varticovski is board-certified in internal medicine and hematology and board-eligible in oncology. She is a member of the American Society for Hematology, American Society of Clinical Oncology and American Association for Cancer Research. In 2003, she joined the National Cancer Institute in Bethesda, Maryland as Staff Clinician and was subsequently promoted to Associate Scientist. Dr. Varticovski directed the Preclinical Models Strategy Team at the Center for Cancer Research (CCR), Molecular Targeting Unit, Lung Cancer Stem Cell Core, and participated in clinical trials at the NIH Clinical Center for patients with drug-resistant tumors. She is currently a member of the Laboratory of Receptor Biology and Gene Expression, CCR, chaired by Dr. Gordon Hager where she focuses on genome-wide characterization of normal and cancer stem cells.


Our work has been focused on drug development, mechanisms of synergy and antagonism using combination of molecular targeted agents and conventional chemotherapies, and drug resistance. In the last several years, cancer stem cells have been identified as a subpopulation of cells responsible for tumor recurrence and drug resistance. Substantial effort towards isolation of cancer stem cells has led to the identification of tumor-specific markers, but characterization of these cells and mechanisms of their resistance to drugs has been largely descriptive. We came to appreciate that in order to develop effective therapies for cancer stem cells, we need a better understanding of stem cell biology and specifically regulation of stemness and differentiation. While gene expression profiling is the end result of multiple processes, the accessibility of transcription factors (TFs) to DNA ultimately controls stemness, reprogramming and differentiation. The LRBGE has pioneered global unbiased landscape analysis of the accessible genome (i.e., all sites in the genome that are accessible to TFs at any time) by combining DNase I hypersensitivity assays with deep sequencing (DHS-seq). In-depth bioinformatic annotation of DNase I accessible sites to all known human and mouse genome sites provides an unbiased view of changes in accessibility for all regulatory elements in any cell type at any given time. This is a powerful tool for identification of novel sites in distant and proximal enhancers and promoters of epigenetic changes that mark stemness and differentiation. We focused on establishing the landscape of all accessible genome in cell lines that are enriched in cancer stem cells and are resistant to conventional chemotherapeutic agents, as well as osteogenic differentiation of inducible pluripotent cells (iPS) cells derived from normal individuals and patients with inheritable disorders, such as osteogenesis imperfecta (OI). Gene replacement therapy using these cells may save many lives and provide an unlimited source of stem cells for regenerative therapy.

This page was last updated on 3/5/2013.