The VICC.ORG Investigator Directory

Elizabeth Yang, M.D., Ph.D.

Associate Professor of Pediatrics (Pediatric Hematology/Oncology)
Associate Professor of Cancer Biology
Associate Professor of Cell & Developmental Biology
VICC Member
Pediatric Hematologist/Oncologist

Patient Contact Information:

Appointments: 615-936-1762
Further Information: 1-800-811-8480

Monroe Carell Jr. Children's Hospital at Vanderbilt
2200 Children's Way
Nashville, TN 37232
Phone: 615-936-1000

Healthcare Provider Contact Information:

Vanderbilt University Medical Center
518 Preston Building
Nashville, TN 37232-6838


Dr. Yang was trained in Pediatrics at Massachusetts General Hospital and in Pediatric Hematology-Oncology at Washington University. She has been involved in cancer-related research at Stanford and at Washington University. She joined Vanderbilt University in 1997 as a member of the Vanderbilt-Ingram Cancer Center. As a physician-scientist, Dr. Yang is active on the Vanderbilt Pediatric Hematology-Oncology clinical service and is committed to cancer research. Her research focus is the molecular mechanisms of apoptosis, or programmed cell death, an important regulatory pathway in cancer. BCL2 is an oncogene which causes cancer by inhibiting cell death and promoting inappropriate cell survival. In studying how the BCL2 family controls cell proliferation, Dr. Yang's laboratory has found that apoptosis and cell cycle are coordinately controlled. The function of many key apoptosis proteins is regulated by phosphorylation. Dr. Yang's group also investigates the complex interactions between specific serine/threonine phosphatases, the phospho-binding protein 14-3-3, and the BCL2 family in regulating apoptosis. Elucidating the basic mechanisms of cell death will enhance understanding of cancer pathogenesis and lead to potential novel cancer therapies.

Research Description:

We have 3 areas of interest. First is how the BCL2 family of apoptosis molecules regulate cell cycle. We found that the pro-apoptotic BCL2 family members BAX and BAK regulate p27 level and reactive oxygen species, and knockout of BAX and BAK result in quiescence. We are interested in how BAX and BAK deletion decreases intracellular ROS and causes the quiescence phenotype.

Second, the oncogenic protein tyrosine phosphatase Shp2 functions both in apoptosis and proliferation. Mutations of this gene are found in human leukemias. When found in the germline, Shp2 mutations predispose to leukemia. We use retroviral gene transduction and bone marrow reconstitution to study cooperating events in Shp2 murine leukemogenesis.

Third, any apoptotic molecules are regulated by reversible phosphorylation. We identified a PP2A as the enzyme dephosphorylating the transcription factor FOXO1 in response to an apoptotic stimulus through complex competitive interactions with 14-3-3. We are elucidating the regulation of the PP2A phosphatase.

Clinical Interest:

Sickle Cell disease

Clincial Research Description:

Sickle cell disease is a single gene disease, but with variable clinical severity. We are interested in genetic modifiers of disease expressivity.



  • M.D. - Stanford University, 1987
  • Ph.D - Stanford University, 1987
  • Pediatric Residency - Massachusetts General Hospital
  • Pediatric Hematology-Oncology Fellowship, Washington University, St. Louis MO.
  • Post-Doctoral Research Fellowship, Washington University, St. Louis, MO

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