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Vanderbilt-Ingram Cancer CenterVanderbilt-Ingram Cancer Center

 
Stephen J.  Brandt

Stephen J. Brandt, M.D.

Professor of Medicine (Hematology/Oncology)
Professor of Cell and Developmental Biology
Professor of Cancer Biology
Researcher

  • Appointments
    615-936-1809
    Physicians: 1-877-936-8422
  • Clinical Trials Information
  • Other Telephone Numbers
    Nashville Veterans Affairs Medical Center
    615-327-4751

    Office
    615-936-1809
  • Faxes
    Nashville Veterans Affairs Medical Center Fax
    615-873-7901
  • Addresses
    Clinic
    Vanderbilt-Ingram Cancer Center
    777 Preston Building
    Nashville, TN 37232-6305

    Nashville Veterans Affairs Medical Center
    1310 24th Ave. South
    Nashville , TN 37212-2637
    Website

    Office
    Vanderbilt-Ingram Cancer Center
    777 Preston Building
    Nashville, TN 37232-6305
Profile

My clinical activities relate to general hematology, including both malignant and non-malignant disorders, and hematopoietic stem cell transplantation, primarily for malignant hematological disorders. I currently see patients exclusively at the Nashville VA Medical Center.

Education
  • B.S., Duke University (1976)
  • M.D., Emory University School of Medicine (1981)
Research Description

Our research focuses on the control of blood cell production and how this is subverted in hematologic malignancy. We have been particularly interested in the oncogene TAL1 (or SCL) that encodes a member of the helix-loop-helix family of transcription factors. Abnormal expression of this gene, originally identified through its involvement by a recurrent chromosomal translocation, constitutes the most frequent gain-of-function mutation in T-cell acute lymphoblastic leukemia (T-ALL). Many helix-loop-helix proteins are important in specification of cell fate, and studies from our lab and others indicate that TAL1 regulates fundamental aspects of hematopoietic differentiation.

We have characterized in detail the expression of TAL1 protein in murine and avian embryogenesis and, most recently, in physiological and pathological vasculogenesis. A series of studies on TAL1 function in erythroid cells have shown this transcription factor undergoes both phosphorylation and acetylation, and we have investigated its interaction with a number of transcriptional coregulators. Work is ongoing to investigate the mechanism by which misexpression of this critical regulator of normal hematopoiesis contributes to leukemic transformation and to identify both its interaction partners and downstream targets. Contemporary techniques of molecular biology and protein biochemistry and both in vitro and in vivo models are used in this research.

Clinical Interest

Leukemias; Lymphomas; Multiple Myeloma

Publications