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Stephen J. Brandt, M.D.

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

Phone

615-936-1809

Email

stephen.brandt@Vanderbilt.Edu
Vanderbilt-Ingram Cancer Center
777 Preston Building
Nashville, TN 37232-6305

Stephen J. Brandt, M.D.

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

615-936-1809

stephen.brandt@Vanderbilt.Edu

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 Emphasis

Transcriptional regulation; basic helix-loop-helix transcription factors; LIM domain proteins; protein dimerization; cell differentiation; hematopoiesis; T-cell leukemia

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.

Publications

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