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Scott W. Hiebert, Ph.D.

  • Associate Director for Basic Science Research and Shared Resources
  • Hortense B. Ingram Professor of Cancer Research
  • Professor of Biochemistry
  • Associate Professor of Medicine

Phone

615-936-3582

Email

scott.hiebert@Vanderbilt.Edu
Vanderbilt University Medical Center
512 Preston Building
Nashville, TN 37232-6838

Scott W. Hiebert, Ph.D.

  • Associate Director for Basic Science Research and Shared Resources
  • Hortense B. Ingram Professor of Cancer Research
  • Professor of Biochemistry
  • Associate Professor of Medicine

615-936-3582

scott.hiebert@Vanderbilt.Edu

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

Profile

Education

Research Emphasis

Genomic analysis, PROseq, ATACseq, RNAseq, ChIPseq, ChIPexo, Molecular Mechanisms of Acute, Leukemia, cell cycle control, and the
action of tumor suppressors, Mechanism of action of anti-cancer drugs that target transcription and the epigenome

Research Description

The work in my laboratory focuses on determining the normal function of the AML1/RUNX1and ETO family of transcription factors in the regulation of stem cells and gene expression, and how disruption of these genes by chromosomal translocations causes myeloid leukemia. We defined AML1 as a transcription factor that binds the "enhancer core" motif, which regulates the expression of a large number of tissue specific genes. We found that AML1 both activates and represses transcription, and that the translocation fusion proteins inhibit expression of AML1-dependent target genes. We have determined that the t(8;21) fusion protein, AML1/ETO, interacts with the mSin3 and nuclear hormone co-repressors that recruit histone deacetylases to repress transcription. This initial observation led us to demonstrate that the t(12;21) and inv(16) proteins also associate with co-repressors and histone deacetylases. Thus, we have identified a common mechanism for transcriptional repression for these three translocations. Given that these fusion proteins recruit epigenetic modifying enzymes, we are targeting these factors to determine if we can cure this leukemia. We use CRISPR-mediated genetics to disrupt these protein interactions, and use cutting-edge genomics methods coupled with small molecule drugs to inhibit this chromatin-modifying enzymes to define the mechanism of tumorigenesis and how to attack this cancer..

Publications

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