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Chi Dang, MD, PhD

The Johns Hopkins Family Professor in Oncology Research
Professor of Medicine, Cell Biology, Oncology and Pathology
Vice Dean for Research, School of Medicine

Dang photo

Departmental Address:
Ross Research Building
Room 1032
720 Rutland Ave.
Baltimore, MD  21205


Administrative Office:
410-955-2773
410-955-0185 (fax)

Additional Contact:
cvdang@jhmi.edu
COS profile:  http://myprofile.cos.com/cvdag

Clinical/Academic Interests

Anemias, Bone Marrow Failure, Myeloproliferative Disorders

Research Interests

My laboratory is studying the mechanisms underlying the neoplastic activities of the MYC oncogene.  MYC encodes a transcription factor, c-MYC, that heterodimerizes with Max to bind specific DNA sequences.  We have contributed extensively to the identification of functional domains of the c-MYC protein.  We, and others, have found that Myc/Max binds to the E-box (CANNTG) sequences to activate transcription and other elements to suppress transcription.  We have recently identified thousands putative c-Myc target genes using representational difference analysis and DNA microarray analysis.  These genes are part of a growing list of putative c-Myc target genes that are estimated to involve about 10% of genes.  We have begun to catalog these genes (www.myc-cancer-gene.org) and are using this database and exploiting phylogenetic footprinting (bioinformatics) to predict in vivo c-Myc binding sequences.  The binding regions are validated by a technique we invented, Scanning Chromatin Immunoprecipitation (SChIP).  We are currently defining the roles of five selected genes in Myc-mediated phenotypes.  Our studies have led to the discovery that c-Myc overexpression activates genes encoding proteins involved in glycolysis and contributes to the Warburg effect or aerobic glycolysis, which is characteristic of essentially all solid tumors.  We recently discovered a key role c-Myc in the regulation of mitochondrial homoeostasis.  In addition, we discovered that c-Myc overexpression contributes to genomic instability by uncoupling S and M phases of the cell cycle; this effect renders c-Myc overexpressing cycle sensitive to anti-miotics.  Our work and those of others have led to the concept that MYC is a central regulator of cell proliferation and cellular metabolism.

Education/Training

  • BS, Chemistry (highest honors), University of Michigan
  • PhD, Chemistry (distinction), Georgetown University
  • MD, (Alpha Omega Alpha), Johns Hopkins University School of Medicine
  • Internship, Department of Medicine, Johns Hopkins Hospital
  • Residency, Department of Medicine, Johns Hopkins Hospital
  • Fellowship, Hematology-Oncology, Cancer Research Institute, UCSF

Academic Positions

  • Assistant Professor of Medicine, Johns Hopkins University 
  • Assistant Professor of Cell Biology & Anatomy, Johns Hopkins University
  • Assistant Professor of Oncology, Johns Hopkins University
  • Associate Professor of Medicine, Johns Hopkins University
  • Director, Division of Hematology, Johns Hopkins University
  • Deputy Director of Research, Department of Medicine, Johns Hopkins University, 
  • Professor of Medicine, Oncology, Pathology, Johns Hopkins University
  • Professor of Cell Biology, Johns Hopkins University

Selected Publications

 
 
 
 
 

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