Lindsey D. Mayo PhD

Phone: 317-278-3173
Office: R4 119

Lindsey D. Mayo, PhD

Associate Professor: Department of Pediatrics

Associate Professor of Biochemistry & Molecular Biology

Member Indiana University Simon Cancer Center

Indiana University School of Medicine


  • BS:Indiana State University
  • PhD:Wright State University
  • Postdoctoral Fellowship:Indiana University School of Medicine
  • Assistant Professor Department of Radiation Oncology, Department of Pharmacology, Case Western Comprehensive Cancer Center, Case Western School of Medicine, Case Western Reserve University.

  • Assistant Professor of Pediatrics, Biochemistry & Molecular Biology, Indiana University Simon Cancer Center, Indiana University School of Medicine

Research Interest:

Current Research Interests: Mdm2 was initially described as an oncogene through its ability to transform cells. Clinically, Mdm2 is not detected in normal tissue but is detectable in 40-80% of various types of late stage cancers (adult and children). It remains unclear whether there are specific transcription factors that are necessary to elevate mdm2 gene expression in response to growth factors and cytokines, which are highly elevated in the tumor microenvironment. In addition, there are major voids in our understanding of how Mdm2 is regulated at the post-translational level to regulate proteins in tumor cells to promote metastasis in response to the growth factors and cytokines in the tumor microenvironment

We recently showed that Smad3, a transcription factor activated by TGF?1, induced mdm2 gene expression. The induction of Mdm2 protein correlated with epithelial to mesenchymal transition, a process associated with metastasis. We also found that preventing complex formation of Mdm2 and p53, using the Nutlin3 compound induced apoptosis. We stained patient samples for Mdm2 and activated Smad3. We found that staining for both proteins correlated with late stage invasive cancer. This work has led to another seminal observation that as cells undergo epithelial to mesenchymal transition (EMT or metastatic phenotype) Mdm2 levels were elevated. Our unpublished data has identified an additional transcription factor, which is necessary for EMT and is also required for the induction of mdm2. We are currently investigating how Mdm2 is driving metastasis and the activity of Mdm2 is regulated in cells that have lost a key tumor suppressor, p53.