Dr Bryan Mitton

Dr Bryan Mitton

Dr Mitton’s research focuses on discovering new drugs that block CREB function

Bryan Mitton, MD, PhD grew up in Mississippi and received his B.S. in Cell and Structural Biology from the University of Illinois Urbana-Champaign. He then pursued combined medical and research training at the University of Cincinnati College of Medicine through the Medical-Scientist Training Program (MSTP). He earned his PhD in 2007 in the Department of Pharmacology and Cell Biophysics, and his M.D. in 2008. He completed clinical residency training in Pediatrics at the University of California, Los Angeles in 2011, and is currently a Hematology-Oncology Clinical Fellow of Pediatrics at the Lucile Packard Children’s Hospital at Stanford University. He has worked in the laboratory of his advisor, Dr Kathleen Sakamoto, MD, PhD, since 2010.

Dr Mitton’s primary research interest is in discovering new therapies for high-risk leukemia
In children, leukemia is the most common form of cancer, and unfortunately, cure rates for both children and adults with Acute Myelogenous Leukemia (AML) remain close to 50%. Previous work had shown that ‘CREB’, a signaling molecule in cells that facilitates cell growth and survival, is elevated and overactive in AML cells compared to normal cells; CREB levels are increased most in patients with high-risk AML, and it therefore also serves as a marker for patients with a poor prognosis. Thus, Dr Mitton’s research focuses on discovering new drugs that block CREB function.

One promising drug designed to block CREB was able to reduce AML cell growth by 80% in a mouse model when used alone; importantly, this compound did so without any toxic effects on the mice studied. This drug also killed cultured AML cells but was not toxic to normal human bone marrow cells, suggesting that CREB inhibition may represent an effective, specific and safe treatment for AML.


Targeting the CREB Proto-Oncogene for Acute Myelogenous Leukemia

Much work remains to be done in characterizing the overall role of CREB in AML, and how well a CREB-inhibiting drug may work in combination with standard chemotherapy. Dr Mitton’s project, Targeting the CREB Proto-Oncogene for Acute Myelogenous Leukemia, will begin to answer these questions.

If successful, Dr Mitton’s work could result in the discovery of a new class of drugs for treating AML in children and adults and address an important clinical problem.