Damon Runyon Researchers

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Catherine C. Smith, MD

Acute myeloid leukemia (AML) is one of the deadliest blood cancers. Mutations in the FLT3 gene are the most common of all mutations in AML and are associated with poor outcomes in both adult and pediatric patients. Despite the importance of FLT3 mutations in AML, we still do not understand the way in which FLT3 is regulated and the functional impact of novel FLT3 mutations identified in recent large AML sequencing studies. Drugs targeting FLT3 have been successful in achieving remissions in AML patients but are limited by the rapid development of drug resistance, particularly due to reactivation of abnormal cancer signaling through the oncogene RAS.  Dr. Smith [Richard Lumsden Foundation Clinical Investigator] proposes studies to better understand how mutations found in AML patients cause dysregulation of FLT3 function and how activation of RAS signaling contributes to drug resistance and AML development. Her goal is to cultivate novel treatment strategies to target FLT3 in patients that will optimize response rates and prevent disease relapse.

Project title: "Defining structure, function and therapeutic impact of oncogenic FLT3 mutations"
Institution: University of California, San Francisco
Named Award: Richard Lumsden Foundation Clinical Investigator
Award Program: Clinical Investigator
Sponsor(s) / Mentor(s): Neil P. Shah, MD, PhD
Cancer Type: Blood
Research Area: Signal Transduction