FLT3 signaling in Acute Myeloid Leukaemia

Key Information

Cancer type: 
Leukaemia
Research Institution: 
UCC, Cork
Grant Amount: 
€116,310
Start date: 
October 1, 2011
End date: 
September 30, 2014

Scientific Project Abstract

AML is a disease that strikes both children and adults and is at the moment a difficult condition to treat. About 35% of AML patients have mutations in a gene called FLT3 and these mutations cause disease progression. The aims of this research project are to investigate how the FLT3 gene turns a normal cell into an aggressive cancer cell. We have several clues and one of these is that FLT3 causes an increase in the production of reactive oxygen molecules. These in turn can increase cell survival and at the same time can cause further damage to the cells DNA. Both of these effects are not desirable and bad for the patient. In this project we will investigate where these molecules are made in the cell and how FLT3 contributes and regulates their production. The more we understand about the underlying molecular mechanisms of leukaemia the better able we will be to develop new treatments.

For the non-scientist

One-line description: 
Undercovering the cellular mechanisms which lead to development of leukemia
What this project involves: 

Approximately 35% of acute myeloid leukaemia (AML) patients have a DNA mutation in a gene called FLT3 and patients with this mutation have a much poorer prognosis than patients without the mutation. This project aims to understand how this FLT3 gene turns a normal cell into a cancer cell in an attempt to better understand the molecular mechanisms of AML and identify potential drug-targets for treatment of the disease.