Acute myeloid leukaemia is a blood cancer cell that changes white blood cells in the human body. Approximately 30% of all AML patients have a modification in a tyrosine kinase known as FLT3. This protein sits on the cover of blood cells and binds to a molecule known as FL outside of the cell.

Normally, the binding of FL activates the FLT3 receptor and causes cell growth. However, when the mutation occurs in FLT3, growth signals are transmitted to leukaemia cells when FL is absent.

Quizartinib is a variety of FLT3 inhibitor that was produced for AML patients with FLT3 mutations. AML patients respond will to Quizartinib initially, but usually, their disease returns presently after treatment. By using blood and marrow specimens donated by AML patients, researchers found that factors produced by done marrow support cell are taken up by leukaemia cells.

Leukaemia cells activating continuance pathways that protect leukaemia cells from occurring killed by Quizartinib. They also determined that these bone marrow factors speed up energy production in leukaemia cells, allowing for cancer cells survival. 

Treating leukaemia cells with a combination of Quizartonib and dasatinib overcame the protective effects of bone marrow support cells in this laboratory study and killed leukaemia cells extra effectively than Quizartinib alone. Insights from this research will be done to develop clinical trials to improve treatment options for leukaemia patients.