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A drug that uses a unique ‘double hit’ to kill leukaemia cells could be a potential new treatment for patients with acute myeloid leukaemia (AML).
The research, led by Dr Spiros Linardopoulos from the Breakthrough Breast Cancer Research Centre at The Institute of Cancer Research (ICR), is published in Leukaemia. Around 30 per cent of patients with AML have faults in the FLT3 gene, which are linked to more aggressive leukaemias and poor survival. While drugs that target these faults are available, the disease eventually builds resistance, leaving treatments ineffective.
To combat this, researchers at The Institute of Cancer Research (ICR) in London, funded by Cancer Research UK and Breakthrough Breast Cancer, developed a unique drug that targets AML cells in a “double hit”. The drug blocks the protein made by the faulty FLT3 gene along with another key protein – called Aurora kinase – which are both involved in driving cancer growth.
Lead author Dr Spiros Linardopoulos, Leader of the Cancer Drug Target Discovery Team at the ICR, said: “There has been great interest in using FLT3 drugs to treat AML, but their effectiveness has been limited because leukaemia cells gain new mistakes in the FLT3 gene, causing resistance.
“Our new drug has the potential to overcome this and has a range of possible uses in AML – as a first line of attack for patients with faulty FLT3, in particular in those over 60 who don’t tolerate chemotherapy well, and also to treat leukaemia patients who have relapsed.”
Professor Paul Workman, director of the Cancer Research UK Cancer Therapeutics Unit at the ICR, said: “We’re excited about the potential of our new ‘double hit’ drug and are now planning to take it into clinical trials to see if it is effective in patients.”
The faults that occur in the FLT3 gene cause rapid cell division, and one particular mistake is linked to a very poor outcome in both adults and children with AML. Each year around 2,380 people are diagnosed with AML in the UK.