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Study leads to better understanding of acute myeloid leukaemia

The Bloodwise logo. Bloodwise appears in black text against a white background
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24 May 2017

A Bloodwise-funded study at the University of Birmingham has made a breakthrough in the understanding of how different genetic mutations cause acute myeloid leukaemia (AML).

A Bloodwise-funded study at the University of Birmingham has made a breakthrough in the understanding of how different genetic mutations cause acute myeloid leukaemia (AML).

Around 2,400 people in the UK are diagnosed with AML each year. Survival rates  are poor, especially for older patients, and new treatments are needed.

Researchers at the Universities of Birmingham and Newcastle worked in collaboration to study the DNA of two types of acute myeloid leukaemia in an effort to explain how clinical prognosis can differ.

Professor Constanze Bonifer, of the Institute of Cancer and Genomic Sciences at the University of Birmingham, said: “Is has been known for a long time that acute myeloid leukaemia is highly heterogeneous, involving different disease-causing genetic mutations. This in turn leads to highly variable clinical outcomes, with some patients responding better to certain treatments than others.

“Prior to this study, the reason for the differences in response to treatment was unknown. We discovered how two closely related oncogenes - genes which have the potential to cause cancer – differently reprogram blood stem cells in acute myeloid leukaemia and send them spiralling out of control.”

The study, published in Cell Reports, highlights the difficulties faced in understanding the heterogeneity of the disease. The research was funded by Bloodwise and Kay Kendall Leukaemia Fund. 

Dr Justin Loke, a Kay Kendall Clinical Fellow from Birmingham Queen Elizabeth Hospital’s Haematology Department which is affiliated with the University of Birmingham’s Institute of Cancer and Genomic Sciences, said: “We used state-of-the-art molecular technology that studies all genes within leukaemic cells to investigate why two types of the disease with mutations in the same gene display a completely different clinical profile.

“We showed that the maintenance of the leukaemic state of these two types of acute myeloid leukaemia is dependent on different sets of normal genes, therefore identifying a route to developing tailored and personalised treatments for patients with different cancer-causing mutations in order to specifically target each tumour.”

AML incidence rates have increased by more than a quarter in the UK since the early 1990s. One in 200 men and one in 255 women will be diagnosed with the disease during their lifetime.