Untangling the complex web of interactions inside AML cells

What if we could understand what controls the abnormal behaviour of acute myeloid leukaemia? Could we find new drug targets to stop people dying?



Dr Bettina Wingelhofer is studying the complex interactions inside acute myeloid leukaemia cells which control their abnormal behaviour. This could reveal new targets for drugs to improve the chances of survival for people with the disease.

The challenge

Acute myeloid leukaemia (AML) affects 3,000 people every year in the UK. Current treatments may be able to keep the disease at bay for a while, but for most patients their disease will eventually come back.

We urgently need to identify new treatments which can cure the disease for good. To do that, we need to identify new drug targets – molecules which, when blocked by drugs, would kill leukaemia cells or stop them from multiplying.

The science behind the research

The uncontrolled growth of leukaemia cells is caused by the abnormal activation of many genes. In both healthy and diseased cells, gene activity is partly controlled by sections of DNA called enhancers, which help to switch genes on and off.

But currently, we’re not clear on the role of enhancers in AML. We don’t know exactly which enhancers are most active in AML cells, nor which specific genes the enhancers control, or what controls their activity.

Understanding this complex web of interactions would help identify the key controllers of disease in AML. This would identify potential targets for disease which could save more lives.

This is what Dr Bettina Wingelhofer is planning to do during her John Goldman Fellowship. With leukaemia cells donated by people with AML, she will use cutting-edge techniques to measure how active different enhancers are, and what genes they control. Bettina also plans to identify the molecules that control the activity of these enhancers.

What difference will this research make?

Bettina’s project will help us to understand the intricate web of interactions between different parts of the DNA inside leukaemia cells. If Bettina can identify the key molecules controlling the behaviour of AML cells, it may reveal new targets for drugs that can tackle the disease. This could lead to new treatments to give everyone with AML the best possible chance of survival.

Project information

Lead researcher

Dr Bettina Wingelhofer


University of Manchester

Blood cancer type


Award type

John Goldman Fellowship

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