Cambridge scientists granted over £500,000 to search for new ways to tackle AML
Two research projects are underway at the University of Cambridge that are seeking to find new ways to treat acute myeloid leukaemia (AML).
Over 2,400 people are diagnosed with AML each year in the UK. It can affect anyone of any age, but the majority of patients are over 60.
The two projects, which will run over three years, have received £535,000 in funding from Bloodwise.
Researchers led by Professor Brian Huntly and Dr George Vassiliou at the Wellcome - MRC Cambridge Stem Cell Institute are tracking the genetic changes that blood cells go through early in their development into leukaemia cells to see whether treatments could be created to prevent AML from fully progressing.
Professor Tony Kouzarides’ team at the Wellcome/Cancer Research UK Gurdon Institute are looking at a new angle on targeting AML, by blocking an enzyme that modifies messages in leukaemia cells.
Dr Alasdair Rankin, Director of Research at Bloodwise, said: “Survival rates for AML remain tragically low, and combination chemotherapy only curing a small proportion of patients. Intensive chemotherapy, often combined with a stem cell transplant, offers the best chance of a permanent cure, but many patients are too elderly to undergo this gruelling treatment, which can have fatal side effects even before it has the chance to work. These exciting research projects at the University of Cambridge are looking completely different ways to treat AML, which we hope will lead to gentler and more effective treatments.”
AML affects a family of blood cells called myeloid cells, which include certain types of white blood cells, red blood cells and platelets. The team at the Cambridge Stem Cell Institute are studying mice with AML to see how early genetic mutations in healthy myeloid cells can kick-start the accumulation of additional DNA damage, leading to the growth of full-blown leukaemia cells with multiple genetic mutations.
Professor Brian Huntly said: “Effective new treatments for AML are desperately needed. By studying which genetic mutations are critical to the development of AML in its early stages, we will identify potential drug targets that could allow earlier and more successful treatment intervention in this highly aggressive disease.”
Strands of molecules called RNA act as ‘messages’ from the genetic instructions contained in the cell’s DNA, which are then translated into the proteins that carry out cell functions.
But not all RNA strands are used to make proteins - many remain as RNA and play a role in regulating cell behaviour. RNA molecules are often modified by enzymes in the cell and sometimes this means that the genetic ‘message’ is hijacked, which can lead to cancer. Professor Tony Kouzarides’ team at The Gurdon Institute team have discovered that AML cells rely on an RNA modifying enzyme called DIMT1 to grow, and now want to understand this more.
Professor Tony Kouzarides said: “We’re trying to understand why this specific enzyme is so influential in the growth of AML. If we can design molecules that can block its activity, we may be able to create a new targeted drug for AML.”