Timeline: How the ICR has led the way in leukaemia research

1980s

• In 1984, Professor Sir Mel Greaves joined the ICR to establish the Leukaemia Research Fund Centre for Cell and Molecular Biology of Leukaemia.
• In 1988, Professor Greaves developed evidence to support the idea that common infections can trigger acute lymphoblastic leukaemia, but only in children who carry a silent pre-leukaemia condition from birth and who had a deficit of immune microbial exposure during infancy. Epidemiological data suggests that the latter exposures derive primarily from the gut microbiome, which formed the basis of Professor Greaves' team's modelling studies in mice.

2000s

• In 2000, ICR researchers led by Professor Sir Mel Greaves discovered that a non-inherited gene abnormality commonly found in childhood leukaemia is present in one per cent of healthy newborn babies. One in a hundred of these babies would go on to develop leukaemia, proving that not every child carrying this genetic abnormality will develop the disease.
• In 2003, as part of the UKCCS, the same team discovered a link between folic acid and leukaemia in children. The research suggested that children exposed to higher levels of folic acid while in the womb have a significantly lower risk of developing leukaemia. Professor Sir Mel Greaves’ work went on to identify possible postnatal triggers that may force blood cells to become leukaemic.
• In 2005, findings from the UKCCS, published in the BMJ, provided significant insights into the development of childhood leukaemia, suggesting that delayed exposure to common infections could trigger the disease in genetically predisposed children.
  

2010s

• In 2010, a study led by Professor Houlston uncovered the location of 10 genetic variants, common in the European population, that are associated with an increased risk of CLL. This discovery provided the first evidence that genetic makeup plays a major role in the risk of ALL and insight into how the disease develops. The results were published in Nature Genetics.
• In 2011, ICR researchers found that a genetic test could be used to identify patients with the most common type of adult leukaemia, CLL, who at the time did not respond well to available drugs and should be considered for experimental treatments instead. The research was published in the Journal of Clinical Oncology.
• In 2011, Cancer Research UK-funded researchers at the ICR, led by Professor Richard Marais, revealed a technique to kill chronic myeloid leukaemia (CML) cells that had stopped responding to imatinib – a targeted drug. They showed that a combination treatment consisting of nilotinib, and drugs called MEK inhibitors, destroyed CML cells by blocking a strong molecular survival signal keeping them alive. The research was published in Cancer Cell.

• In 2016, Dr Spiros Linardopoulos discovered a new drug, later named EP0042, that could help counteract drug resistance in cancers such as acute myeloid leukaemia (AML). The drug works by targeting key proteins involved in cancer growth.  
• In 2016, an international study co-led by Professor Houlston linked the increased risk of developing CLL to the inheritance of nine separate regions of DNA, each containing genetic variants associated with the disease. The research was published in Nature Communications.
• In 2017, research led by Professor Houlston found that when a specific region of DNA has certain genetic changes, is linked to an increased risk of high-hypodiploid ALL – the most common genetic subtype of ALL, which is associated with good outcomes. Published in Nature Communications, the research points to a likely biological process or event at the cellular level behind the development of the childhood cancer.
• In 2017, Professor Greaves was awarded the Royal Society’s prestigious Royal Medal in recognition of his research on childhood leukaemia. 
• In 2018, research led by Professor Houlston and published in Nature Communications identified that two single-letter changes to DNA are linked to an increased risk of developing ALL.
• In 2018, Professor Greaves received a Knighthood for his work advancing the diagnosis, treatment and prevention of childhood leukaemia. 

• In 2023, The US Food and Drug Administration (FDA) granted Orphan Drug Designation (ODD) to EP0042 for patients with AML.
• In 2024, Dr David Taussig led a phase I trial of the ICR-founded drug, EP0042, in collaboration with Ellipses Pharma – which rapidly progressed the development of the drug following successful negotiations led by the ICR’s Business Innovation Office. The clinical trial data was presented at the 66^th American Society of Haematology Annual Meeting and published in Blood.
• In 2024, research co-led by Professor Kamil Kranc and the University of Oxford uncovered a promising treatment strategy for AML by targeting the enzymes that AML cells typically use to sense and adapt to changing oxygen levels. The research, published in Nature Cancer, revealed that blocking these oxygen-sensing enzymes can significantly halt AML in mice and in patient samples without affecting the normal production of blood cells.
• In 2024, Dr Alex Radzisheuskaya and Professor Kristian Helin identified a key weakness in AML by focusing on disrupting the function of a protein complex that cancer cells, including leukaemia cells, rely on to maintain their abnormal growth. The research, published in The EMBO Journal, offers a promising strategy to delay the progression of the aggressive cancer.