For the first time, a team of international researchers have mapped the family trees of cancer cells in acute myeloid leukaemia (AML) to understand how this blood cancer responds to a new drug, enasidenib. The work also explains what happens when a patient stops responding to the treatment, providing important clues about how to combine enasidenib with other anti-cancer drugs to produce longer-lasting remissions and to prevent relapse.
The study published in Nature Medicine today (Monday), is an international collaboration between researchers from the Gustave Roussy Cancer Campus and Inserm in Paris (France), the MRC Molecular Haematology Unit and the MRC Weatherall Institute of Molecular Medicine at the University of Oxford (UK), Memorial Sloan Kettering Cancer Center (USA) and Celgene (USA).
AML is the most common and aggressive blood cancer in adults and is incurable in most patients. About 12-15% of AML patients have a mutation in the IDH2 gene that stops bone marrow cells from differentiating, or maturing, into blood cells that are required for life. Instead these immature cells accumulate in the bone marrow and blood, which is a hallmark of AML. Previous research from the same team  showed that enasidenib prompts blood cell differentiation and restores normal blood
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