The mouse model study, led by Dr Mary Clarke and Professor Jon Frampton and recently published in Blood, showed that low levels of the protein lead to a more abnormal blood stem cells over time, eventually developing into bone marrow cancers or disorders in older age.
MYB plays a key role in gene regulation in blood cell supply and in the maintenance of normal haematopoietic stem cells (HSC). HSC are immature cells that can develop into all types of blood cells, including red and white blood cells, as well as platelets.
Genetic dysregulation of MYB is involved in the cause of many types of leukaemia. Inherited non-coding variants of the MYB gene can also make a person susceptible to certain haematological conditions. The mechanisms that link variations in MYB levels to being predisposed to disease are not well understood.
In this study, the researchers have advanced understanding of these mechanisms by describing a mouse model of MYB insufficiency, which led to haematological conditions and leukaemia in later life, matching the age profile of the same diseases in humans.
The publication was also accompanied by an editorial in Blood written by Tom Gonda, who is one of the pioneers of the MYB field.