Causes

Acute myeloid leukaemia (AML) is caused by a DNA mutation in the stem cells in your bone marrow that produce red blood cells, platelets and infection-fighting white blood cells.

The mutation causes the stem cells to produce many more white blood cells than are needed.

The white blood cells produced are still immature, so they do not have the infection-fighting properties of fully developed white blood cells.

As the number of immature cells increases, the amount of healthy red blood cells and platelets decrease, and it's this fall that causes many of the symptoms of leukaemia.

Increased risk

It's not known what triggers the genetic mutation in AML, although a number of different things can increase your risk of developing the condition.

Radiation exposure

Being exposed to a significant level of radiation can increase your chances of developing AML, although this usually requires exposure at very high levels.

In the UK, most people are unlikely to be exposed to levels of radiation high enough to cause AML. 

But some people who have had radiotherapy as part of a previous cancer treatment may have a bigger chance of getting AML.

Benzene and smoking

Exposure to the chemical benzene is a known risk factor for AML in adults.

Benzene is found in petrol, and it's also used in the rubber industry, although there are strict controls to protect people from prolonged exposure.

Benzene is also found in cigarette smoke, which could explain why people who smoke have an increased risk of developing AML.

Previous cancer treatment

Treatment with radiotherapy and certain chemotherapy medications for an earlier, unrelated cancer can increase your risk of developing AML many years later.

Blood disorders

People with certain blood disorders, such as myelodysplasia, myelofibrosis or polycythaemia vera, have an increased risk of developing AML.

Genetic disorders

People with certain genetic conditions, including Down's syndrome and Fanconi's anaemia, have an increased risk of developing leukaemia.

Page last reviewed: Mon Feb 2022 Next review due: Fri Feb 2020