Causes and Risk Factors
For most people who have chronic myeloid leukemia (CML), there are no obvious reasons why they develop the disease. Few risk factors are associated with CML. Two known risk factors are:
- exposure to very high doses of radiation
- high-dose radiation therapy (radiotherapy) used to treat other cancers such as lymphoma
However, most people treated for cancer with radiation don't develop CML. And most people with CML were never exposed to high-dose radiation. The proportion of people who are exposed to radiotherapy and develop CML is small.
Research hasn't shown any association between dental or medical x-rays and CML. Furthermore, you can't catch CML from someone else.
How Does CML Develop?
CML starts with a mutation (change) to a single stem cell in the bone marrow. Stem cells form blood cells (red cells, white cells and platelets). The mutated marrow cell multiplies into many cells (CML cells). The CML cells grow and survive better than normal cells. Uncontrolled growth of CML cells in the marrow leads to an increase of CML cells in the blood.
CML doesn't completely interfere with the development of mature red cells, white cells and platelets. As a result, chronic phase CML is generally less severe than acute leukemia.
If not treated, CML can lead to:
- low numbers of red cells that can no longer supply an adequate amount of oxygen, resulting in anemia
- the immune system's inability to guard against infection effectively because of a lack of neutrophils (a type of white cell), a condition called neutropenia
- low numbers of platelets, which can cause bleeding and easy bruising with no apparent cause, a condition called thrombocytopenia
The Philadelphia Chromosome
People with CML have an abnormal chromosome called the Philadelphia chromosome (Ph chromosome). The Ph chromosome is the result of a translocation between chromosomes 22 and 9. The translocation leads to the development of a cancer-causing gene (oncogene) called the Bcr-Abl gene.
The Bcr-Abl oncogene gives a stem cell instructions to make a dysfunctional protein called Bcr-Abl tyrosine kinase, which leads to the development of CML.