Acute myeloid leukaemia (AML) starts when the DNA and genes in the stem cells of the bone marrow undergo change known as genetic mutation. This leads to uncontrolled growth and proliferation of the cells and these immature white blood cells called blasts are released into the blood stream before they attain maturity.
Normally mutations and changes in DNA are self-corrected or the cell undergoes a programmed death. When cancer occurs this rogue cell continues to divide and the cancer spreads. What exactly causes the cancerous change is not yet known.
Risk factors for AML
There are several risk factors that can raise the risk of getting AML. However, all persons who have exposure to these risk factors may not develop the cancer.
These triggers or risk factors may be present since childhood and may manifest into cancers much later in life.
Most experts suggest a “two hit” theory for childhood leukemias. The theory speculates that the first hit may be if the child is born with a genetic mutation and the second hit is exposure to an environmental or life style trigger that causes the cancer.
The risk factors for AML include:-
Exposure to cigarette smoke
The best known proven lifestyle-related risk factor for AML is smoking. Smoking cigarettes has been associated with cancers of the lungs, mouth, throat, and larynx and leukemias like AML.
Exposure to certain chemicals
The risk of AML rises when there is exposure to certain toxins in the environment and chemicals. These include benzene. Benzene is used as a solvent in several industries like rubber, chemical plants, shoe manufacturing, oil refineries, gasoline-related industries etc. It is also present in glues, cleaning products, detergents, paints and cigarette smoke. Exposure to formaldehyde has also been linked to AML but the exact association is not known.
Previous exposure to chemotherapy
Patients who have had chemotherapy before are more likely to develop AML. Some of the drugs linked with these secondary leukemias (also known as treatment related leukemias) include mechlorethamine, procarbazine, chlorambucil, melphalan, etoposide, teniposide and cyclophosphamide.
The risk rises if these agents are given along with radiation therapy. Secondary leukemias are seen around 10 years after treatment of Hodgkin disease, non-Hodgkin lymphoma, or childhood acute lymphocytic leukemia (ALL). Secondary leukemias may also occur after treatment of breast, ovarian, or other cancers.
Exposure to radiation
Exposure to high levels of radiation is a known risk factor for AML as well as acute lymphoblastic leukemia (ALL). This was first noted among the Japanese atomic bomb survivors who had a greatly increased risk of getting acute leukemia, usually within 6 to 8 years after exposure.
Radiation may arise from radiation therapy for cancers, radiation from imaging studies like X rays and CT scans etc. Exposure of an unborn baby to radiation within the first months of development may also raise the risk of acute leukemia.
Some blood disorders themselves may raise the risk of getting AML. These include chronic myeloproliferative disorders such as polycythemia vera, essential thrombocytopenia, and idiopathic myelofibrosis. Those with myelodysplastic syndrome (a pre-leukemic condition) may develop AML.
Those with chronic myelogenous leukemia (CML) may later develop a form of AML. Treatment for these disorders with chemotherapy and radiation therapy also raises the risk of AML.
Some congenital syndromes that run in families have been associated with AML. These include Down syndrome, Klinefelter syndrome, Fanconi’s anemia, Ataxia-telangiectasia, Bloom syndrome, Blackfan-Diamond syndrome etc.
AML is slightly more common in males than in females and the reasons are not clear.
Ethnicity and race
AML is seen more commonly among Caucasians than in African Americans.
Other potential risk factors
Other unproven risk factors include exposure to electromagnetic fields like living near power grids and cell phone towers etc, exposure to pesticides, and certain other chemicals, hair dyes and bleaches and cigarette smoke.
Reviewed by April Cashin-Garbutt, BA Hons (Cantab)