Acute myeloid leukemia (AML) is a fast-moving blood cancer that starts in the bone marrow, where blood cells are made. Immature white blood cells multiply out of control and crowd out the healthy red blood cells, white blood cells, and platelets your body needs to function. It is the most common acute leukemia in adults, and its five-year survival rate ranges from roughly 80% in the youngest patients down to about 20% in the oldest age groups.
How AML Develops in the Bone Marrow
Your bone marrow normally produces stem cells that mature into three types of blood cells: red blood cells that carry oxygen, white blood cells that fight infection, and platelets that help your blood clot. In AML, DNA changes in early-stage white blood cells cause them to get stuck partway through development. These immature cells, called blasts, keep dividing but never become functional.
As blasts pile up, they physically crowd out the production lines for healthy blood cells. Red blood cell production drops, leading to anemia. Platelet production falls, which means your blood can’t clot properly. And even though the body is churning out huge numbers of white blood cells, they don’t work, leaving you vulnerable to infections. This bone marrow failure happens relatively quickly compared to chronic leukemias, which is why AML is classified as “acute.”
Recognizing the Symptoms
AML symptoms trace directly back to those missing healthy blood cells. Low red blood cells cause persistent fatigue, shortness of breath, and pale or noticeably changed skin color. Low platelets lead to easy bruising and unexplained bleeding, often from the gums or nose. And the lack of working white blood cells shows up as frequent infections and fevers that don’t resolve.
Bone pain, back pain, and stomach pain are also common. These symptoms can appear suddenly and worsen over days to weeks. Because many of them overlap with far less serious conditions, AML is sometimes mistaken for the flu or general exhaustion before blood work reveals the problem.
What Causes AML
Most cases of AML arise from acquired DNA mutations, meaning they develop during a person’s lifetime rather than being inherited. What triggers those mutations isn’t always clear, but several risk factors increase the odds significantly.
Long-term benzene exposure roughly doubles the risk. Workers exposed to soot, coal dust, or creosote face two to four times the risk of the general population. Shorter-term contact with certain industrial chemicals, including vinyl chloride, inks, dyes, and fertilizers, has also been linked to higher rates. Age is the strongest non-environmental factor: AML becomes more common with each decade of life.
Therapy-Related AML
A distinct form of AML can develop as a late complication of previous cancer treatment. Chemotherapy and radiation used to treat an earlier cancer can damage the DNA of bone marrow cells, sometimes triggering AML years later. About 70% of these therapy-related cases carry high-risk genetic changes, compared to roughly 20% in AML that arises on its own. That makes therapy-related AML harder to treat: the cancer cells have, in a sense, already survived one round of selection pressure and tend to be more resistant to standard chemotherapy.
How AML Is Diagnosed
Diagnosis starts with a blood test that reveals abnormal cell counts, but confirmation requires a bone marrow biopsy. A pathologist examines the sample under a microscope and counts the percentage of blast cells. The standard threshold is 20% or more blasts in the marrow or blood. Before 2001, the cutoff was 30%, but it was lowered after research showed that patients with 20% to 29% blasts had outcomes more like AML than like the slower-growing condition called myelodysplastic syndrome (MDS).
Genetic testing on the biopsy sample is now just as important as the blast count. Modern classification prioritizes specific DNA abnormalities because they determine both how aggressive the leukemia is and which treatments are most likely to work. Two mutations that doctors routinely test for, called FLT3 and IDH, have targeted drugs available. Other genetic patterns help place the disease into low, moderate, or high-risk categories, which directly shapes the treatment plan.
Treatment: What to Expect
The backbone of AML treatment for nearly five decades has been an intensive chemotherapy regimen commonly called “7+3.” It combines two drugs: one given over seven consecutive days and another over three. The goal of this initial phase, called induction, is to kill enough blast cells to push the disease into remission. Patients typically spend several weeks in the hospital during induction because their blood counts drop dangerously low before recovering.
If remission is achieved, the next question is how to keep it. For patients whose genetic profile suggests a high risk of relapse, a stem cell transplant (sometimes called a bone marrow transplant) offers the best chance of long-term cure. In this procedure, a donor’s healthy stem cells replace the patient’s bone marrow, and the donor’s immune system helps attack any remaining leukemia cells. The decision to transplant weighs three things against each other: the likelihood the cancer will come back without it, the patient’s overall health and other medical conditions, and the risks of the transplant itself, which include serious immune complications. Patients up to about age 75 may be evaluated for transplant, though it is most commonly performed in younger, fitter patients.
Targeted Therapies
For patients whose leukemia carries certain genetic mutations, newer targeted drugs can be added to treatment or used on their own. FLT3 inhibitors block a protein that drives growth in roughly a quarter of AML cases. One was the first targeted drug approved for AML and is used alongside chemotherapy during initial treatment; another is approved for patients whose disease returns after first-line therapy. IDH inhibitors work differently, targeting a metabolic enzyme that, when mutated, prevents blast cells from maturing. Two are currently approved, each for a specific version of the IDH mutation. These drugs don’t replace chemotherapy for most patients but have meaningfully expanded options, particularly for older adults who can’t tolerate intensive treatment.
Survival and Prognosis
Survival in AML depends heavily on two factors: age and the genetic profile of the leukemia. Data from Nordic cancer registries covering cases through 2021 show five-year survival of about 80% for the youngest patients, dropping to roughly 70% for those in early adulthood, 45% for middle-aged adults, and around 20% for the oldest groups. These numbers represent a dramatic improvement over past decades, driven largely by better supportive care, genetic risk classification, and the introduction of targeted therapies.
Within any age group, genetics create wide variation. Patients with favorable-risk mutations can have cure rates well above the average for their age, while those with high-risk or complex genetic changes face significantly tougher odds. Therapy-related AML carries an independently worse prognosis even when age and genetics are accounted for, because of the higher rate of resistant disease and the toll of prior treatment on the body.