NORD gratefully acknowledges Amy E. DeZern, MD, MHS, Assistant Professor of Oncology and Medicine, Division of Hematologic Malignancies, Johns Hopkins Sidney Kimmel Comprehensive Cancer Center, for assistance in the preparation of this report.
Acute myeloid leukemia (AML) is a group of blood and bone marrow cancers. This disorder is characterized by incomplete maturation of blood cells and reduced production of other normal hematopoietic stem cells. Hematopoietic stem cells are specialized cells that are formed in the bone marrow, the soft, spongy material found in the center of long bones. Hematopoietic stem cells develop, or mature, into the three main blood cells – red blood cells, white blood cells and platelets. In AML, a change in the genetic material (DNA) of a single immature cell, called a blast cell or a myeloblast cell causes the altered cell to continually reproduce itself. Eventually, these altered cells crowd out normal, healthy cells in the marrow. They also cause damage and scarring in the marrow, further disrupting the production of red cells, white cells, and platelets. These altered blast cells can be released into the bloodstream where they travel to other areas or organs in the body, potentially damaging these organs or interfering with their normal function. Without treatment, AML progresses rapidly (acute disease). AML is the most common acute form of leukemia in adults. Most people who develop this form of cancer are older adults; more than half of the affected individuals are 65 years old or older. Although uncommon, AML can occur in children.
There are several subtypes of AML recognized in the 2016 World Health Organization classification:
• AML with recurrent genetic abnormalities
• AML with myelodysplasia-related changes
• Therapy-related myeloid neoplasms
• AML, not otherwise specified
• Myeloid sarcoma
• Myeloid proliferations related to Down syndrome
These subtypes are described in greater detail in the Causes section. Another subtype of AML is acute promyelocytic leukemia (APL). APL is not discussed in this report, although it is briefly described in the Related Disorders section.
Some symptoms of acute myeloid leukemia result from disruption of the normal formation of blood cells. There are three main types of blood cells – red blood cells, white blood cells, and platelets. These cells are formed in the bone marrow and they arise from hematopoietic stem cells, a type of adult stem cell.
In AML, immature cells known as myeloblasts build up in the bone marrow, crowding out healthy cells and interfering with the normal production of blood cells. This leads to a deficiency of these mature blood cells, a condition called pancytopenia. Red blood cells deliver oxygen to the body, white blood cells help in fighting infections, and platelets allow the body to form clots to stop bleeding. A low level of circulating red blood cells is called anemia. A low level of white blood cells is called leukopenia. A low level of platelets is called thrombocytopenia.
Because of the lack of healthy blood cells, affected individuals may experience weakness, fatigue, shortness of breath (dyspnea), recurrent infections (which can cause fever, body aches, and night sweats), and prolonged bleeding. Affected individuals may appear pale and they may bruise easily (including with minor injury or without a reason). There may be a loss in appetite and unintended weight loss. Inflammation of tissue in the mouth can cause swollen, bleeding gums, sores and be painful.
Some individuals develop small red or purples spots on the skin called petechiae that are caused by bleeding under the skin, or larger, purple spots called ecchymoses caused by bleeding from ruptured blood vessels under the skin. Some people have chronic or severe nosebleeds. Some women will have abnormally heavy or prolonged bleeding during their menstrual periods (menorrhagia).
Some people may have sternal tenderness, which refers to chronic pain or tenders in the breastbone (sternum). Affected individuals may have abnormally enlarged lymph nodes (lymphadenopathy). Less often, the liver and/or spleen may be enlarged, which is called hepatosplenomegaly.
Some people with AML, mainly those who have not been treated or received a delayed diagnosis, develop hyperleukocytosis and leukostasis. Hyperleukocytosis means that a person’s white blood cell levels are at abnormally high levels. This can cause symptoms, particularly affecting the lungs or central nervous system. When symptoms occur, this is called leukostasis. Leukostasis can be characterized by headaches, confusion, seizures, visual disturbances, difficulty breathing, respiratory failure, or coma. Both conditions are medical emergencies, even in people without noticeable symptoms.
Myeloid sarcoma is when a group of leukemic (malignant) cells form a mass or tumor outside of the bone marrow (extramedullary disease). This is a rare occurrence in AML. Common sites for a myeloid sarcoma include bone, soft tissues, lymph nodes, and the periosteum, a dense layer of fibrous tissue that covers bone. Myeloid sarcoma is also known as chloroma, granulocytic sarcoma, or myeloblastoma. Sometimes, a myeloid sarcoma will develop without any evidence of leukemic cells in the bone marrow or circulating blood.
Some individuals will develop leukemia cutis, which is when cancer cells travel (migrate) to the skin. This can cause a variety of skin problems including spots, bumps, or rashes. Leukemia cutis is estimated to affect fewer than 10% of people with AML.
Although uncommon, leukemic cells can spread to affect the brain and spinal cord (central nervous system).
Leukemias are clonal disorders, which means that cancer arises from a change in one original cell. In AML, this occurs in a hematopoietic stem cell, specifically a myeloblast. A myeloblast is an immature precursor cell found in the bone marrow. This means that a myeloblast will change (mature or differentiate) into a healthy white blood cell called an agranulocyte or a monocyte. In AML, myeloblasts do not mature, and grow and multiply out-of-control. Because myeloblasts are immature cells, they cannot perform the normal functions of mature blood cells. These abnormal cells build up in the bone marrow, preventing the development of healthy red blood cells, white blood cells, and platelets. Leukemic myeloblasts also survive better than normal blood cells. People with AML eventually develop pancytopenia, a condition in which they lack healthy red and white blood cells and platelets.
There is a genetic component in most people with AML. Most people have changes or alterations to specific genes. There are certain genes in the body that control how cells grow and divide and multiply and die. These genes are either oncogenes, which control cell growth and division, or tumor suppressor genes, which slow down cell division and make sure cells die at the right time. A change or alteration to an oncogene or a tumor suppressor gene can cause out-of-control cell growth and multiplication. These changes or alterations are usually acquired during a person’s life (they are not inherited), usually randomly for unknown reasons (de novo). People with AML usually have a change in a few genes, both oncogenes and tumor suppressor genes. Researchers believe that the interaction of these genetic changes plays a significant role in the development of AML.
These genetic alterations are very important. They can be used by doctors to guide treatment and predict how the disease will progress. Understanding the genetic aspects of AML is difficult; this is a very complex topic. Doctors and researchers are still learning about how these changes play a role in the development and progression of AML. Patients and parents of affected children should discuss the genetic aspects of their individual situations with their physicians and entire medical team.
The genetic changes in AML can be a change in a gene called a mutation. This is a permanent change in the DNA sequence that makes up the gene. Common mutations associated with AML including changes to the FLT3, NPM1, DNMT3A, IDH1 or IDH2, NRAS or KRAS, or RUNX1 genes. These gene changes contribute to the growth and spread of AML in the body. The identification of these genes has allowed researchers to look for targeted therapies, which are therapies that directly target the altered gene or the protein that the gene produces as a way to control the disease.
Some people have translocations, which occur when regions of certain chromosomes break off and are rearranged, resulting in shifting of genetic material and an altered set of chromosomes. Chromosomes are in the nucleus of human cells and carry the genetic information for each individual. Human body cells normally have 46 chromosomes. Pairs of human chromosomes numbered from 1 through 22 are called autosomes and the sex chromosomes are designated X and Y. Males have one X and one Y chromosome and females have two X chromosomes. Some genetic changes in AML are inversions in which there is a breakage within a single chromosome at two points and a “rejoining” of the chromosome with a reversal (inversion) of the two breakpoints.
Researchers have been able to determine certain risk factors that, when present, increase a person’s chances of developing AML. These risk factors include several environmental factors including exposure to benzene, certain pesticides, ionizing radiation, and smoking. Most people with AML develop the disease without any known risk factors.
Some people have therapy-related AML. In these people, AML results from treatments people underwent earlier in their lives. Often, this can be radiation therapy or chemotherapy that was used to treat a different form of cancer.
Some people with AML have another blood disorder first, such as a form of myelodysplastic syndrome. Myelodysplastic syndromes are a rare group of blood disorders that occur because of disordered development of blood cells within the bone marrow. About half of the people who have a myelodysplastic syndrome eventually develop AML. Myelodysplastic syndromes were once called pre-leukemia or smoldering leukemia. In rare instances, people with other blood disorders such as essential thrombocythemia or polycythemia vera can eventually develop AML. This is much less likely, however, than it is in people with a myelodysplastic syndrome. (For more information on these disorders, choose the specific disorder name as your search term in the NORD Rare Disease Database.)
People who have certain rare disorders including Down syndrome, Fanconi anemia, ataxia-telangiectasia, and Bloom syndrome have a slightly increased risk of developing AML. (For more information, choose the specific disorder name as your search term in the NORD Rare Disease Database.)
Acute myeloid leukemia is the most common form of acute leukemia in adults, making up about 80% of people with acute leukemia. In the United States, it is estimated that 3-5 people per every 100,000 people in the general population has the disease. More than half the people diagnosed with AML are 65 years of age or older. Slightly more men than women are affected by the disease, and it occurs with slightly more frequency in people of European heritage.
A diagnosis of acute myeloid leukemia is based upon identification of characteristic symptoms, a detailed patient history, a thorough clinical evaluation, and a variety of specialized tests. During a complete physical examination, physicians may feel (i.e., palpate) the lymph nodes in certain regions to detect any swelling.
Clinical Testing and Workup
Laboratory tests will include a complete blood count and a peripheral blood smear. A complete blood count will tell the doctor whether the levels of red blood cells, white blood cells and platelets are low, how much hemoglobin (the red, iron-rich, oxygen-containing pigment of the blood) is in the blood, and the portion of the blood that is made up of red blood cells. A peripheral blood smear is a test that involves studying a sample of the circulating blood in the body and is used to look for abnormalities in blood cells including changes in the shape of cells or the presence of immature blood cells (myeloblasts).
A suspected diagnosis of AML can be confirmed by a bone marrow biopsy. A biopsy is a test that involves taking a sample of tissue (in this situation bone marrow tissue) and studying the sample under a microscope. Often, a tissue sample is taken from the hip bone. During a bone marrow biopsy, the skin and tissue over the bone is numbed with a local anesthetic, and a needle is inserted into the bone through which a bone marrow sample is withdrawn. This may be painful and sometimes a mild, calming medication (sedative) may be offered beforehand. There may be bruising and discomfort for a few days after the procedure as well. After the sample is withdrawn, it is examined under a microscope by a pathologist, who is a specialist in the cause and development of disease, and who can diagnose disease through laboratory testing.
Cytogenetic analysis may be used to help diagnose AML. Doctors know now that cancerous cells have certain genetic abnormalities or rearrangements. AML is associated with many different, specific genetic abnormalities. Cancerous cells are studied in order to detect these genetic changes.
A procedure called immunophenotyping is often used to help distinguish blood cell cancers. This test involves using antibodies that react to certain markers (antigens) on the surface of cancer cells. This test can help to distinguish different types of leukemia from one another.
The World Health Organization (WHO) has published diagnostic criteria for AML based on any of the following:
• Greater than (≥) 20% blasts in blood or marrow (based on 200 nucleated cells from blood and 500 nucleated cells from bone marrow)
• clonal, recurring cytogenetic abnormalities t(8;21)(q22;q22), inv(16)(p13q22) or t(16;16)(p13;q22), and t(15;17)(q22;q12) (regardless of blast percentage)
• myeloid sarcoma (regardless of blast percentage)
The “t” in bullet two refers to a translocation and the “inv” refers to an inversion. These cytogenetic abnormalities are described in the Causes section above.
Sometimes regular and specialized imaging techniques like traditional X-rays, computerized tomography (CT) scanning or magnetic resonance imaging (MRI) may be used to help to assess the extent of disease. A chest x-ray may be given to assess the lungs and other organs and bones in the chest. During CT scanning, a computer and x-rays are used to create a film showing cross-sectional images of certain organ or tissue structures. An MRI uses a magnetic field and radio waves to produce cross-sectional images of organs and bodily tissues. These tests can help to determine whether leukemia has spread to affect other organs or areas of the body.
Some people may undergo a test called a lumbar puncture, also known as a spinal tap. This procedure is given if doctors suspect that AML has spread to the central nervous stem. During a lumbar puncture, a needle is inserted into the spinal canal in the lower back to retrieve a sample of cerebrospinal fluid (CSF). CSF is the fluid that surrounds the brain and spinal cord.
The diagnosis and therapeutic management of acute myeloid leukemia may require the coordinated efforts of a team of medical professionals, such as physicians who specialize in the diagnosis and treatment of cancer (medical oncologists), disorders of the blood and blood-forming tissues (hematologists), or the use of radiation to treat cancers (radiation oncologists); oncology nurses; surgeons; dietitians; and/or other healthcare professionals. Psychosocial support for the entire family is essential as well.
Specific therapeutic procedures and interventions may vary, depending upon numerous factors, such as disease stage; specific genetic alterations present and specific AML subtype; the presence or absence of certain symptoms; whether leukemia has spread outside of the blood and bone marrow and what specific organ systems are involved; an individual’s age and general health; a person’s physical ability, ability to care for oneself, and ability to perform normal, daily activities (performance status); and/or other elements. Decisions concerning the use of specific drug regimens and/or other treatments should be made by physicians and other members of the health care team in careful consultation with the patient based upon the specifics of his or her case; a thorough discussion of the potential benefits and risks, including possible side effects and long-term effects; patient preference; and other appropriate factors. Doctors may use these factors to establish a classification or stratification of risk for a person with AML to offer a prognosis and to best guide treatment.
For most people, the initial treatment for AML is induction therapy. The goal of induction therapy is to achieve a complete remission of the disease. This involves the use of chemotherapy, a combination of drugs that are harmful to cancerous cells and tissue. Chemotherapy can reduce the number of cancerous cells in the body and prevent new cells from forming. For young adults (i.e. under 60 years of age), an anthracycline chemotherapy drug like daunorubicin or idarubicin in combination with cytarabine, is usually used and may be referred to as the “7 + 3 regimen” (7 days of therapy with cytarabine, plus 3 days of an anthracycline drug). There are other options as well including regimens with higher doses of cytarabine. These different options need to be discussed in detail with a patient’s physician and medical team. Induction therapy has very high success rates in achieving remission, but there are also high rates of cancer coming back, called a relapse. Induction therapy is a highly toxic treatment regimen and requires close monitoring.
It is common for a small number of leukemic cells to remain after induction therapy. This may be referred to as minimal residual disease. Consequently, after induction therapy, individuals may undergo a second phase of treatment, called the consolidation phase or postinduction therapy. This is done after a person has had time to recover from the side effects of induction therapy, and is performed to destroy any cancerous cells that remain and achieve long-term remission. In general, consolidation therapy consists of more chemotherapy or an allogeneic stem cell transplant.
Consolidation phase chemotherapy may consist of another round of the chemotherapy regimen used in induction therapy, different doses of drugs used in the initial induction therapy, or treatment with different drugs. For instance, higher doses of cytarabine either alone or in combination with other drugs are often used. One such combination is the FLAG-IDA regimen (cytarabine, fludarabine, granulocyte colony stimulating factor and idarubicin). New chemotherapy drugs and new regimens (combinations of drugs) are being studied in clinical trials. A physician may recommend that a person with AML join a clinical trial, especially if their disease seems resistant to standard treatment options.
Sometimes, doctors may recommend an allogeneic stem cell transplant for consolidation therapy. Whether to undergo this procedure is based on many factors including those discussed in the second paragraph of this section. An allogeneic stem cell transplant is a type of bone marrow transplant. Hematopoietic stem cells are special cells found in bone marrow that manufacture different types of blood cells (e.g., red blood cells, white blood cells, platelets). In allogeneic stem cell transplantation, stem cells are donated from another person, usually from a closely matched family member. In people with AML, this procedure follows treatment with strong doses of chemotherapy to wipe out leukemic cells. Sometimes, radiation therapy may also be used. In some people, the new (donated) cells that are infused into the patient will recognize any remaining leukemic cells as foreign and destroy them. This is called graft-versus-leukemia effect, but it does not always occur. Allogeneic stem cell transplants can be associated with severe, even life-threatening complications. Generally, this therapy is reserved for people who do not respond to other treatment options and younger patients who meet specific criteria.
Some people such as certain older individuals who meet specific criteria may elect to undergo a reduced-intensity (nonmyeloablative) allogeneic stem cell transplant. These transplants involve an initial chemotherapy regimen given at lower doses (reduced intensity), and thus are mild enough for people who are not eligible for a regular allogeneic stem cell transplant.
In 2017, the following drugs were approved to treat AML:
Midostaurin (Rydapt) was approved for the treatment of adult patients with newly diagnosed FLT3 gene positive AML in combination with standard cytarabine and daunorubicin induction and cytarabine consolidation. Rydapt is manufactured by Novartis Pharmaceuticals Corp.
Idhifa (enasidenib) was approved to treat adult patients with relapsed or refractory AML who have a IDH2 gene mutation. The drug was approved for use with the RealTime IDH2 Assay, which is used to detect specific mutations in the IDH2 gene in patients with AML. Idhifa is manufactured by the Celgene Corporation. The RealTime IDH2 Assay is manufactured by Abbott Laboratories.
Vyxeos was approved to treat adults with two types of AML: newly diagnosed therapy-related AML (t-AML) and AML with myelodysplasia-related changes (AML-MRC). Vyxeos is a fixed-combination of chemotherapy drugs daunorubicin and cytarabine that is manufactured by Jazz Pharmaceuticals.
Mylotarg (gemtuzumab ozogamicin) was approved to treat adults with newly diagnosed AML whose tumors express the CD33 antigen (CD33-positive AML) and to treat patients aged 2 years and older with CD33-positive AML who have experienced a relapse or who have not responded to initial treatment. Mylotarg is manufactured by Pfizer Inc.
More than 50% of people with AML experience a return of cancer, called a relapse. If relapse occurs within the first year, then physicians may recommend that individuals participate in a clinical trial for a new treatment option. Another option is to try another round of induction therapy with a different chemotherapy regimen and new drugs. If a relapse is over a year later, then physicians may recommend an allogeneic stem cell transplant, or they may recommend repeating the chemotherapy used during induction therapy, or they may recommend both. People who experience a relapse or for whom further treatment is ineffective, may be encouraged to participate in a clinical trial.
There is no clear age that distinguishes between younger adult and older adult. In most studies, older adults have been defined as people over the age of 60. Treatment for older adults is difficult because they are more likely to have conditions unrelated to AML (e.g. heart disease, diabetes) that may limit treatment options. AML also tends to be more resistant to chemotherapy in older adults and they are more susceptible to side effects from treatment. There is no agreed upon, optimal approach to treating older adults with AML. Treatment for older adults is highly individualized.
The treatment of AML in children is similar to that for younger adults. Induction therapy with chemotherapy, often cytarabine and anthracycline drugs including daunorubicin or doxorubicin, are used. However, there are different induction therapy regimens that can be used to treat children with AML. Decisions concerning treatment are made based on the factors discussed in the beginning of this section. As with adults, children with AML will go through a consolidation phase of treatment as well. Treatment of relapse in children is similar to treatment in younger adults. Physicians may recommend participation in a clinical trial.
As of February 2017, there are multiple drugs and drug combinations being studied as potential therapies for AML. Some of these are targeted agents for select AML populations while others are for patients who have not responded to other treatments or those just beginning their first treatment for AML. The eligibility criteria are select and best assessed by the treating physician.
Targeted therapies are being studied as potential treatments for AML. Targeted therapies are medications that directly target a gene mutation associated with AML. There are several genes that have been shown to be involved in the development of AML in some people including the FLT3, NPM1, DNMT3A, IDH1 or IDH2, NRAS or KRAS, or RUNX1 genes. These medications are being studied as single agents (by themselves) or in conjunction with standard chemotherapy regimens. These medications usually work by blocking (inhibiting) the protein product of the altered gene, which researchers believe contribute to the growth and spread of AML. More research is necessary to determine the long-term safety and effectiveness of targeted therapies for people with AML.
Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.
For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:
Toll-free: (800) 411-1222
TTY: (866) 411-1010
Some current clinical trials also are posted on the following page on the NORD website:
For information about clinical trials sponsored by private sources, in the main, contact:
For more information about clinical trials conducted in Europe, contact: https://www.clinicaltrialsregister.eu/
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