Acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) are two types of leukemia that start in the bone marrow — the spongy tissue in the center of your bones, where blood cells are made. Leukemia is a type of cancer that develops when cells in the bone marrow start to grow out of control.

Although both types of leukemia affect cells that give rise to the same types of white blood cells, they differ in development, potential symptoms, treatment options, and outlook.

Types of Leukemia

Leukemia can be classified in two ways: how quickly it progresses — categorized as either acute or chronic — and the type of blood cells that are growing abnormally.

Acute vs. Chronic Leukemia

AML progresses rapidly and involves white blood cells that aren’t fully developed, called blasts. CML progresses more slowly and involves blood cells that are more mature.

Myeloid Leukemia

Leukemia can arise from two types of blood-forming cells — myeloid and lymphoid cells. Because they develop from myeloid cells that grow abnormally and don’t function properly, both AML and CML are known as myelogenous leukemias. Myeloid cells can develop into red blood cells, platelets (involved in blood clotting), and white blood cells such as neutrophils, basophils, eosinophils, and monocytes.

By comparison, lymphocytic leukemias, such as acute lymphocytic leukemia and chronic lymphocytic leukemia, cause the bone marrow to produce too many lymphocytes — white blood cells known as B cells and T cells.

What Causes AML and CML?

Leukemia is caused by mutations (changes) in the DNA of bone marrow cells that affect how the cells grow, divide, and die. DNA changes can occur throughout a person’s lifetime as a result of exposure to certain chemicals or radiation or because of random chance. The risk of a mutation that can cause leukemia increases with age.

AML cells commonly have mutations in genes that either stop bone marrow cells from maturing or help the cells grow uncontrollably. Examples of these genes are the following:

• FLT3
• c-KIT
• RAS
• IDH1 and IDH2

Almost all CML cells have an abnormal chromosome called the Philadelphia chromosome. This chromosome is the result of a gene called BCR-ABL, which makes a protein called tyrosine kinase. Tyrosine kinase causes CML cells to grow and divide out of control.

Who Gets AML vs. CML?

AML is more common than CML. The American Cancer Society estimates that in 2022, more than 20,000 new cases of AML and more than 8,000 new cases of CML will be diagnosed in the United States. Both AML and CML are more common in adults than children.

Risk Factors

Certain factors can increase your risk of developing either AML or CML.

According to the American Cancer Society, risk factors for both AML and CML include:

• Older age
• Male gender
• Exposure to radiation

The following risk factors have been shown to raise the risk of AML but don’t seem to increase the risk of CML:

• Smoking
• Exposure to certain chemicals
• Previous chemotherapy
• Blood disorders like myelodysplastic syndrome
• Certain genetic syndromes
• Family history of AML

People with Down syndrome are also at an increased risk of developing AML.

Symptoms of AML and CML

AML and CML may cause similar symptoms. However, because CML progresses more slowly, people with CML usually have less severe symptoms than those with AML.

Shared symptoms of AML and CML include:

• Weight loss
• Tiredness
• Fever
• Night sweats
• Loss of appetite
• Bone pain
• Swelling or pain in the abdomen

Many AML and CML symptoms occur because of the high number of leukemia cells, which can crowd out healthy, functional cells. Having too few red blood cells can result in anemia, causing symptoms such as:

• Weakness
• Tiredness
• Shortness of breath

When you have too many blast cells and not enough functional white blood cells or neutrophils, your risk of infection rises. If you don’t have enough platelets, your risk of bleeding arises.

Classification of AML and CML

Most cancers are classified into stages based on the size of the tumor and how far it has spread. AML and CML don’t usually form tumors, so their classification differs from other kinds of cancer.

AML is classified into subtypes based on the cancer cells’ characteristics, such as appearance under the microscope, genetic abnormalities, and blood cell counts.

CML is classified by phases — chronic, accelerated, and blast. Compared with people who have chronic phase CML, people with accelerated or blast-phase CML have more leukemia cells. If CML progresses to the blast phase, the symptoms can be very similar to those of AML.

Treatments for AML and CML

Chemotherapy and targeted therapy are the mainstays of treatment for AML and CML. The type of treatment your doctor recommends depends on the type of cancer you have. AML requires rapid treatment because it progresses very quickly.

Chemotherapy

The primary treatment for AML is often chemotherapy. The most common chemotherapy drugs used to treat AML include:

• Cytarabine (Ara-C)
• Daunorubicin (Cerubidine)
• Idarubicin (Idamycin)
• Azacitidine (sold as Onureg and Vidaza) combined with venetoclax (Venclexta)
• Decitabine (Dacogen) combined with venetoclax

In contrast, chemotherapy is rarely used to treat CML. Chemotherapy is typically used only in people who have accelerated or blast-phase CML or are resistant to targeted therapies.

Targeted Therapy

Targeted therapies attack a gene or protein specific to the cancer cell. Because AML and CML are caused by different gene mutations, the targets are different.

Venetoclax, a treatment for AML, zeroes in on the BCL-2 protein. In addition, several AML drugs target gene mutations. These drugs can be taken with chemotherapy or used alone by people who are older or not strong enough to tolerate chemotherapy.

• People with a mutation in the FTL3 gene can use midostaurin (Rydapt) or gilteritinib (Xospata).
• People with a mutation in the IDH1 gene can use ivosidenib (Tibsovo).
• People with a mutation in the IDH2 gene can use Enasidenib (Idhifa).

Because almost all CML cells have the same mutation causing abnormal tyrosine kinase activity, certain targeted therapies inhibit this protein. Known as tyrosine kinase inhibitors (TKIs), these drugs are very effective and provide the first-line treatment for CML. TKIs often used first in CML include:

• Imatinib (Gleevec)
• Dasatinib (Sprycel)
• Nilotinib (Tasigna)

Outlook for AML vs. CML

People with CML often have a better prognosis (outlook) than those with AML. According to studies, about 90 percent of people with CML and about 30 percent of individuals with AML survive for five years or more after diagnosis. If you have AML or CML, talk to your doctor to learn more about your prognosis.

Talk With Others Who Understand

MyLeukemiaTeam is the social network for people with leukemia and their loved ones. On MyLeukemiaTeam, more than 12,000 members come together to ask questions, give advice, and share their stories with others who understand life with leukemia.

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