AML vs. CML: What Are the Differences?

Acute and chronic myeloid leukemia

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Acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) differ in how the condition develops and worsens, their symptoms, diagnosis, and treatment. In AML, the disease comes on quickly and rapidly deteriorates without treatment. With CML, the condition comes on slowly and worsens over time.

Learn what sets AML apart from CML and help ensure that you get the proper care from a physician specializing in this area.

AML vs. CML Symptoms

Verywell / Jessica Olah


It's not always easy to distinguish between acute and chronic myeloid leukemia based on symptoms alone. These can be remarkably similar in some cases. Some of the symptoms that both have in common include the following:

  • Tiredness
  • Weakness
  • Fever

However, there can also be differences as well. With acute myeloid leukemia, patients may also experience signs such as:

  • Feeling short of breath
  • Bruising easily
  • Loss of appetite with potential weight loss
  • Petechiae: Pinpoint spots underneath the skin caused by bleeding
  • Bone pain
  • Frequent infections
  • Painless lumps on the body

Meanwhile, those with chronic myeloid leukemia may experience signs such as:


While both AML and CML may seem similar in some respects, there are some definite distinctions. The underlying causes here are actually different.

Acute Myeloid Leukemia

With acute myeloid leukemia, a mutation in the stem cells causes more white blood cells to be produced than are needed. However, these white cells are still immature (not maturing beyond the early blast stage) and lack the infection-fighting capabilities of fully developed white blood cells.

As the number of these immature blast cells increases, this also leaves less room for needed red blood cells (which carry oxygen) and platelets (which help in clotting), which begin to decrease. When these healthy cells are crowded out, this gives rise to AML leukemia symptoms.

Chronic Myeloid Leukemia

In many cases of chronic myeloid leukemia, some DNA between chromosomes 9 and 22 is partially swapped in a process known as translocation. In almost all CML patients, this makes chromosome 22 shorter than usual—something dubbed the Philadelphia chromosome.

This also leads to the formation of the BCR-ABL oncogene, which produces a protein that causes CML cells to grow and divide uncontrollably. These DNA changes are not passed to you from your parents (inherited) but rather occur during your lifetime.

CML cells mature more than their AML counterparts. While these more closely resemble normal white blood cells, they don't fight infection as well. They also end up crowding out normal cells from the bone marrow.

With CML, it can take much longer for the condition to cause problems. However, it may be more challenging to cure CML than AML.


Determining whether you may have either AML or CML will mean undergoing a battery of tests. With CML, there may be no symptoms. Rather, this may be flagged during a routine checkup or a blood test done for something unrelated.

For both AML and CML, you can expect to undergo blood, bone marrow, and genetic tests such as the following:

AML Testing

When diagnosing AML, some factors doctors may be looking for in the lab samples include:

  • Leukemic blast cells in the bone marrow
  • An increased percentage of blast cells in the marrow
  • Unique antigen markers on the blast cell surface, such as cluster designation (CD)13 or (CD)33

CML Testing

In looking for a case of CML, doctors are on alert for:

  • An increased white blood cell count together with reduced red blood cell numbers and a possible decrease in platelets
  • Any changing proportion of fully mature white blood cells to immature ones
  • The type of blood cells and their size and shape
  • Signs of the BCR-ABL1 gene, which can sometimes be identified by the FISH test or in other cases may require a more sensitive quantitative polymerase chain reaction test to find


Finding the right treatment for your particular type of leukemia is key because approaches can vary.

AML Approaches

Chemotherapy is the primary treatment for those diagnosed with AML. This involves the use of drugs to kill cancer cells, in most cases by interfering with their ability to divide and grow. Chemotherapy will likely be divided into two phases: induction and consolidation.

Induction therapy takes place right after diagnosis, aiming to put you into complete remission. In younger people, a combination of cytarabine (Cytosar-U) and Cerubidine (daunorubicin) or Idamycin (idarubicin) is commonly given.

Older adults with conditions that rule out the use of intensive chemotherapy may be given lower intensity therapies, such as Dacogen (decitabine), Vidaza (azacitidine), or low dose cytarabine. These therapies may be used alone or in combination with Venclexta (venetoclax), a BCL2 inhibitor, or Tibsovo (ivosidenib), an IDH1 inhibitor, if mutations are present.

Consolidation therapy is done by giving different medications following induction therapy to mop up any lingering AML cells that may not have been detected. Younger patients are often given two to four rounds of at least an intermediate dose of an agent like cytarabine.

As part of the therapy, particularly for those at higher risk of relapse, a stem cell transplant is often suggested.

In some AML cases, targeted therapy aimed at specific genes or proteins or even the environment of the tissue itself may be an option. This can target mutations in genes such as IDH1, IDH2, and FLT3.

Radiation therapy, in which cancer cells are destroyed by beams of X-rays or other particles, tends to be given only in select cases as it would not target the AML cells circulating in the blood. This may involve cases in which AML has spread to the brain or where a specific tumor needs to be shrunk.

CML Therapy

The usual treatment for the majority of people with CML is targeted therapy, with other options such as chemotherapy, immunotherapy, and bone marrow (stem cell) transplantation used much less often than they were in the past.

The targeted approach for CML patients takes aim at the BCR-ABL tyrosine kinase enzyme, with the idea of inhibiting this protein. When tyrosine kinase inhibitors are used, these keep the BCR-ABL enzyme from working and kills off CML cells. These usually come in pill form.

Some tyrosine kinase inhibitors that may be offered to those with CML include the following:

  • Gleevec (imatinib): Approved in 2001, this was the first targeted therapy for CML.
  • Sprycel (dasatinib): This can be used either as an initial treatment or substituted for other drugs that are not working.
  • Tasigna (nilotinib): This agent is another initial option or a possibility if another targeted medication is not working.
  • Bosulif (bosutinib): This medication is offered to those experiencing a lot of side effects or in cases where other targeted agents are not effective.
  • Iclusig (ponatinib): Those on this medication have the T3151 mutation and have not had luck with other agents, either finding these ineffective or experiencing a large number of side effects.

Chemotherapy may also be a possibility in some CML cases with Droxia or Hydrea (hydroxyurea). This may be used initially to normalize blood cell levels and also reduce spleen size. The downside is that this alone does not prevent blasts from developing, and it also doesn't reduce the number of cells with Philadelphia chromosome.

Another option may be immunotherapy, which relies on the body's own immune system to destroy the cancer. The immunotherapy agent interferon, given by an injection under the skin, can help lower white blood cell counts and, in some cases, can reduce those cells with the Philadelphia chromosome.

Stem cell transplantation (formerly called bone marrow transplantation) may be an option for some CML patients. With this, bone marrow with leukemia is replaced by hematopoietic (blood-producing) stem cells, which have the ability to develop into normal bone marrow. These can either come from your own stem cells or be donated by someone else.


Heading off AML or CML before it develops can be an appealing idea. Unfortunately, for CML, there are no known lifestyle risk factors that can be altered.

With AML, most of those affected do not have any lifestyle risk factors that can be changed. Quitting smoking is one of the few actions that may have a preventive effect. Also, your risk may be lowered by avoiding the cancer-causing chemical benzene. However, this is likely a risk factor for AML in only a few cases.

Some rare cases of AML occur after a person has a different type of cancer that is treated with chemotherapy or radiation. The doctor will weigh the need for treating this other cancer with the slightly increased risk that it may result in AML.


AML and CML are blood and bone marrow cancers that affect the same lines of white blood cells. AML comes on suddenly as very immature cells crowd out normal cells in the bone marrow. CML comes on more slowly, with the CML cells growing out of control.

AML is vigorously treated upon detection with chemotherapy and stem cell transplantation. CML is primarily treated with targeted therapy, but may also be treated with chemotherapy, immunotherapy, or stem cell transplantation.

A Word From Verywell

Whether you are dealing with a case of AML or CML, it may feel overwhelming. However, by familiarizing yourself with leukemia in general as well as the particular form with which you may be contending, you optimize your chances for a good outcome in both the near term and the long term.

Frequently Asked Questions

How do you get leukemia?

AML is caused by a DNA mutation that results in an overabundance of immature white blood cells. These do not effectively fight infection and may crowd out healthy blood cells. It is not known why this mutation develops. But it is known that both smoking and prolonged exposure to the chemical benzene might put you at increased risk.

In CML, there seems to be a genetic component. Often a mutation producing the Philadelphia chromosome is seen. It produces a protein that causes CML cells to grow out of control. However, mutations here are not passed down by your parents but rather are something that occurs during your own lifetime.

What's the difference between acute and chronic myeloid leukemia?

While some of the symptoms of AML and CML are similar, these are two different conditions. The speed of occurrence can be a distinction here.

AML occurs when too many white blood cells are produced in the marrow. These don't mature properly and can crowd out other blood cells. This is a condition that can arise rapidly, occurring over days to weeks.

Likewise, with CML, too many immature white blood cells don't leave enough room for healthy cells. This is a process, however, that occurs over months to years.

What is the survival rate of leukemia in adults?

For both adults and children, AML is the second most common type of leukemia diagnosed. Most of the time, it occurs in adults. For those ages 20 and older, there is a 26% five-year survival rate. The survival rate under the age of 20 is 68%.

CML accounts for about 15% of all leukemia, with about 50% occurring in those over 64. This is very rare in children. New drugs have significantly increased the five-year survival rates here, with these more than tripling from around 22% surviving with the condition in the mid-1970s to around 72% today.

15 Sources
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
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By Maxine Lipner
Maxine Lipner is a long-time health and medical writer with over 30 years of experience covering ophthalmology, oncology, and general health and wellness.