Acute myeloid leukemia is a cancer that starts in the bone marrow, where the body makes blood, and it develops quickly, so it usually needs treatment to start soon after it is found [1,2].
This page provides general information. It does not replace advice from a doctor or another qualified healthcare professional.
Bone marrow, the soft inner part of some bones, is where blood is made. It holds stem cells, which become red blood cells that carry oxygen, platelets that stop bleeding, and white cells that help protect against infection [3]. These follow a myeloid or a lymphoid path, and AML starts on the myeloid side [3].
In AML the marrow makes large numbers of immature myeloid white cells called blasts. They do not work properly, crowd out healthy cells and often spill into the blood [2,17]. AML is usually diagnosed when blasts reach 20 in every 100 marrow cells, or fewer where certain gene changes are present [2,16]. Acute means fast-developing, so treatment starts right away [3].
Another name is acute myelogenous leukemia [3]. Chronic myeloid leukemia starts in the same cells and grows slowly, while acute lymphoblastic leukemia is fast like AML and starts in lymphoid cells [3,11].
AML is uncommon. About 22,720 people in the United States were expected to be diagnosed in 2026, around 1.1 percent of all new cancer cases, with about 11,500 deaths [1,4]. The rate was 4.4 new cases per 100,000 a year, the median age at diagnosis is 70, and about 62 in every 100 new cases are in people aged 65 or over [1,5].
Cancer Research UK reports around 2,700 diagnoses a year in the United Kingdom [13], the NHS around 3,100, the counts using different diagnostic codes [11]. Australia has around 900 a year [17]. A Global Burden of Disease analysis estimated 144,645 cases worldwide in 2021, up from 79,372 in 1990, largely because people live longer [28]. Recorded rates are higher in higher-income countries, partly because AML is a disease of later life and partly because the tests needed to name it are not available everywhere, so lower-income figures are probably undercounts [28].
In most cases no cause can be identified [11]. AML begins when something goes wrong in the DNA, the instruction set inside developing blood cells, of which a gene is one section. Nobody knows why this happens, and nothing a person did brought it on [15].
Several things raise the risk, though most people who have them never develop AML [5,15]:
Families ask about inheritance constantly, and the answer is reassuring. AML is not usually inherited: the gene changes almost always happened inside the leukemia cells during the person’s life, and most people diagnosed have no affected relative [5,15]. A close relative raises the risk slightly, and rare families pass on an altered gene [5,17].
Symptoms appear over a few weeks and get worse [11]. Most come from having too few healthy blood cells [6]:
Weight loss, night sweats and bone pain are common too, and occasionally there are no symptoms [6,17].
When to seek urgent help. Contact a doctor or the hospital team the same day for a fever or any sign of infection, unexplained bleeding or bruising, or new breathlessness [6,11]. Very high blast numbers can slow blood flow, which is rare and treatable, causing headache, weakness on one side, slurred speech or confusion, and needs emergency care [6]. United Kingdom guidance advises a blood count within 48 hours for adults with unexplained pallor, tiredness, fever, repeated infection, bruising or bleeding, and immediate referral once a test reports acute leukemia [25,26].
A family doctor usually orders a blood test. A very high number of abnormal white cells, or a very low count, points toward leukemia, and the person is referred urgently to a hematologist, a blood specialist [12]. Further tests use blood and marrow [2]:
The genetic results are not just labels. The World Health Organization’s 2022 classification defines many types of AML by their genetic change rather than by how the cells look [19]. European LeukemiaNet guidance sorts people into three risk groups, favorable, intermediate or adverse, guiding treatment intensity and whether a transplant may help [18,29].
Treatment starts quickly, sometimes before every result is back, given by a hospital hematology team [7].
Intensive chemotherapy. For people fit enough, induction chemotherapy, usually cytarabine with an anthracycline such as daunorubicin, clears as many leukemia cells as possible, and consolidation follows once in remission [7]. Counts stay low for weeks, so antibiotics, antifungals and transfusions are routine [2,7]. A donor stem cell transplant may replace or follow consolidation where the risk grouping suggests a likely return [7].
Lower-intensity treatment. For some people intensive chemotherapy would do more harm than good. A common alternative pairs azacitidine with venetoclax, a tablet blocking a protein leukemia cells use to survive [7,8]. In a trial of 431 people unfit for intensive treatment, median age 76, adding venetoclax lengthened median survival from 9.6 to 14.7 months [21]. Supportive care alone is also a legitimate choice [7].
Targeted medicines. Where the cells carry a particular gene change, a matching tablet may be used: midostaurin, quizartinib or gilteritinib for FLT3, ivosidenib for IDH1, enasidenib for IDH2, and the menin inhibitors revumenib or ziftomenib for NPM1-changed leukemia that has returned [8,23,24]. Those are United States approvals; availability varies.
Acute promyelocytic leukemia. This subtype is treated differently, and the news is better. It carries a high early bleeding risk, so treatment may begin as soon as it is suspected [9]. The main medicines are not chemotherapy: all-trans retinoic acid (ATRA) and arsenic trioxide push the cells to mature [9,22]. About 9 in 10 people reach remission, and 9 in 10 of those stay in long-term remission [10].
Measurable residual disease. Counts can look normal while a few leukemia cells remain, too few to see under a microscope. Sensitive tests find them, and the result, called measurable residual disease or MRD, can change what is advised next [16,20].
What the survival figures show. These figures are hard reading and worth stating plainly. In the United States, five-year relative survival was 33.4 percent for people diagnosed between 2016 and 2022, measured against people of the same age without cancer [1]. Age changes the picture sharply: among people diagnosed in one area of England between 2010 and 2019, five-year survival was 55 in every 100 for those under 40 and 1 in 100 for those aged 80 and over [14]. Such figures are averages and cannot say what will happen to one person, since outlook depends on subtype, genetics, age and fitness. They also describe people diagnosed years ago, before some current treatments existed [1,14,27].
A diagnosis of AML arrives suddenly and treatment starts fast, which is a lot to absorb. Finding out which type it is and what the plan involves often helps people feel more in control [12].
Daily life during treatment centers on infection and blood counts. While counts are low, a fever needs same-day contact with the team, and transfusions and preventive antibiotics are normal rather than a sign something has gone wrong [2,7]. Repeat marrow tests show whether the leukemia is responding [16]. AML and its treatment can affect sex life and fertility, so raise fertility before treatment starts [32]. Tiredness often lasts long after treatment ends [13].
Clinical trials test whether a treatment works and is safe. AML is an active research area, so studies come up reasonably often, including after the leukemia has come back. Deciding whether to look into one is personal, and it helps to take it in steps.
Be clear on what a study involves:
Every trial has rules about who can take part, called eligibility criteria. Some describe who can join, others who cannot. For an AML study they might include a confirmed diagnosis, a specific gene change such as FLT3, IDH1, IDH2 or NPM1, whether the leukemia is newly diagnosed or has come back, previous treatments, organ test results within set ranges, general fitness, and reliable contraception for some medicines.
trialport’s medifit helps people consider information related to possible medical suitability. It does not diagnose a condition, confirm eligibility or replace formal screening by the study team.
Explore acute myeloid leukemia clinical trials through trialport
A study can look right on paper and still be hard in practice. Worth thinking through:
trialport’s readifit helps people reflect on their understanding, motivation, time, routines, support, emotions and practical arrangements.
Questions to put to a research team:
Taking part is voluntary. A person can ask questions, speak with people they trust and choose not to participate.
Search for clinical trials at app.trialport.com.
Research is moving toward treatment chosen by the genetics of each leukemia. Main areas include:
Study status checked: 3 August 2026. Research moves quickly, so this list will date. For current information, search at app.trialport.com.
In the United States, the National Cancer Institute publishes a plain-language treatment summary in English and Spanish [2], and the American Cancer Society covers subtypes and treatment in depth [3].
In the United Kingdom, Blood Cancer UK has quality-marked information and a free line on 0808 2080 888 [15]. Leukaemia Care runs a helpline on 08088 010 444 [30]. Cancer Research UK has the fullest detail on subtypes and survival, with nurses on 0808 800 4040 [13,14], and the NHS has an overview [11].
In Australia, the Leukaemia Foundation provides information, accommodation and transport support on 1800 620 420 [17]. Coverage elsewhere is uneven, and where no local group exists a national cancer organization is the best starting point.
Evan Handler, the American actor known for Sex and the City and Californication, was diagnosed with acute myeloid leukemia in his mid-twenties in the 1980s, when it was widely regarded as incurable. He described his memoir, Time on Fire, on NPR as “a book about a 24 year old’s really angry journey through acute myeloid leukemia” [31].
Leukemia has several distinct types and public reports often do not say which one, so this page names only people who have described this condition publicly themselves.
Is AML curable?
For some people, yes. About 2 in 3 people who have intensive induction reach remission, and up to half of those who then have consolidation reach long-term remission and may be cured [10]. For others, particularly older people who cannot have intensive treatment, the aim is to control the leukemia and keep life as good as possible for as long as possible [7].
Why does AML have to be treated so quickly?
The cells multiply fast and crowd out healthy blood cells, so counts fall and the risks from infection and bleeding rise [3,11].
Is AML inherited?
Not usually. The gene changes almost always happened inside the leukemia cells during the person’s life, and most people diagnosed have no affected relative [5,15]. A close relative raises the risk slightly, so mention family history [5,17].
What is acute promyelocytic leukemia?
A subtype caused by a swap of genetic material between two chromosomes. It needs emergency treatment because of the early bleeding risk, and responds far better than other subtypes [2,9,10].
Do the survival figures apply to me?
No published figure applies to any individual. They are averages across large groups diagnosed years ago [1,14,27]. The hematology team is the right source for a personal answer.
Written by: trialport editorial team
Reviewed by: Keith Berelowitz, Founder and CEO, trialport
Reviewed on: 3 August 2026
Next review due: 3 August 2027
References last checked: 3 August 2026