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Acute Myeloid Leukaemia (AML)

C92-C94WHO Vol. 11 (2024)
Haematolymphoid System

Key facts

Estimated new cases (US, 2026)
22,720 (SEER)
Estimated deaths (US, 2026)
11,500 (SEER)
5-year relative survival
33.4% (SEER, 2016–2022 data)
Typical age at diagnosis
median 70 years; most cases diagnosed at 65–74
Main risk factors
smoking, previous chemotherapy or radiotherapy, benzene exposure, prior blood disorders (e.g. myelodysplastic syndrome)
Screening
no screening test; detected through blood counts when symptoms appear

Acute myeloid leukaemia (AML) is a fast-progressing blood cancer in which the bone marrow produces large numbers of abnormal, immature white blood cells (myeloblasts) that crowd out healthy red cells, white cells and platelets. It arises from myeloid stem cells, and its subtypes are distinguished by features of the leukaemia cells, including the genetic changes found in them; a distinct example is acute promyelocytic leukaemia (APL), driven by the PML::RARA fusion gene. AML is mainly a disease of older adults, with a median age at diagnosis of 70 years. Symptoms usually build up over a few weeks and reflect bone marrow failure: fatigue and pallor from anaemia, fevers and infections from a lack of working white cells, and easy bruising or bleeding from low platelets. The disease is detected with blood counts and confirmed by bone marrow aspiration and biopsy, with cytogenetic and molecular testing used to establish the subtype and guide treatment, which typically proceeds in remission-induction and consolidation phases.

Prognosis

AML is not staged like solid tumours; the outlook depends above all on the genetic (cytogenetic and molecular) subtype of the leukaemia, the patient's age and overall fitness, and factors such as the white blood cell count at diagnosis. In the US SEER registry, 5-year relative survival for AML overall is 33.4% (based on 2016–2022 data), and death rates have been slowly declining, by about 0.9% per year over 2015–2024. Outcomes differ widely between risk groups: younger patients and those with favourable genetic subtypes, such as acute promyelocytic leukaemia, generally respond to treatment much better than older patients or those with high-risk disease. These figures are population statistics drawn from many past patients — they cannot predict the course of any individual's illness, which the treating haematology team assesses from that person's specific results.

🔬 Histological Types

📚 Latest Research

2026-09-09

Exosomal METTL16 from mesenchymal stem cells promotes malignant progression and M2 macrophage polarization in acute myeloid leukemia via IGF2BP2-dependent GPX1 m6A modification.

Shang Z, et al

A new study identifies GPX1 as a critical hub gene in acute myeloid leukemia (AML), showing that exosomal METTL16 secreted by AML-associated mesenchymal stem cells (MSCs) stabilizes GPX1 mRNA through IGF2BP2-dependent m6A modification, thereby fueling leukemic cell survival and immunosuppressive M2 macrophage polarization. GPX1 expression was significantly upregulated in AML and closely linked to monocyte-macrophage differentiation, while its silencing suppressed AML cell malignancy, induced oxidative stress, enhanced cytarabine sensitivity, and inhibited M2 polarization (p < 0.05). METTL16 was found to be highly enriched in exosomes isolated from both AML patient serum and AML-MSCs (p < 0.05), and METTL16-deficient exosomes reversed pro-tumoral effects in vitro and in vivo by downregulating GPX1 (p < 0.05). These findings establish the exosomal METTL16–IGF2BP2–GPX1 axis as a potential therapeutic target for disrupting the bone marrow microenvironment crosstalk that sustains AML progression.

Biochimica et biophysica acta. Molecular basis of disease

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2026-09-09 • AI

High-Content Imaging Workflow for Single-Cell Drug Response Profiling of Acute Myeloid Leukemia Subtypes.

Isigkeit L, et al

Researchers have developed a high-content fluorescence imaging platform that profiles drug responses in Acute Myeloid Leukaemia (AML) at the level of individual cells, overcoming the limitations of conventional bulk viability assays that mask tumour heterogeneity. The workflow integrates three non-toxic fluorescent dyes capturing nuclear morphology, mitochondrial function, and apoptosis, and applies supervised machine learning to classify thousands of cells per sample as viable, apoptotic, or dead, enabling the derivation of IC50 values and drug sensitivity scores (DSS) at single-cell resolution. Validation across seven AML cell lines — including models of acquired and mutation-driven resistance to BCL-2 inhibition — showed strong concordance with the established ATP-based CellTiterGlo assay, and a 16-compound panel screen confirmed robust agreement between image- and CTG-based profiles. In a pilot primary-patient experiment using a 31-compound screen, BCL-2 inhibitors emerged as the most active agents, consistent with the patient's molecular profile, underscoring the platform's potential for functional precision oncology and combination therapy optimisation.

SLAS discovery : advancing life sciences R & D

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2026-09-09

The stress-sensing MARCH5 axis governs blood cancer apoptotic resilience via tractable protein-protein interactions.

Lew TE, et al

Researchers have identified a mitochondrial stress-sensing protein complex — comprising MARCH5, UBE2J2, and MFN2 — that enables blood cancer cells to resist apoptosis, and demonstrated that disrupting this complex restores sensitivity to the approved drug venetoclax in models of refractory lymphoma and cytokine-stimulated, drug-resistant chronic lymphocytic leukemia (CLL). The complex assembles at mitochondria-ER contact sites (MERCS) and co-localizes specifically with the anti-apoptotic proteins BCL-2 and BCL-XL but not MCL-1, creating a spatially encoded mechanism that integrates diverse cellular damage signals into life-or-death decisions in hematopoietic malignancies. Critically, non-blood cell lines show a phenotype largely restricted to BCL-XL dependence, suggesting a tissue-selective therapeutic window that would allow venetoclax combinations to target blood cancers with reduced toxicity to normal tissues. Genetic deletion of MARCH5 or UBE2J2 reversed BH3-mimetic resistance in primary CLL cells, and disrupting key protein-protein interactions within the complex prolonged survival in a murine model of refractory lymphoma, establishing these protein interfaces as tractable drug targets.

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💊 Therapies

Chemotherapy
Immunotherapy
Targeted therapies
Hematopoietic stem cell transplantation

🥗 Diet

Low-bacterial (neutropenic) diet Enteral and parenteral nutrition (tube feeding and intravenous feeding)

🫙 Supplements

Probiotics for diarrhoea caused by chemotherapy and radiotherapy

🧪 Tumor markers

Lactate dehydrogenase

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🩺 Centers for this diagnosis

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See all › Outpatient clinics for this diagnosis (14) ›

Sources

  1. NCI SEER Cancer Stat Facts: Acute Myeloid Leukemia (AML) ↗
  2. NCI PDQ: Acute Myeloid Leukemia Treatment (Patient Version) ↗
  3. ESMO: Acute Myeloblastic Leukaemia — A Guide for Patients ↗