Acute Myeloid Leukemia

Disease / Phenomenon

Acute myeloid leukemia (AML) is an aggressive cancer of the blood-forming tissue inside bone marrow. It begins when a myeloid progenitor cell acquires genetic damage that halts normal maturation, leaving the marrow crowded with immature blasts that divide relentlessly yet never become functioning granulocytes, red cells, or platelets. As blasts accumulate they displace healthy hematopoiesis, producing the disease's characteristic triad of anemia, infection susceptibility, and bleeding or bruising. Onset is typically rapid, measured in weeks rather than years, and incidence rises sharply after age sixty, although AML occurs at any age. Recognized risk factors include prior chemotherapy or radiation exposure, benzene, smoking, and antecedent marrow disorders such as myelodysplastic syndrome.

At the molecular level AML is strikingly heterogeneous. Recurrent mutations in FLT3, NPM1, IDH1 and IDH2, DNMT3A, and TET2, together with fusion genes such as PML-RARA and RUNX1-RUNX1T1, define biologically distinct subtypes that behave very differently. These lesions converge on a few shared themes: blocked differentiation, resistance to programmed cell death, disordered epigenetic control, and metabolic rewiring that sustains proliferation. Signals from the marrow niche and inflammatory cytokines further support blast survival. This page decomposes AML into its component biological processes, the molecular pathways operating within each, and the biomarkers that make them measurable.