Acute myeloid leukemia (AML) is an aggressive blood cancer that arises from immature myeloid cells in the bone marrow. These abnormal cells proliferate rapidly and crowd out normal blood cell production, leading to anemia, infections, and bleeding. AML is biologically diverse, driven by various genetic and chromosomal abnormalities that influence prognosis and treatment response.

Research has identified recurrent mutations in genes that regulate cell growth, differentiation, and epigenetic control, such as FLT3, NPM1, IDH1/2, DNMT3A, and others. These discoveries have enabled more refined diagnostic classification and risk stratification, replacing older systems based largely on morphology. Cytogenetic profiles and molecular markers now guide treatment intensity and decisions about stem cell transplantation.

Targeted therapies have transformed the treatment landscape for specific AML subtypes. FLT3 inhibitors, IDH inhibitors, and BCL2 inhibitors are used in patients whose leukemias harbor these vulnerabilities, often in combination with hypomethylating agents or traditional chemotherapy. For some older or unfit patients, lower intensity regimens with targeted agents offer improved survival and quality of life compared with intensive chemotherapy alone.

Despite these advances, many patients relapse, and minimal residual disease monitoring is increasingly used to detect early recurrence and refine therapy. Ongoing research focuses on overcoming drug resistance, exploiting leukemic stem cell biology, and integrating immunotherapies such as antibody drug conjugates and cellular therapies. The overarching trend is toward personalized treatment based on the genetic and molecular features of each patient’s leukemia, with the goal of improving long term survival while reducing treatment toxicity.