Luara L. Arana-LunaMartha Alvarado‐IbarraLuis G. Silva-MichelAdrián Morales-MaravillaMaría del C. González-RubioLénica A. Chávez-AguilarMa. Fernanda Tena-IturraldeLiliana Mojica-BalcerasNidia Zapata-CantoPatricia Galindo-Delgado2026-03-222026-03-22202210.24875/gmm.m21000597https://doi.org/10.24875/gmm.m21000597https://andeanlibrary.org/handle/123456789/58193Citaciones: 1Acute myeloid leukemia (AML) comprises a heterogeneous group of hematopoietic cell neoplasms of myeloid lineage that arise from the clonal expansion of their precursors in the bone marrow, interfering with cell differentiation, leading to a syndrome of bone marrow failure. AML is a consequence of genetic and epigenetic changes (point mutations, gene rearrangements, deletions, amplifications, and arrangements in epigenetic changes that influence gene expression) in hematopoietic precursor cells, which create a clone of abnormal cells that are capable of proliferating but cannot differentiate into mature hematopoietic cells or undergo programmed cell death. The diagnosis requires more than 20% myeloid blasts in the bone marrow and certain cytogenic abnormalities. Treatment will depend on age, comorbidities, and cytogenetic risk among the most frequent.esMedicinearticle