تسجيل الدخول

تسجيل

Phenotype of Acute Myeloid Leukemia

المؤلف:  Hoffman, R., Benz, E. J., Silberstein, L. E., Heslop, H., Weitz, J., & Salama, M. E.

المصدر:  Hematology : Basic Principles and Practice

الجزء والصفحة:  8th E , P937

2026-10-04

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Normal hematopoiesis is characterized by self-renewal and differentiation of long-term hematopoietic stem cells (HSCs) to short-term HSCs, multipotent progenitors, and common lymphoid and myeloid progenitors. These lineage-committed progenitors further differentiate to mature lymphoid or myeloid cells, including erythrocytes, granulocytes, macrophages, and platelets. This process is regulated by lineage-specific transcription factors at key points during normal hematopoiesis. Functional analysis of recurrent chromosomal, molecular, and epigenetic alterations in AML has revealed that many of these lesions corrupt hematopoietic differentiation programs, impacting proliferation, survival, and maturation of myeloid progenitor cells. Consequently, a hallmark of the AML phenotype is an accumulation of immature myeloid precursors. A myeloblast count of 20% or greater distinguishes AML from other myeloid malignancies.

Historically, leukemias were classified according to morphologic criteria using the French-American-British (FAB) classification, first proposed in 1976. This system classifies AML by the extent of maturation and lineage specificity, ranging from M0 (undifferentiated) to M3 (promyelocytic), M4eo (myelomonocytic with eosinophilia), M6 (erythroid), or M7 (megakaryocytic). Certain FAB subtypes were subsequently found to correlate with underlying cytogenetic abnormalities, notably M3 with t(15;17), M4eo with inv(16), and M2 with t(8;21). As greater understanding of recurrent cytogenetic and now molecular and epigenetic aberrations has developed, it has become clear that morphology alone is inadequate to fully describe the disease spectrum of AML.