Acute Myelogenous Leukemia

AML and Its Morphology

The AML, commonly called as acute myeloid leukemia, is a class of heterogeneous disease caused in the bone marrow and peripheral blood cells due to the clonal enhancement of myeloid progenitors. Previously, AML could not be cured due to limitations in the availability of resources, but the advancement of technologies has rehabilitated 35%-40% of patients below 60years. However, it still remains challenging to cure patients older than 60years. Many studies have showm that this disease arises from the mutations recurrently accumulated in hematopoietic stem cells w'ith age. As the NGS technologies develop, primary and relapsed tumors have been identified w'ith their therapeutic approaches (Ding et al. 2012). It has been characterized morphologically that the progenitors of AML have varying sizes and shapes from as small as lymphocytes to as large as monocytes, with a large-size nucleus usually containing several nucleoli. The precursors of AML are present on fit and fine undeveloped myeloid cells such as common differentiation (CD) markers including CD-13, CD-33, and CD-34 (Campos et al. 1989) and are usually expressed based on morphological subclassification of AML and differentiation of immature cells. Additionally, it can also co-express T-cell and B-cell antigens such as terminal deoxynucleotidyl transferase, human leukocyte antigen- antigen D related, CD-7, and CD-19.

Classification Systems for AML

Many different classification systems have been discovered for AML in the past years according to their morphology, etiology, phenotypic immunity, and genetics study, and in the early 1970s, it was classified based on the French-American-British system of classification through the criteria of morphological appearances and phenotypic and cytochemical immunity, to elucidate eight AML subtypes such as FAB MO, Ml, М2, М3, M4, M5, M6, and M7. But the old French-American-British system of AML classification is now replaced by the classification of WHO. WHO classification has been renewed in 2008 and defines seven subtypes of AML such as AML having myelodysplasia-related changes; AML having repeated genetic aberrations such as aberrations in RUNXJ-RUNX1TJ translocation t(8;21)(q22;q22), CBFB-MYHl 1 inversion Inv(16)(pl3.1q22), and translocation t(16;16)(pl3.1;q22), PML-RARA translocation t( 15,17)(q22:ql2), MLL llq23, and with mutated genes such as NPM1 and СЕВРА; NOS-AML; therapy-related myeloid neoplasms; the proliferation of myeloid based on Down’s syndrome; myeloid sarcoma; and blastic plasmacytoid neoplasm in dendritic cells (Vardiman et al. 2009). According to the classified system of etiology, AML can be categorized as secondary AML, therapy-related AML, and de novo AML (Lindsley et al. 2015).

 
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