M2 AML
| Acute myeloblastic leukemia with maturation | |
|---|---|
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| Myeloblast | |
| Classification and external resources | |
| Specialty | Hematology and oncology |
| ICD-O | M9874/3 |
| MeSH | D015470 |
M2 is a subtype of AML (Acute Myeloid Leukemia).
It is also known as "Acute Myeloblastic Leukemia with Maturation".
Acute myeloid leukemia (AML) is a type of cancer affecting blood cells that eventually develop into non-lymphocyte white blood cells. The disease originates from the bone marrow, the soft inner portion of select bones where blood stem cells develop into either lymphocyte or in this particular condition, myeloid cells. This acute disease prevents bone marrow cells from properly maturing, thus causing an accumulation of immature myeloblast cells in the bone marrow.
Acute myeloid leukemia is more lethal than chronic myeloid leukemia, a disease that affects the same myeloid cells, but at a different pace. Many of the immature blast cells in acute myeloid leukemia have a higher loss of function and thus, a higher inability to carry out normal functions than those more developed immature myeloblast cells in chronic myeloid leukemia (O’Donnell et al. 2012). Acute in acute myeloid leukemia means that the amounts of blast cells are increasing at a very high rate. Myeloid refers to the type of white blood cells that are affected by the condition.
Acute myeloid leukemia is the most common acute leukemia that is affecting the adult population. The 5-year survival rate for the cancer stands at around 26% (ACS, 2016).
M2 acute myeloblastic leukemia with maturation refers to the subtype of acute myeloid leukemia characterized by the maturation stages of the myeloid cell development and the location of the AML1 gene. One of the hallmarks of M2 subtype acute myeloid leukemia is the formation of a fusion protein, AML1-ETO or RUNX1-RUNX1T1, due to a translocation of chromosome 8 to chromosome 21 or t(8;21) (Miyoshi et al., 1991, Andrieu et al., 1996). This cytogenetic abnormality has been found in 90% of M2 acute myeloblastic leukemia; while the other 10% constitutes a mix of M1 and M4 acute myeloid leukemia (GFHC, 1990).
Another translocation between chromosome 6p23 and chromosome 9q34 is also associated with the M2 subtype. The t(6;9) causes the formation of a fusion oncogene made of DEK (6p23) and CAN/NUP214 (9q34). This rare translocation has a poor prognosis compared to the t(8;21) because 70% of t(6;9) acute myeloid leukemia patients have the FLT3-ITD mutation (Schwartz et al., 1983, Kottaridis, 2001). The FLT-ITD mutation is one of the most lethal mutations in acute myeloid leukemia (Chi et al., 2008).
The first red flag that indicates M2 acute myeloblastic leukemia with maturation is the skewed ratio of white blood cells to red blood cells. Leukemia is initially diagnosed by a peripheral blood smear, a procedure used to check for cell count and cell shapes. Then a bone marrow aspiration and biopsy would be conducted to collect and view the bone, bone marrow, and blood under a microscope. Cytogenetic assays, such as fluorescence in situ hybridization (FISH) would help evaluate the structure and function of the cell’s chromosomes.
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