Acute Myeloid Leukemia (AML)

 

AML is a malignancy of immature bone marrow cells including high numbers of blasts and with subtypes M0 to M7. The subtypes indicate degree or lack of maturation of the cells.

  • M0 and M1 are characterized by blasts with no or little maturation, including no or little myeloperoxidase reaction, respectively.
  • M2 is characterized by some maturation including the presence of promyelocytes or more mature neutrophils. In one form of M2, there is an increase in basophils.
  • M3 is characterized by presence of many abnormal promyelocytes and is also referred to as acute promyelocytic leukemia (APL).
  • M4 and M5 are characterized by some monocytic differentiation. M4E is a subtype of M4 and is characterized by presence of abnormal eosinophils. M5 is divided into M5A, which is characterized by the presence of many monoblasts, and M5B, which is characterized by the presence of more mature monocytic cells. M4 is also referred to as acute myelomonocytic leukemia, and M5 is also referred to as acute monocytic leukemia.
  • M6 is characterized by some erythroid differentiation and is also referred to as erythroleukemia and can be considered a form of di Guglielmo’s syndrome.
  • M7 is characterized by some megakaryocytic differentiation and is also referred to as acute megakaryoblastic leukemia.
  • A distinct and rare form of AML is acute basophilic leukemia (without an M number), characterized by the presence of basophilic granules that may require electron microscopy for identification.

AML may be primary or secondary (therapy-related). Many subtypes are associated with distinct chromosomal abnormalities. AML occurring in an extramedullary site is also referred to as granulocytic sarcoma.

 


AML Abnormalities

 

-7
 +21
del(5)(q13q35) most characteristic of “5q-” syndrome
del(7)(q11.2-q36)
del(9)(q21-q22) secondary changes in AML, interstitial or terminal
del(12)(p12) approx breakpt.
del(20)(q11.2)
del(20)(q11.2q13.1)
i(17)(q10)
idic(X)(q13)
ins(3;3)(q26;q21q26)
inv(3)(q21q26.2)
inv(16)(p13.1q22) M4-E0
t(1;3)(p36.1;q21) M1,M4
t(1;11)(q21;q23) M4,M5
t(1;22)(p13;q13) M7
t(3;3)(q21;q26) M1,M4,M6
t(3;5)(q21-25;q31-35) M6, sometimes MDS precedes
t(3;21)(q26.2;q22) genotoxic exposure
t(6;9)(p23;q34) M2,M4, BM basophilia
t(6;11)(q27;q23) M4, M5
t(7;11)(p15;p15) M2
t(8;16)(p11;p13) M5b
t(8;21)(q22;q22) M2
t(9;11)(p21-22;q23) M5
t(9;22)(q34;q11.2)
t(10;11)(p11-15;q13-23) M5
t(11;15)(q23;q21) M3
t(11;17)(q23;q21) M3
t(11;17)(q23;q25) M2,M4,M5
t(11;19)(q23;p13.1) M4, M5
t(11;19)(q23;p13.3) M4, M5
t(15;17)(q24;q21) M3
t(16;16)(p13.1;q22) M4 w/increased eosinophils, variant of inv(16)
t(16;21)(p11;q22)

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