The Fab And Who Classification Of

The FAB classification was composed of eight AML subtypes: M0-M7. These subtypes were distinguished based on both the degree of differentiation and the cell lineage.3 Cytochemical stains, including myeloper-oxidase, nonspecific esterase, and sudan black B, were used in conjunction with morphology to identify the subtype.47 This classification system did not require immunophenotyping to make a diagnosis, except in the M0 subtype (minimally differentiated AML subtype). Cytogenetics were also not incorporated into this classification system. The WHO classification system differs from the FAB classification in several aspects. The blast percentage for AML is decreased from 30 to 20%. In addition, biological, clinical, and prognostic markers (such as cytogenetics) are incorporated into the classification. Such factors allow us to better define the disease and risk-adapt therapy. The new WHO classification for AML recognizes four distinct entities: (1) AML with specific cytogenetic abnormalities, (2) AML with multilineage dysplasia

t(8;21)(q22;q22)

inv(16)(p13q22)

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8 der(8) 21 der(21)

16 der(16)

t(15;17)(q22;q21)

t(9;11)(p22;q23)

Pi 3 ™ 3 —

15 der(15) 17der(17)

9 der(9) 11der(11)

Figure 3.6 Critical nonrandom chromosome abnormalities that define disease subtypes included in the WHO entity "acute myeloid leukemia with recurrent genetic abnormalities" include t(8;21), t(15;17) and variants, inv(16) and variants, and 11q23 abnormalities. For each pair of GTG-banded chromosomes shown, the normal homologues are shown on the left, and abnormal homologues on the right; arrows mark chromosome breakpoints. These abnormalities can also be detected by molecular methods, including RT-PCR and FISH

Figure 3.6 Critical nonrandom chromosome abnormalities that define disease subtypes included in the WHO entity "acute myeloid leukemia with recurrent genetic abnormalities" include t(8;21), t(15;17) and variants, inv(16) and variants, and 11q23 abnormalities. For each pair of GTG-banded chromosomes shown, the normal homologues are shown on the left, and abnormal homologues on the right; arrows mark chromosome breakpoints. These abnormalities can also be detected by molecular methods, including RT-PCR and FISH

(with or without prior MDS), (3) therapy-related AML and MDS (alkylating-agent-related or epipodophyllo-toxin-related), and (4) AML not otherwise classifi-

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