P | Sex | Age (years) | WHO type | Disease stage | PB blast % | BM blast % | Molecular | Cytogenetics |
|---|
A | f | 51 | AML-nos | R1 | 6.5 | 16.2 | WT1+
| nl |
B | m | 51 | AML-rga | Dx | 50 | 64.4 | NPM1+, WT1+
| nl |
C | m | 62 | AML-nos | Dx | 2 | 72 | ASXL1+
| Trisomy 8 |
D | m | 61 | AML-nos | Dx CR1 | 47.8 0 | 79.8 0.6 | Negative | Deletion 17p |
E | f | 76 | AML-mds | Evolution from MDS | 18 | ND | ND | ND |
F | m | 52 | AML-rga | Dx | 92.5 | 94.5 | WT1+, NPM1+, FLT3-ITD+
| inv(3)(q21q26) |
G | f | 62 | AML-nos | CR1 | 0 | 0.8 | ASXL1+
| trisomy 8 |
-
AML acute myeloid leukemia, P Patient, f female, m male, WHO World Health Organization (WHO) 2008 classification for AML, AML-nos AML not otherwise specified, AML-rga AML with recurrent genetic abnormalities, AML-mds AML with myelodysplasia (MDS)-related changes, R1 first relapse of AML, Dx diagnosis stage, CR1 first complete hematological remission of AML, PB blast % percentage of AML blasts in peripheral blood, BM blast % percentage of AML blasts in bone marrow, ND no data, WT1 overexpression of Wilms’ tumor 1 (WT1) gene transcript, NPM1 presence of mutated nucleophosmin 1 (NPM1), ASXL1 presence of mutation in additional sex combs 1 (ASXL1) gene, FLT3-ITD presence of internal tandem duplication of fms-like tyrosine kinase 3 (FLT3), nl normal karyotype
