Figure 1.
Distribution of CNAs recognized by array CGH in 24 patients with AML-M5.
A total of 117 CNAs with 51 genomic gains (43.1%) and 66 genomic losses (56.9%) was observed. 70 CNAs (59.8%) were cryptic with size less than 5 Mb and invisible to karyotype. The arrows indicated recurrent CNAs and harbored interesting genes.
Table 1.
The recurrent chromosomal abnormalities of 24 cases of AML-M5.
Table 2.
Recurrent CNAs reported by previous studies of MDS/AML and this study.
Figure 2.
FOXN3 gene (14q31.3-q32.11) deletions in two patients with AML-M5.
(A) Array CGH showed a lower signal ratio spanning 14q22.3-q32.33 (55,109,046–106,342,076 bp). FOXN3 gene was one of the genes located at the deleted region. (B) The microdeletion of 14q32.11 (89,027,534–89,236,808 bp) involving FOXN3 gene was inferred by array CGH.
Figure 3.
Gain of 11q23.3 and loss of 9p21.3 coexisting in case #18.
(A) Lower signal of 21,755,226–22,097,452 on chromosome 9 was recognized by array CGH analysis. (B) A gain in the region of 116,893,506–119,524,806 was observed on chromosome 11 by array CGH. (C) UCSC genome browser (hg18) indicated the RefSeq genes involved CDKN2A/B genes and MLL gene. (D) FISH analysis showed the concurrent CDKN2A gene deletion and MLL gene amplication in interphase nuclei. The left nucleus showed the homogenous deletion of CDKN2A and the right nucleus demonstrated the heterogenous deletion of CDKN2A.
Table 3.
Candidate AML-M5 associated genes inferred by array CGH.
Table 4.
Comparative clinico-biological parameters and number of CR by number of CNAs.