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Double minutes (dmin), the cytogenetic hallmark of genomic amplification, are found in ∼1% of karyotypically abnormal acute myeloid leukemias (AML) and myelodysplastic syndromes (MDS). TheMYCgene at 8q24 has been reported to be amplified in the majority of the cases, and generally it has been assumed thatMYCis the target gene. However, only a few studies have focused on the extent of the amplicon or on the expression patterns of the amplified genes. We have studied six cases (five AML and one MDS) withMYC-containing dmin. Detailed fluorescencein situhybridization analyses identified a common 4.3 Mb amplicon, with clustered proximal and distal breakpoints, harboring eight known genes (C8FW,NSE2,POU5FLC20,MYC,PVT1,AK093424,MGC27434andMLZE). The corresponding region was deleted in one of the chromosome 8 homologues in five of the six cases, suggesting that the dmin originated through extra replication (or loop-formation)–excision–amplification. Northern blot analysis revealed thatMYCwas not overexpressed. Instead, theC8FWgene, encoding a phosphoprotein regulated by mitogenic pathways, displayed increased expression. These results excludeMYCas the target gene and indicate that overexpression ofC8FWmay be the functionally important consequence of 8q24 amplicons in AML and MDS.

human molecular genetics

Identification of a commonly amplified 4.3 Mb region with overexpression of               C8FW              , but not               MYC               in               MYC              -containing double minutes in myeloid malignancies