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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-1-2
pubmed:abstractText
Gene amplifications occur rarely in hematologic neoplasms. We characterized two cases of acute myeloid leukemia (AML) with marker chromosomes and 11q23-25 amplicons. Case 1 was a 14-year-old male with an additional ring of chromosome 11 material as the sole karyotypic abnormality, as determined by G-banding and multicolor fluorescence in situ hybridization. Standard comparative genomic hybridization (CGH) showed amplification in 11q23-qter. However, the MLL gene, in 11q23, was not amplified by FISH. Case 2 was a 38-year-old male with the G-banding karyotype 51,XY,+8,+19,+3mar and with 11q22-qter amplification by standard CGH. This patient also had the MLL-LARG fusion gene. We used microarray-based CGH (array-CGH) to characterize the amplicons. In case 1, the amplified region in 11q24.3-25 (5.5 Mb) was continuous, and MLL was not amplified, as expected. In case 2, the amplicon was divided into two distinct parts, in 11q23.3 (1.2 Mb) and in 11q23.3-25 (13.3 Mb). It contained a loss ( approximately 1 Mb) in 11q23.3, and the amplicon breakpoint was in the middle of MLL. Although the amplicon size varied, the patients had a common amplified region in 11q24-25 that comprised 14 genes. Expression microarray of case 1 revealed that three of these genes, FLI1, NFRKB, and SNX19, were also overexpressed. The results indicate that the 11q24-q25 region may harbor new candidate oncogenes. In addition, the complex amplicon of case 2 suggests some intriguing chromosomal mechanisms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1045-2257
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
257-64
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Amplified, lost, and fused genes in 11q23-25 amplicon in acute myeloid leukemia, an array-CGH study.
pubmed:affiliation
Department of Pathology, Haartman Institute and HUSLAB, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't