Source:http://linkedlifedata.com/resource/pubmed/id/16283618
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2006-1-2
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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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/MLL protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Myeloid-Lymphoid Leukemia Protein,
http://linkedlifedata.com/resource/pubmed/chemical/NFRKB protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Protein c-fli-1
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1045-2257
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
45
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
257-64
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16283618-Acute Disease,
pubmed-meshheading:16283618-Adolescent,
pubmed-meshheading:16283618-Adult,
pubmed-meshheading:16283618-Chromosome Aberrations,
pubmed-meshheading:16283618-Chromosomes, Human, Pair 11,
pubmed-meshheading:16283618-DNA-Binding Proteins,
pubmed-meshheading:16283618-Gene Amplification,
pubmed-meshheading:16283618-Gene Deletion,
pubmed-meshheading:16283618-Humans,
pubmed-meshheading:16283618-Leukemia, Myeloid,
pubmed-meshheading:16283618-Male,
pubmed-meshheading:16283618-Myeloid-Lymphoid Leukemia Protein,
pubmed-meshheading:16283618-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:16283618-Oncogenes,
pubmed-meshheading:16283618-Proto-Oncogene Protein c-fli-1
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pubmed:year |
2006
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pubmed:articleTitle |
Amplified, lost, and fused genes in 11q23-25 amplicon in acute myeloid leukemia, an array-CGH study.
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pubmed:affiliation |
Department of Pathology, Haartman Institute and HUSLAB, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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