PMID- 14978788
OWN - NLM
STAT- MEDLINE
DCOM- 20040504
LR  - 20190816
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 39
IP  - 4
DP  - 2004 Apr
TI  - Distinct sequences on 11q13.5 and 11q23-24 are frequently coamplified with MLL in 
      complexly organized 11q amplicons in AML/MDS patients.
PG  - 263-76
AB  - Amplification within chromosome arm 11q involving the mixed-lineage leukemia gene 
      (MLL) locus is a rare but recurrent aberration in acute myeloid leukemia and 
      myelodysplastic syndrome (AML/MDS). We and others have observed that 11q 
      amplifications in most AML/MDS cases have not been restricted to the chromosomal 
      region surrounding the MLL gene. Therefore, we implemented a strategy to 
      characterize comprehensively 11q amplicons in a series of 13 AML/MDS patients 
      with MLL amplification. Analysis of 4 of the 13 cases by restriction landmark 
      genomic scanning in combination with virtual genome scan and by matrix-based 
      comparative genomic hybridization demonstrated that the 11q amplicon in these 
      four cases consisted of at least three discontinuous sequences derived from 
      different regions of the long arm of chromosome 11. We defined a maximally 700-kb 
      sequence around the MLL gene that was amplified in all cases. Apart from the core 
      MLL amplicon, we detected two additional 11q regions that were coamplified. Using 
      fluorescence in situ hybridization (FISH) analysis, we demonstrated that 
      sequences in 11q13.5 and 11q23-24 were amplified in 8 of 13 and 10 of 12 AML/MDS 
      cases, respectively. Both regions harbor a number of potentially oncogenic genes. 
      In all 13 cases, either one or both of these regions were coamplified with the 
      MLL amplicon. Thus, we demonstrated that 11q amplicons in AML/MDS patients 
      display a complex organization and have provided evidence for coamplification of 
      two additional regions on the long arm of chromosome 11 that may harbor candidate 
      target genes.
CI  - Copyright 2004 Wiley-Liss, Inc.
FAU - Zatkova, Andrea
AU  - Zatkova A
AD  - Institut fur Medizinische Biologie, Universitat Wien, Wien, Austria.
FAU - Ullmann, Reinhard
AU  - Ullmann R
FAU - Rouillard, Jean Marie
AU  - Rouillard JM
FAU - Lamb, Barbara J
AU  - Lamb BJ
FAU - Kuick, Rork
AU  - Kuick R
FAU - Hanash, Sam M
AU  - Hanash SM
FAU - Schnittger, Susanne
AU  - Schnittger S
FAU - Schoch, Claudia
AU  - Schoch C
FAU - Fonatsch, Christa
AU  - Fonatsch C
FAU - Wimmer, Katharina
AU  - Wimmer K
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (DNA Probes)
RN  - 0 (DNA, Neoplasm)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Genetic Markers)
RN  - 0 (KMT2A protein, human)
RN  - 0 (Transcription Factors)
RN  - 149025-06-9 (Myeloid-Lymphoid Leukemia Protein)
RN  - EC 2.1.1.43 (Histone-Lysine N-Methyltransferase)
SB  - IM
MH  - Acute Disease
MH  - Aged
MH  - Aged, 80 and over
MH  - Chromosomes, Human, Pair 11/*genetics
MH  - Cytogenetic Analysis/methods
MH  - DNA Probes/genetics
MH  - DNA, Neoplasm/genetics
MH  - DNA-Binding Proteins/*genetics
MH  - Female
MH  - Gene Amplification/*genetics
MH  - Gene Dosage
MH  - Genetic Markers/genetics
MH  - Histone-Lysine N-Methyltransferase
MH  - Humans
MH  - In Situ Hybridization, Fluorescence/methods
MH  - Leukemia, Myeloid/*genetics
MH  - Male
MH  - Middle Aged
MH  - Myelodysplastic Syndromes/*genetics
MH  - Myeloid-Lymphoid Leukemia Protein
MH  - Nucleic Acid Hybridization/methods
MH  - Oligonucleotide Array Sequence Analysis/methods
MH  - Polymerase Chain Reaction/methods
MH  - *Proto-Oncogenes
MH  - Restriction Mapping/methods
MH  - *Transcription Factors
EDAT- 2004/02/24 05:00
MHDA- 2004/05/05 05:00
CRDT- 2004/02/24 05:00
PHST- 2004/02/24 05:00 [pubmed]
PHST- 2004/05/05 05:00 [medline]
PHST- 2004/02/24 05:00 [entrez]
AID - 10.1002/gcc.20002 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2004 Apr;39(4):263-76. doi: 10.1002/gcc.20002.