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Tiling resolution array CGH of dic(7;9)(p11 approximately 13;p11 approximately 13) in B-cell precursor acute lymphoblastic leukemia reveals clustered breakpoints at 7p11.2 approximately 12.1 and 9p13.1.

Lundin, Catarina LU ; Heidenblad, Markus LU ; Strömbeck, Bodil LU ; Borg, Åke LU ; Hovland, R ; Heim, S and Johansson, Bertil LU (2007) In Cytogenetic and Genome Research 118(1). p.13-18
Abstract
The dic( 7; 9)( p11 similar to 13; p11 similar to 13) is a recurrent chromosomal abnormality in acute lymphoblastic leukemia (ALL), mainly of B-lineage. Although more than 20 dic(7; 9)-positive ALLs have been reported to date, the molecular genetic consequences of this aberration are unknown. We performed tiling resolution (32K) genome-wide array-based comparative genomic hybridization ( array CGH) analysis of three cases with dic(7; 9) in order to characterize the breakpoints on 7p and 9p. The analysis showed a clustering of breakpoints within 9p13.1 in all three cases and within 7p11.2 in two cases; the array CGH revealed two different breakpoints - 7p12.1 and 7p14.1 - in the remaining case. Based on these findings the abnormality should... (More)
The dic( 7; 9)( p11 similar to 13; p11 similar to 13) is a recurrent chromosomal abnormality in acute lymphoblastic leukemia (ALL), mainly of B-lineage. Although more than 20 dic(7; 9)-positive ALLs have been reported to date, the molecular genetic consequences of this aberration are unknown. We performed tiling resolution (32K) genome-wide array-based comparative genomic hybridization ( array CGH) analysis of three cases with dic(7; 9) in order to characterize the breakpoints on 7p and 9p. The analysis showed a clustering of breakpoints within 9p13.1 in all three cases and within 7p11.2 in two cases; the array CGH revealed two different breakpoints - 7p12.1 and 7p14.1 - in the remaining case. Based on these findings the abnormality should hence be designated dic(7; 9)(p11.2 similar to 12.1; p13.1). Locus-specific fluorescence in situ hybridization analysis of one of the cases narrowed down the 7p11.2 breakpoint to a < 500-kb segment in this sub-band, a region containing three known genes. Unfortunately, lack of material precluded further molecular genetic studies, and it thus remains unknown whether the pathogenetically important outcome of the dic(7; 9) is formation of a chimeric gene or loss of 7p and/or 9p material. Copyright (c) 2007 S. Karger AG, Basel. (Less)
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author
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cytogenetic and Genome Research
volume
118
issue
1
pages
13 - 18
publisher
Karger
external identifiers
  • wos:000249981000003
  • scopus:34848834513
  • pmid:17901695
ISSN
1424-859X
DOI
10.1159/000106436
language
English
LU publication?
yes
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87266d95-4c52-422e-8289-89ef7ae280af (old id 607452)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17901695&dopt=Abstract
date added to LUP
2016-04-01 11:56:40
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2022-01-26 20:32:50
@article{87266d95-4c52-422e-8289-89ef7ae280af,
  abstract     = {{The dic( 7; 9)( p11 similar to 13; p11 similar to 13) is a recurrent chromosomal abnormality in acute lymphoblastic leukemia (ALL), mainly of B-lineage. Although more than 20 dic(7; 9)-positive ALLs have been reported to date, the molecular genetic consequences of this aberration are unknown. We performed tiling resolution (32K) genome-wide array-based comparative genomic hybridization ( array CGH) analysis of three cases with dic(7; 9) in order to characterize the breakpoints on 7p and 9p. The analysis showed a clustering of breakpoints within 9p13.1 in all three cases and within 7p11.2 in two cases; the array CGH revealed two different breakpoints - 7p12.1 and 7p14.1 - in the remaining case. Based on these findings the abnormality should hence be designated dic(7; 9)(p11.2 similar to 12.1; p13.1). Locus-specific fluorescence in situ hybridization analysis of one of the cases narrowed down the 7p11.2 breakpoint to a &lt; 500-kb segment in this sub-band, a region containing three known genes. Unfortunately, lack of material precluded further molecular genetic studies, and it thus remains unknown whether the pathogenetically important outcome of the dic(7; 9) is formation of a chimeric gene or loss of 7p and/or 9p material. Copyright (c) 2007 S. Karger AG, Basel.}},
  author       = {{Lundin, Catarina and Heidenblad, Markus and Strömbeck, Bodil and Borg, Åke and Hovland, R and Heim, S and Johansson, Bertil}},
  issn         = {{1424-859X}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{13--18}},
  publisher    = {{Karger}},
  series       = {{Cytogenetic and Genome Research}},
  title        = {{Tiling resolution array CGH of dic(7;9)(p11 approximately 13;p11 approximately 13) in B-cell precursor acute lymphoblastic leukemia reveals clustered breakpoints at 7p11.2 approximately 12.1 and 9p13.1.}},
  url          = {{http://dx.doi.org/10.1159/000106436}},
  doi          = {{10.1159/000106436}},
  volume       = {{118}},
  year         = {{2007}},
}