Characterisation of dic(9;20)(p11-13;q11) in childhood B-cell precursor acute lymphoblastic leukaemia by tiling resolution array-based comparative genomic hybridisation reveals clustered breakpoints at 9p13.2 and 20q11.2.
Details
Serval ID
serval:BIB_4B4AA01EA0FC
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Characterisation of dic(9;20)(p11-13;q11) in childhood B-cell precursor acute lymphoblastic leukaemia by tiling resolution array-based comparative genomic hybridisation reveals clustered breakpoints at 9p13.2 and 20q11.2.
Journal
British Journal of Haematology
ISSN
0007-1048 (Print)
ISSN-L
0007-1048
Publication state
Published
Issued date
2006
Volume
135
Number
4
Pages
492-499
Language
english
Notes
Publication types: Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov'tPublication Status: ppublish
Abstract
Although the dic(9;20)(p11-13;q11) is a recurrent chromosomal abnormality in paediatric B-cell precursor acute lymphoblastic leukaemia (BCP ALL), occurring in approximately 2% of the cases, its molecular genetic consequences have not been elucidated. In the present study, high-resolution genome-wide array-based comparative genomic hybridisation (array-CGH) and fluorescence in situ hybridisation (FISH) were used to characterise the 9p and 20q breakpoints (BPs) in seven childhood BCP ALLs with dic(9;20), which was shown to be unbalanced in all of them, resulting in loss of 9p13.2-pter. Five of the cases had loss of 20q11.2-qter, whereas two displayed gain of 20cen-pter. All BPs on 9p clustered in a 1.5 Mb segment of the sub-band 9p13.2; in three of the cases, the 20q BPs mapped to three adjacent clones covering a distance of 350 kb at 20q11.2. Thus, the aberration should be designated dic(9;20)(p13.2;q11.2). One of the ALLs, shown to have a complex dic(9;20), was further investigated by FISH, revealing a rearrangement of the haemapoietic cell kinase isoform p61 (HCK) gene at 20q11. The disruption of HCK may result in a fusion gene or in loss of function. Unfortunately, lack of material precluded further analyses of HCK. Thus, it remains to be elucidated whether dic(9;20)(p13.2;q11.2) leads to a chimaeric gene or whether the functionally important outcome is loss of 9p and 20q material.
Keywords
Adolescent, Burkitt Lymphoma/genetics, Child, Child, Preschool, Chromosome Aberrations, Chromosome Deletion, Chromosome Mapping/methods, Chromosomes, Human, Pair 20/genetics, Chromosomes, Human, Pair 9/genetics, DNA, Neoplasm/genetics, Female, Humans, In Situ Hybridization, Fluorescence/methods, Infant, Karyotyping, Male, Nucleic Acid Hybridization/methods, Oligonucleotide Array Sequence Analysis/methods
Pubmed
Web of science
Open Access
Yes
Create date
17/09/2011 9:28
Last modification date
20/08/2019 13:59