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Expression profiles of leukemia cells of acute-type adult T-cell leukemia (ATL) patients

ABSTRACT: We recently mapped 605 chromosomal breakpoints in 61 ATL cases by spectral karyotyping and identified chromosome 14q11 as one of the most common chromosomal breakpoint regions. To map the precise location of chromosomal breakpoints at 14q11, we performed single-nucleotide polymorphism (SNP)-based comparative genomic hybridization on leukemia cells from acute-type ATL patients. The breakpoints accumulated frequently adjacent to the T cell receptor alpha/delta chain locus (TCRα/δ) with chromosomal deletions at 14q11 and a recurrent 0.9 Mb interstitial deletion was identified at a region including part of the TCRα/δ locus. Because leukemia-associated genes are frequently located near the breakpoint cluster regions, we then analyzed the gene expression profiles of ATL cells and identified N-myc downstream regulated gene 2 (NDRG2) as one of the genes that are down-regulated in ATLL cells among the 25 genes mapped to the region adjacent to the recurrently deleted regions at 14q11.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43017 | GEO | 2012/12/20

SECONDARY ACCESSION(S): PRJNA184059

REPOSITORIES: GEO

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Expression profiles of leukemia cells of acute-type adult T-cell leukemia (ATL) patients

Project description:We recently mapped 605 chromosomal breakpoints in 61 ATL cases by spectral karyotyping and identified chromosome 14q11 as one of the most common chromosomal breakpoint regions. To map the precise location of chromosomal breakpoints at 14q11, we performed single-nucleotide polymorphism (SNP)-based comparative genomic hybridization on leukemia cells from acute-type ATL patients. The breakpoints accumulated frequently adjacent to the T cell receptor alpha/delta chain locus (TCRα/δ) with chromosomal deletions at 14q11 and a recurrent 0.9 Mb interstitial deletion was identified at a region including part of the TCRα/δ locus. Because leukemia-associated genes are frequently located near the breakpoint cluster regions, we then analyzed the gene expression profiles of ATL cells and identified N-myc downstream regulated gene 2 (NDRG2) as one of the genes that are down-regulated in ATLL cells among the 25 genes mapped to the region adjacent to the recurrently deleted regions at 14q11. We compared the gene expression profiles of ATL cells from seven acute-type ATL patients and CD4+ T lymphocytes from the peripheral blood of five healthy volunteers as references using oligonucleotide microarrays.

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Affymetrix SNP array data for acute-type adult T-cell leukemia (ATL) samples

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Transcription profiling of kidney samples from Wilms tumor patients to examine down- and up-regulation of genes either side of 1p13 breakpoints

Project description:Wilms tumour karyotypes frequently exhibit recurrent, large-scale chromosomal imbalances, among the most common of which are concurrent loss of 1p and gain of 1q. We have previously identified a novel breakpoint at 1p13 by 1Mb-spaced array CGH, and undertook a fine-tiling oligonucleotide array approach to accurately map the region in four tumours exhibiting rearrangements at this locus. The use of a 10 bpspaced platform revealed that all four tumours in fact harboured different breakpoints, which were mapped to target four distinct genes PHTF1, DCLRE1B, TRIM33 and NRAS. The precise breakpoint interval was confirmed for one case to lie within intron 3 of DCLRE1B by quantitative copy number PCR and RT-PCR. In addition, expression profiling revealed a pattern of down- and up-regulation of genes either side of the breakpoint in all cases. Although it appears that no single gene is the driver of this rearrangement, this study highlights the power of fine-tiling oligonucleotide arrays to delineate breakpoint regions identified by other genome-wide screens. RElated experimement E-TABM-155

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Non-allelic homologous recombination between retrotransposable elements is a major driver of de novo unbalanced translocations.

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Non-allelic homologous recombination between retrotransposable elements is a major driver of de novo unbalanced translocations.

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Germline unbalanced translocations arise from diverse mutational mechanisms including chromothripsis

Project description:Unbalanced translocations are a relatively common type of copy number variation and are a major contributor to neurodevelopmental disorders. We analyzed the breakpoints of 57 unique unbalanced translocations to investigate the mechanisms of how they form. 51 are simple unbalanced translocations between two different chromosome ends, and six rearrangements have more than three breakpoints involving two to five chromosomes. Sequencing 37 breakpoint junctions revealed that simple translocations have between zero and four basepairs (bp) of microhomology (n=26), short inserted sequences (n=8), or paralogous repeats (n=3) at the junctions, indicating that translocations do not arise primarily from non-allelic homologous recombination, but instead form most often via non-homologous end joining or microhomology-mediated break-induced replication. Three simple translocations fuse genes that are predicted to produce in-frame transcripts of SIRPG-WWOX, SMOC2-PROX1, and PIEZO2-MTA1, which may lead to gain of function. Three complex translocations have inversions, insertions, and multiple breakpoint junctions between only two chromosomes. Whole- genome sequencing and fluorescence in situ hybridization analysis of two de novo translocations revealed at least 18 and 33 breakpoints involving five different chromosomes. Breakpoint sequencing of one inherited translocation involving four chromosomes uncovered multiple breakpoints with inversions and insertions. All of these breakpoint junctions had zero to four bp of microhomology consistent with germline chromothripsis, and both de novo events occurred on paternal alleles. Breakpoint sequencing of our large collection of chromosome rearrangements offers a comprehensive analysis of the molecular mechanisms behind germline translocation formation.

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