ArticleHuman genetics2006
Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.
Article in Human genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
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- Matrix association region/scaffold attachment region (MAR/SAR) sequence: its vital role in mediating chromosome breakages in nasopharyngeal epithelial cells via oxidative stress-induced apoptosis.BMC molecular biology · 2018Article
- Anthracyclines as Topoisomerase II Poisons: From Early Studies to New Perspectives.International journal of molecular sciences · 2018Review
- Oxidative stress-induced chromosome breaks within the ABL gene: a model for chromosome rearrangement in nasopharyngeal carcinoma.Human genomics · 2018Article
- Bile acids at neutral and acidic pH induce apoptosis and gene cleavages in nasopharyngeal epithelial cells: implications in chromosome rearrangement.BMC cancer · 2018Article
- Potential role of oxidative stress-induced apoptosis in mediating chromosomal rearrangements in nasopharyngeal carcinoma.Cell & bioscience · 2016Article
- Inhibitor of caspase-activated DNase expression enhances caspase-activated DNase expression and inhibits oxidative stress-induced chromosome breaks at the mixed lineage leukaemia gene in nasopharyngeal carcinoma cells.Cancer cell international · 2015Article
- Leukemogenic rearrangements at the mixed lineage leukemia gene (MLL)-multiple rather than a single mechanism.Frontiers in cell and developmental biology · 2015Review
- Genetic and epigenetic determinants mediate proneness of oncogene breakpoint sites for involvement in TCR translocations.Genes and immunity · 2014Article
- Do non-genomically encoded fusion transcripts cause recurrent chromosomal translocations?Cancers · 2012Article
- Mechanism of generation of therapy related leukemia in response to anti-topoisomerase II agents.International journal of environmental research and public health · 2012Review
- Evaluating translocation gene fusions by SNP array data.Cancer informatics · 2012Article
- Premature transcript termination, trans-splicing and DNA repair: a vicious path to cancer.American journal of blood research · 2011Article
- High cell density and latent membrane protein 1 expression induce cleavage of the mixed lineage leukemia gene at 11q23 in nasopharyngeal carcinoma cell line.Journal of biomedical science · 2010Article
- ABL tyrosine kinases: evolution of function, regulation, and specificity.Science signaling · 2010Review
- Models for chromosomal replication-independent non-B DNA structure-induced genetic instability.Molecular carcinogenesis · 2009Review
- Preferential induction of MLL(Mixed Lineage Leukemia) rearrangements in human lymphocyte cultures treated with etoposide.Genetics and molecular biology · 2009Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The t(9;22) BCR/ABL fusion is associated with over 90% of chronic myelogenous and 25% of acute lymphocytic leukemia. Chromosome 11q23 translocations in acute myeloid and lymphoid leukemia cells demonstrate myeloid lymphoid leukemia (MLL) fusions with over 40 gene partners, like AF9 and AF4 on chromosomes 9 and 4, respectively. Therapy-related leukemia is associated with the above gene rearrangements following the treatment with topoisomerase II (topo II) inhibitors. BCR, ABL, MLL, AF9 and AF4 have defined patient breakpoint cluster regions. Chromatin structural elements including topo II and DNase I cleavage sites and scaffold attachment sites have previously been shown to closely associate with the MLL and AF9 breakpoint cluster regions, implicating these elements in non-homologous recombination (NHR). In this report, using cell lines and primary cells, chromatin structural elements were analyzed in BCR, ABL and AF4 and, for comparison, in MLL2, which is a homolog to MLL, but not associated with chromosome translocations. Topo II and DNase I cleavage sites associated with all breakpoint cluster regions, whereas SARs associated with ABL and AF4, but not with BCR. No close breakpoint clustering with the topo II/DNase I sites were observed; however, a statistically significant 5' or 3' distribution of patient breakpoints to the topo II DNase I sites was found, implicating DNA repair and exonucleases. Although MLL2 was expressed in all cell lines tested, except for the presence of one DNAse I site in the promoter, no other structural elements were found in MLL2. A NHR model presented demonstrates the importance of chromatin structure in chromosome translocations involved with leukemia.
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