ArticleGenes, chromosomes & cancer2009
Rearrangements of the MLL gene are influenced by DNA secondary structure, potentially mediated by topoisomerase II binding.
Article in Genes, chromosomes & cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- Genetic and epigenetic bases of long-term adverse effects of childhood cancer therapy.Nature reviews. Cancer · 2025Review
- Selective pressures of platinum compounds shape the evolution of therapy-related myeloid neoplasms.Nature communications · 2024Article
- DNA fragility at topologically associated domain boundaries is promoted by alternative DNA secondary structure and topoisomerase II activity.Nucleic acids research · 2024Article
- Preleukemic Fusion Genes Induced via Ionizing Radiation.International journal of molecular sciences · 2023Review
- Therapy-selected clonal hematopoiesis and its role in myeloid neoplasms.Leukemia research · 2023Article
- DNA fragility at theOpen biology · 2023Review
- Elevated Mutational Age in Blood of Children Treated for Cancer Contributes to Therapy-Related Myeloid Neoplasms.Cancer discovery · 2022Article
- Topoisomerase II contributes to DNA secondary structure-mediated double-stranded breaks.Nucleic acids research · 2020Article
- Review
- DNA damage signalling from the placenta to foetal blood as a potential mechanism for childhood leukaemia initiation.Scientific reports · 2019Article
- Bioflavonoids promote stable translocations between MLL-AF9 breakpoint cluster regions independent of normal chromosomal context: Model system to screen environmental risks.Environmental and molecular mutagenesis · 2019Article
- Environmental and chemotherapeutic agents induce breakage at genes involved in leukemia-causing gene rearrangements in human hematopoietic stem/progenitor cells.Mutation research · 2015Article
- Leukemogenic rearrangements at the mixed lineage leukemia gene (MLL)-multiple rather than a single mechanism.Frontiers in cell and developmental biology · 2015Review
- Topoisomerase II and leukemia.Annals of the New York Academy of Sciences · 2014Review
- Chemotherapy induced microsatellite instability and loss of heterozygosity in chromosomes 2, 5, 10, and 17 in solid tumor patients.Cancer cell international · 2014Article
- TDP2-dependent non-homologous end-joining protects against topoisomerase II-induced DNA breaks and genome instability in cells and in vivo.PLoS genetics · 2013Article
- Zinc Finger Nuclease induced DNA double stranded breaks and rearrangements in MLL.Mutation research · 2012Article
- Multiple clonal MLL fusions in a patient receiving CHOP-based chemotherapy.British journal of haematology · 2012Article
- Suberoylanilide hydroxyamic acid modification of chromatin architecture affects DNA break formation and repair.International journal of radiation oncology, biology, physics · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
The location of MLL translocation breakpoints within therapy-related acute myeloid leukemia linked to drugs targeting Topoisomerase II and infant acute leukemia (IAL) are biased toward the intron 11-exon 12 region of MLL, although lacking a comprehensive explanation. To address this, blood samples were taken from breast cancer and lymphoma patients receiving Topoisomerase II inhibitor therapy. Inverse PCR analysis was used to interrogate the exon 12 region of MLL for rearrangements. Eleven of 19 observed translocations showed breakpoint junctions restricted to a single 5 bp location within exon 12. A similarly restricted distribution (11/20 breakpoint junctions) was observed in TK6 cells exposed to either estrogen (linked to IAL) or anti-CD95 antibody. The translocation hotspot was at the 5' edge of a 10-bp tract matched with a perfect palindrome, 101 bp distant. A high stringency Topoisomerase II consensus sequence binding site was noted at the geometric midpoint of the palindromes. Ligation-mediated PCR to screen TK6 cells exposed to anti-CD95 antibody showed 14/37 (38%) of DNA breaks adjacent to the 5' palindrome and 10/37 (27%) at the 3' partner. We propose a model whereby Topoisomerase II facilitates the organization of nuclease-sensitive secondary structures, stabilized by palindrome association, which are prone to rearrangement.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.