ArticleLeukemia2005
Cleavage of the MLL gene by activators of apoptosis is independent of topoisomerase II activity.
Article in Leukemia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- DNA fragility at theOpen biology · 2023Review
- Human topoisomerases and their roles in genome stability and organization.Nature reviews. Molecular cell biology · 2022Review
- Mutagenic Consequences of Sublethal Cell Death Signaling.International journal of molecular sciences · 2021Review
- Bioflavonoids cause DNA double-strand breaks and chromosomal translocations through topoisomerase II-dependent and -independent mechanisms.Mutation research. Genetic toxicology and environmental mutagenesis · 2020Article
- MLL-Rearranged Leukemias-An Update on Science and Clinical Approaches.Frontiers in pediatrics · 2017Review
- Topoisomerase-mediated chromosomal break repair: an emerging player in many games.Nature reviews. Cancer · 2015Review
- 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
- Zinc Finger Nuclease induced DNA double stranded breaks and rearrangements in MLL.Mutation research · 2012Article
- Prolonged mitotic arrest triggers partial activation of apoptosis, resulting in DNA damage and p53 induction.Molecular biology of the cell · 2012Article
- Exploring the contextual sensitivity of factors that determine cell-to-cell variability in receptor-mediated apoptosis.PLoS computational biology · 2012Article
- Etoposide quinone is a redox-dependent topoisomerase II poison.Biochemistry · 2011Article
- Review
- Genistein induces topoisomerase IIbeta- and proteasome-mediated DNA sequence rearrangements: Implications in infant leukemia.Biochemical and biophysical research communications · 2010Article
- Suberoylanilide hydroxyamic acid modification of chromatin architecture affects DNA break formation and repair.International journal of radiation oncology, biology, physics · 2010Article
- Estrogen treatment induces MLL aberrations in human lymphoblastoid cells.Leukemia research · 2009Article
- Rearrangements of the MLL gene are influenced by DNA secondary structure, potentially mediated by topoisomerase II binding.Genes, chromosomes & cancer · 2009Article
- Quantitative analysis of pathways controlling extrinsic apoptosis in single cells.Molecular cell · 2008Article
- Roles of DNA topoisomerase II isozymes in chemotherapy and secondary malignancies.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Transcription linked to recombination: a gene-internal promoter coincides with the recombination hot spot II of the human MLL gene.Oncogene · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Exposure to topoisomerase II inhibitors is linked to the generation of leukemia involving translocations of the MLL gene, normally restricted to an 8.3 kbp tract, the breakpoint cluster region (BCR). Using an in vitro assay, apoptotic activators, including radiation and anti-CD95 antibody, trigger site-specific cleavage adjacent to exon 12 within the MLL BCR and promote translocation of the MLL gene in cells that can survive. To explore the mechanism of cleavage and rearrangement in more detail, the entire MLL BCR was placed into the pREP4 episomal vector and transfected into human lymphoblastoid TK6 cells. Episomes containing either the MLL BCR, or deletion constructs of 367 bp or larger, were cleaved at the same position as genomic MLL after exposure to apoptotic stimuli. Further analysis of sequence motifs surrounding the cleaved region of MLL showed the presence of both a predicted nuclear matrix attachment sequence and a potential strong binding site for topoisomerase II, flanking the site of cleavage. Inactivation of topoisomerase II by the catalytic inhibitor merbarone did not inhibit MLL cleavage, suggesting that the initial cleavage step for MLL rearrangement is not mediated by topoisomerase II.
Indexed as
Identifiers
What OpenQuestion holds
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.