ArticleNucleic acids research2004
Chemotherapeutic deletion of CTG repeats in lymphoblast cells from DM1 patients.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
24 citing papers in PubMed, 58 citations in OpenAlex.
- Targeting Expanded CUG and CTG Repeats as a Therapeutic Approach for Myotonic Dystrophy Type 1 (DM1).ChemMedChem · 2026Review
- DNA Base Damage Repair Crosstalks with Chromatin Structures to Contract Expanded GAA Repeats in Friedreich's Ataxia.Biomolecules · 2024Article
- Multifaceted nucleic acid probing with a rationally upgraded molecular rotor.Chemical science · 2024Article
- Gene-Environment Interactions in Repeat Expansion Diseases: Mechanisms of Environmentally Induced Repeat Instability.Biomedicines · 2023Review
- Modifiers of CAG/CTG Repeat Instability: Insights from Mammalian Models.Journal of Huntington's disease · 2021Review
- Trinucleotide repeat instability via DNA base excision repair.DNA repair · 2020Review
- CoInternational journal of molecular sciences · 2018Article
- Daunorubicin reduces MBNL1 sequestration caused by CUG-repeat expansion and rescues cardiac dysfunctions in aDisease models & mechanisms · 2018Article
- FANCJ is essential to maintain microsatellite structure genome-wide during replication stress.Nucleic acids research · 2016Article
- Article
- Length-dependent CTG·CAG triplet-repeat expansion in myotonic dystrophy patient-derived induced pluripotent stem cells.Human molecular genetics · 2013Article
- The structural basis of actinomycin D-binding induces nucleotide flipping out, a sharp bend and a left-handed twist in CGG triplet repeats.Nucleic acids research · 2013Article
- Trinucleotide repeat deletion via a unique hairpin bypass by DNA polymerase β and alternate flap cleavage by flap endonuclease 1.Nucleic acids research · 2013Article
- Investigating the binding mode of an inhibitor of the MBNL1·RNA complex in myotonic dystrophy type 1 (DM1) leads to the unexpected discovery of a DNA-selective binder.Chembiochem : a European journal of chemical biology · 2012Article
- Altered replication in human cells promotes DMPK (CTG)(n) · (CAG)(n) repeat instability.Molecular and cellular biology · 2012Article
- Instability of (CTG)n•(CAG)n trinucleotide repeats and DNA synthesis.Cell & bioscience · 2012Article
- Myotonic dystrophy mouse models: towards rational therapy development.Trends in molecular medicine · 2011Review
- Topoisomerase 1 and single-strand break repair modulate transcription-induced CAG repeat contraction in human cells.Molecular and cellular biology · 2011Article
- Replication-dependent instability at (CTG) x (CAG) repeat hairpins in human cells.Nature chemical biology · 2010Article
- Repeat instability as the basis for human diseases and as a potential target for therapy.Nature reviews. Molecular cell biology · 2010Review
Corrections and comments
- Erratum issuedKhajav, Merhdad [corrected to Khajavi, Mehrdad]
Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myotonic dystrophy type 1 (DM1) is caused by the expansion of a (CTG).(CAG) repeat in the DMPK gene on chromosome 19q13.3. At least 17 neurological diseases have similar genetic mutations, the expansion of DNA repeats. In most of these disorders, the disease severity is related to the length of the repeat expansion, and in DM1 the expanded repeat undergoes further elongation in somatic and germline tissues. At present, in this class of diseases, no therapeutic approach exists to prevent or slow the repeat expansion and thereby reduce disease severity or delay disease onset. We present initial results testing the hypothesis that repeat deletion may be mediated by various chemotherapeutic agents. Three lymphoblast cell lines derived from two DM1 patients treated with either ethylmethanesulfonate (EMS), mitomycin C, mitoxantrone or doxorubicin, at therapeutic concentrations, accumulated deletions following treatment. Treatment with EMS frequently prevented the repeat expansion observed during growth in culture. A significant reduction of CTG repeat length by 100-350 (CTG).(CAG) repeats often occurred in the cell population following treatment with these drugs. Potential mechanisms of drug-induced deletion are presented.
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.