ReviewEnvironmental and molecular mutagenesis2010
Targeting and processing of site-specific DNA interstrand crosslinks.
Review in Environmental and molecular mutagenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 55 citations in OpenAlex.
- Article
- Replication-Independent ICL Repair: From Chemotherapy to Cell Homeostasis.Journal of molecular biology · 2024Review
- Fance deficiency inhibits primordial germ cell proliferation associated with transcription-replication conflicts accumulate and DNA repair defects.Journal of ovarian research · 2023Article
- Triplex-forming oligonucleotides as an anti-gene technique for cancer therapy.Frontiers in pharmacology · 2022Review
- Targeting Chromosomal Architectural HMGB Proteins Could Be the Next Frontier in Cancer Therapy.Cancer research · 2020Review
- Polyphenolic contents of Teucrium polium L. and Teucrium scordium L. associated with their protective effects against MMC-induced chromosomal damage in cultured human peripheral blood lymphocytes.Turkish journal of biology = Turk biyoloji dergisi · 2018Article
- Systematic analysis of DNA crosslink repair pathways during development and aging in Caenorhabditis elegans.Nucleic acids research · 2017Article
- The homologous recombination protein RAD51D protects the genome from large deletions.Nucleic acids research · 2017Article
- Tools to Study the Role of Architectural Protein HMGB1 in the Processing of Helix Distorting, Site-specific DNA Interstrand Crosslinks.Journal of visualized experiments : JoVE · 2016Article
- HMGB1 interacts with XPA to facilitate the processing of DNA interstrand crosslinks in human cells.Nucleic acids research · 2016Article
- Effects of Anticancer Drugs on Chromosome Instability and New Clinical Implications for Tumor-Suppressing Therapies.Cancer research · 2016Article
- DNA damage response in cisplatin-induced nephrotoxicity.Archives of toxicology · 2015Review
- Review
- UHRF1 is a sensor for DNA interstrand crosslinks and recruits FANCD2 to initiate the Fanconi anemia pathway.Cell reports · 2015Article
- Physical and genetic-interaction density reveals functional organization and informs significance cutoffs in genome-wide screens.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- An inverse switch in DNA base excision and strand break repair contributes to melphalan resistance in multiple myeloma cells.PloS one · 2013Article
- Relationships between chromatin remodeling and DNA damage repair induced by 8-methoxypsoralen and UVA in yeast Saccharomyces cerevisiae.Genetics and molecular biology · 2012Article
- REV1 and DNA polymerase zeta in DNA interstrand crosslink repair.Environmental and molecular mutagenesis · 2012Review
- Fanconi-like crosslink repair in yeast.Genome integrity · 2012Article
- Rad5-dependent DNA repair functions of the Saccharomyces cerevisiae FANCM protein homolog Mph1.The Journal of biological chemistry · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
DNA interstrand crosslinks (ICLs) are among the most cytotoxic types of DNA damage, and thus ICL-inducing agents such as cyclophosphamide, melphalan, cisplatin, psoralen, and mitomycin C have been used clinically as anticancer drugs for decades. ICLs can also be formed endogenously as a consequence of cellular metabolic processes. ICL-inducing agents continue to be among the most effective chemotherapeutic treatments for many cancers; however, treatment with these agents can lead to secondary malignancies, in part due to mutagenic processing of the DNA lesions. The mechanisms of ICL repair have been characterized more thoroughly in bacteria and yeast than in mammalian cells. Thus, a better understanding of the molecular mechanisms of ICL processing offers the potential to improve the efficacy of these drugs in cancer therapy. In mammalian cells, it is thought that ICLs are repaired by the coordination of proteins from several pathways, including nucleotide excision repair (NER), base excision repair (BER), mismatch repair (MMR), homologous recombination (HR), translesion synthesis (TLS), and proteins involved in Fanconi anemia (FA). In this review, we focus on the potential functions of NER, MMR, and HR proteins in the repair of and response to ICLs in human cells and in mice. We will also discuss a unique approach, using psoralen covalently linked to triplex-forming oligonucleotides to direct ICLs to specific sites in the mammalian genome.
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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.