ArticleOncotarget2017
Crosstalk between mismatch repair and base excision repair in human gastric cancer.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 21 citations in OpenAlex.
- Novel De NovoInternational journal of molecular sciences · 2025Article
- Accidental Encounter of Repair Intermediates in Alkylated DNA May Lead to Double-Strand Breaks in Resting Cells.International journal of molecular sciences · 2024Review
- Double-strand breaks: When DNA repair events accidentally meet.DNA repair · 2022Review
- Article
- Yeast-based assays for the functional characterization of cancer-associated variants of human DNA repair genes.Microbial cell (Graz, Austria) · 2020Review
- A Review of Research Progress in Multidrug-Resistance Mechanisms in Gastric Cancer.OncoTargets and therapy · 2020Review
- Two-way crosstalk between BER and c-NHEJ repair pathway is mediated by Pol-β and Ku70.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Exploring new potential role of DDB2 by host cell reactivation assay in human tumorigenic cells.BMC cancer · 2019Article
- Functional Interaction BetweenFrontiers in genetics · 2018Article
- Regulation of DNA Alkylation Damage Repair: Lessons and Therapeutic Opportunities.Trends in biochemical sciences · 2017Review
- DNA ligase I fidelity mediates the mutagenic ligation of pol β oxidized and mismatch nucleotide insertion products in base excision repair.The Journal of biological chemistryArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
DNA repair gene expression in a set of gastric cancers suggested an inverse association between the expression of the mismatch repair (MMR) gene MLH1 and that of the base excision repair (BER) gene DNA polymerase β (Polβ). To gain insight into possible crosstalk of these two repair pathways in cancer, we analysed human gastric adenocarcinoma AGS cells over-expressing Polβ or Polβ active site mutants, alone or in combination with MLH1 silencing. Next, we investigated the cellular response to the alkylating agent methyl methanesulfonate (MMS) and the purine analogue 6-thioguanine (6-TG), agents that induce lesions that are substrates for BER and/or MMR. AGS cells over-expressing Polβ were resistant to 6-TG to a similar extent as when MLH1 was inactivated while inhibition of O
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.