ReviewCurrent medicinal chemistry2012
Base excision repair: contribution to tumorigenesis and target in anticancer treatment paradigms.
Review in Current medicinal chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 43 citations in OpenAlex.
- Molecular editing ofRSC medicinal chemistry · 2024Article
- Identification of Novel Pathways Regulated by APE1/Ref-1 in Human Retinal Endothelial Cells.International journal of molecular sciences · 2023Article
- Inhibition of human APE1 and MTH1 DNA repair proteins by dextran-coated γ-FeNanomedicine (London, England) · 2022Article
- Article
- Polymorphic mutations in the polb gene promoter and their impact on transcriptional activity.Thoracic cancer · 2022Article
- Article
- Base excision repair accessory factors in senescence avoidance and resistance to treatments.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Fragment- and structure-based drug discovery for developing therapeutic agents targeting the DNA Damage Response.Progress in biophysics and molecular biology · 2021Article
- DNA polymerase β deficiency promotes the occurrence of esophageal precancerous lesions in mice.Neoplasia (New York, N.Y.) · 2021Review
- FEN1 is a prognostic biomarker for ER+ breast cancer and associated with tamoxifen resistance through the ERα/cyclin D1/Rb axis.Annals of translational medicine · 2021Article
- Non-muscle invasive bladder cancer tissues have increased base excision repair capacity.Scientific reports · 2020Article
- Base Excision Repair in the Immune System: Small DNA Lesions With Big Consequences.Frontiers in immunology · 2020Review
- BRCA1 identified as a modulator of temozolomide resistance in P53 wild-type GBM using a high-throughput shRNA-based synthetic lethality screening.American journal of cancer research · 2019Article
- Interacting partners of FEN1 and its role in the development of anticancer therapeutics.Oncotarget · 2017Review
- Cellularly active N-hydroxyurea FEN1 inhibitors block substrate entry to the active site.Nature chemical biology · 2016Article
- Inhibitors of the apurinic/apyrimidinic endonuclease 1 (APE1)/nucleophosmin (NPM1) interaction that display anti-tumor properties.Molecular carcinogenesis · 2016Article
- p53 coordinates base excision repair to prevent genomic instability.Nucleic acids research · 2016Article
- Production, Purification, and Characterization of ¹⁵N-Labeled DNA Repair Proteins as Internal Standards for Mass Spectrometric Measurements.Methods in enzymology · 2016Article
- YU238259 Is a Novel Inhibitor of Homology-Dependent DNA Repair That Exhibits Synthetic Lethality and Radiosensitization in Repair-Deficient Tumors.Molecular cancer research : MCR · 2015Article
- Emerging roles of the nucleolus in regulating the DNA damage response: the noncanonical DNA repair enzyme APE1/Ref-1 as a paradigmatical example.Antioxidants & redox signaling · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer treatments often lose their effectiveness due to the development of multiple drug resistance. Thus, identification of key proteins involved in the tumorigenic process and the survival mechanism(s), coupled with the design of novel therapeutic compounds (such as small molecule inhibitors), are essential steps towards the establishment of improved anticancer treatment strategies. DNA repair pathways and their proteins have been exposed as potential targets for combinatorial anticancer therapies that involve DNA-interactive cytotoxins, such as alkylating agents, because of their central role in providing resistance against DNA damage. In addition, an understanding of the tumor-specific genetics and associated DNA repair capacity has allowed research scientists and clinicians to begin to devise more targeted treatment strategies based on the concept of synthetic lethality. In this review, the repair mechanisms, as well as the links to cancer progression and treatment, of three key proteins that function in the base excision repair pathway, i.e. APE1, POLβ, and FEN1, are discussed.
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.