ReviewAntioxidants & redox signaling2009
Going ape as an approach to cancer therapeutics.
Review in Antioxidants & redox signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 109 citations in OpenAlex.
- A phase I study targeting the APE1/Ref-1 redox signaling protein with APX3330: first clinical agent targeting APE1/Ref-1 in cancer.The oncologist · 2026Article
- Real-Time, Light-Activated, and Multiplexed Monitoring of Base Excision Repair in Living Cells Using Chimeric d/l-DNA Molecular Beacons.ACS sensors · 2025Article
- The human AP-endonuclease 1 (APE1) is a DNA G-quadruplex structure binding protein and regulates KRAS expression in pancreatic ductal adenocarcinoma cells.Nucleic acids research · 2022Article
- Changes in the Plasma Apurinic/Apyrimidinic Endonuclease 1/Redox Factor-1(APE1/Ref-1) Level during Cancer Surgery: An Observational Study.Medicina (Kaunas, Lithuania) · 2021Observational
- Elevated APE1/Ref-1 Levels of Synovial Fluids in Patients with Rheumatoid Arthritis: Reflection of Disease Activity.Journal of clinical medicine · 2021Article
- Molecular Mechanisms Regulating the DNA Repair Protein APE1: A Focus on Its Flexible N-Terminal Tail Domain.International journal of molecular sciences · 2021Review
- DNA alkylation lesion repair: outcomes and implications in cancer chemotherapy.Journal of Zhejiang University. Science. B · 2021Review
- Licochalcone B Ameliorates Liver Cancer via Targeting of Apoptotic Genes, DNA Repair Systems, and Cell Cycle Control.Iranian journal of pharmaceutical research : IJPR · 2020Article
- P53 supports endothelial barrier function via APE1/Ref1 suppression.Immunobiology · 2019Article
- Targeting Base Excision Repair Glycosylases with DNA Containing Transition State Mimics Prepared via Click Chemistry.ACS chemical biology · 2019Article
- Therapeutic positioning of secretory acetylated APE1/Ref-1 requirement for suppression of tumor growth in triple-negative breast cancer in vivo.Scientific reports · 2018Article
- Suppression of STAT3 NHMolecular carcinogenesis · 2018Article
- APE1/Ref-1 redox-specific inhibition decreases survivin protein levels and induces cell cycle arrest in prostate cancer cells.Oncotarget · 2018Article
- The Anti-Apoptotic Properties of APEX1 in the Endothelium Require the First 20 Amino Acids and Converge on Thioredoxin-1.Antioxidants & redox signaling · 2017Article
- Natural Bioactive Compounds: Alternative Approach to the Treatment of Glioblastoma Multiforme.BioMed research international · 2017Review
- The anti-inflammatory role of extranuclear apurinic/apyrimidinic endonuclease 1/redox effector factor-1 in reactive astrocytes.Molecular brain · 2016Article
- Article
- APE1 overexpression promotes the progression of ovarian cancer and serves as a potential therapeutic target.Cancer biomarkers : section A of Disease markers · 2016Article
- Regulation of limited N-terminal proteolysis of APE1 in tumor via acetylation and its role in cell proliferation.Oncotarget · 2016Article
- Endothelial cell tumor growth is Ape/ref-1 dependent.American journal of physiology. Cell physiology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The DNA base excision repair (BER) pathway repairs alkylation and oxidative DNA damage caused by endogenous and exogenous agents, including chemotherapeutic agents. Upon removal of the damaged base AP endonuclease 1 (Ape1), a critical component of the pathway cleaves the abasic site to facilitate repair. Ape1 is a multifunctional protein which plays a role not only in DNA repair but it also functions as a reduction-oxidation factor, known as Ref-1 in the literature, to increase the DNA binding ability of several transcription factors involved in different growth signaling pathways. Elevated levels of Ape1 have been linked to resistance to chemotherapy, poor prognosis, and poor survival. Reducing the amount of Ape1 protein in cancer cells and tumors using RNA interference and anti-sense oligonucleotide technology sensitizes mammalian tumor cells to a variety of laboratory and chemotherapeutic agents. Therefore, selective inhibition of Ape1's DNA repair activity is a promising avenue to develop novel cancer therapeutics.
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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.