ArticleCancers2013
PARP-1: Friend or Foe of DNA Damage and Repair in Tumorigenesis?
Article in Cancers, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 118 citations in OpenAlex.
- Moderate NADH supplementation prevents early colon carcinogenesis by modulating inflammation and oxidative stress in a mouse model.Journal of molecular histology · 2025Article
- Integrating machine learning driven virtual screening and molecular dynamics simulations to identify potential inhibitors targeting PARP1 against prostate cancer.Scientific reports · 2025Article
- A psychiatric medication, clozapine, induces autophagy and apoptosis in breast cancer cells through reactive oxygen species.PloS one · 2025Article
- Mechanistic insights into Rho/MRTF inhibition-induced apoptotic events and prevention of drug resistance in melanoma: implications for the involvement of pirin.Frontiers in pharmacology · 2025Article
- Novel inhibitors of PARP1 and PARP14: design, synthesis, and potentiation of cisplatin efficacy in cancer.Future medicinal chemistry · 2025Article
- Lactylation-Related Gene CALM1 Promotes Aortic Dissection via Immune Microenvironment Remodeling: Insights from Bioinformatics and Clinical Evidence.Journal of inflammation research · 2025Article
- Poly (ADP-Ribose) Polymerase-1 (PARP-1) Inhibitors in Diabetic Retinopathy: An Attractive but Elusive Choice for Drug Development.Pharmaceutics · 2024Review
- PARP-1 selectively impairsGut · 2024Article
- Globospiramine fromCells · 2024Article
- Frontier knowledge and future directions of programmed cell death in clear cell renal cell carcinoma.Cell death discovery · 2024Review
- Inhibition of host PARP1 contributes to the anti-inflammatory and antitubercular activity of pyrazinamide.Nature communications · 2023Article
- Elucidating the Therapeutic Utility of Olaparib in Sulfatide-Induced Human Astrocyte Toxicity and Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Article
- Olaparib Attenuates Demyelination and Neuroinflammation in an Organotypic Slice Culture Model of Metachromatic Leukodystrophy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Regulation of Biomolecular Condensates by Poly(ADP-ribose).Chemical reviews · 2023Review
- DNA Repair Inhibitors: Potential Targets and Partners for Targeted Radionuclide Therapy.Pharmaceutics · 2023Review
- Methyltransferase Set7/9 as a Multifaceted Regulator of ROS Response.International journal of biological sciences · 2023Review
- Oxidative Stress Markers Are Associated with a Poor Prognosis in Patients with Pancreatic Cancer.Antioxidants (Basel, Switzerland) · 2022Article
- Existing Evidence for the Repurposing of PARP-1 Inhibitors in Rare Demyelinating Diseases.Cancers · 2022Review
- Pleiotropic role of PARP1: an overview.3 Biotech · 2022Review
- The protective effect of 17 β-estradiol on human uterosacral ligament fibroblasts from postmenopausal women with pelvic organ prolapse.Frontiers in physiology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress induced by reactive oxygen species can result in DNA damage within cells and subsequently increase risk for carcinogenesis. This may be averted by repair of DNA damage through the base or nucleotide excision repair (BER/NER) pathways. PARP, a BER protein, is known for its role in DNA-repair. However, multiple lesions can occur within a small range of DNA, known as oxidative clustered DNA lesions (OCDLs), which are difficult to repair and may lead to the more severe DNA double-strand break (DSB). Inefficient DSB repair can then result in increased mutagenesis and neoplastic transformation. OCDLs occur more frequently within a variety of tumor tissues. Interestingly, PARP is highly expressed in several human cancers. Additionally, chronic inflammation may contribute to tumorigenesis through ROS-induced DNA damage. Furthermore, PARP can modulate inflammation through interaction with NFκB and regulating the expression of inflammatory signaling molecules. Thus, the upregulation of PARP may present a double-edged sword. PARP is needed to repair ROS-induced DNA lesions, but PARP expression may lead to increased inflammation via upregulation of NFκB signaling. Here, we discuss the role of PARP in the repair of oxidative damage versus the formation of OCDLs and speculate on the feasibility of PARP inhibition for the treatment and prevention of cancers by exploiting its role in inflammation.
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.