ReviewJournal of molecular histology2006
New tricks for old drugs: the anticarcinogenic potential of DNA repair inhibitors.
Review in Journal of molecular histology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 67 citations in OpenAlex.
- Open-Sourced In Silico Drug Screening.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Controlled Self-Immolative Release of β-Lapachone via an OptimizedJournal of the American Chemical Society · 2025Article
- Chlorogenic Acid Enhances Beta-Lapachone-Induced Cell Death by Suppressing Autophagy in NQO1-Positive Cancer Cells.Cell biology international · 2025Article
- DNA damage induced by KP372-1 hyperactivates PARP1 and enhances lethality of pancreatic cancer cells with PARP inhibition.Scientific reports · 2020Article
- Phase 1 study of ARQ 761, a β-lapachone analogue that promotes NQO1-mediated programmed cancer cell necrosis.British journal of cancer · 2018Article
- Using a novel NQO1 bioactivatable drug, beta-lapachone (ARQ761), to enhance chemotherapeutic effects by metabolic modulation in pancreatic cancer.Journal of surgical oncology · 2017Article
- NAMPT inhibition sensitizes pancreatic adenocarcinoma cells to tumor-selective, PAR-independent metabolic catastrophe and cell death induced by β-lapachone.Cell death & disease · 2015Article
- Tumor-selective, futile redox cycle-induced bystander effects elicited by NQO1 bioactivatable radiosensitizing drugs in triple-negative breast cancers.Antioxidants & redox signaling · 2014Article
- Catalase abrogates β-lapachone-induced PARP1 hyperactivation-directed programmed necrosis in NQO1-positive breast cancers.Molecular cancer therapeutics · 2013Article
- Structural simplification of bioactive natural products with multicomponent synthesis. 4. 4H-pyrano-[2,3-b]naphthoquinones with anticancer activity.Bioorganic & medicinal chemistry letters · 2012Article
- The effects of resveratrol and selected metabolites on the radiation and antioxidant response.Cancer biology & therapy · 2011Article
- The small GTPase RhoA localizes to the nucleus and is activated by Net1 and DNA damage signals.PloS one · 2011Article
- Harnessing the complexity of DNA-damage response pathways to improve cancer treatment outcomes.Oncogene · 2010Review
- Prostate cancer radiosensitization through poly(ADP-Ribose) polymerase-1 hyperactivation.Cancer research · 2010Article
- Differential oxidative stress gene expression profile in mouse brain after proton exposure.In vitro cellular & developmental biology. Animal · 2010Article
- Expression profile of DNA damage signaling genes in 2 Gy proton exposed mouse brain.Molecular and cellular biochemistry · 2010Article
- Beta-lapachone micellar nanotherapeutics for non-small cell lung cancer therapy.Cancer research · 2010Article
- The trypanocidal activity of naphthoquinones: a review.Molecules (Basel, Switzerland) · 2009Review
- DNA damage-induced cell death: lessons from the central nervous system.Cell research · 2008Review
- An NQO1- and PARP-1-mediated cell death pathway induced in non-small-cell lung cancer cells by beta-lapachone.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Defective or abortive repair of DNA lesions has been associated with carcinogenesis. Therefore it is imperative for a cell to accurately repair its DNA after damage if it is to return to a normal cellular phenotype. In certain circumstances, if DNA damage cannot be repaired completely and with high fidelity, it is more advantageous for an organism to have some of its more severely damaged cells die rather than survive as neoplastic transformants. A number of DNA repair inhibitors have the potential to act as anticarcinogenic compounds. These drugs are capable of modulating DNA repair, thus promoting cell death rather than repair of potentially carcinogenic DNA damage mediated by error-prone DNA repair processes. In theory, exposure to a DNA repair inhibitor during, or immediately after, carcinogenic exposure should decrease or prevent tumorigenesis. However, the ability of DNA repair inhibitors to prevent cancer development is difficult to interpret depending upon the system used and the type of genotoxic stress. Inhibitors may act on multiple aspects of DNA repair as well as the cellular signaling pathways activated in response to the initial damage. In this review, we summarize basic DNA repair mechanisms and explore the effects of a number of DNA repair inhibitors that not only potentiate DNA-damaging agents but also decrease carcinogenicity. In particular, we focus on a novel anti-tumor agent, beta-lapachone, and its potential to block transformation by modulating poly(ADP-ribose) polymerase-1.
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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.