ArticleCancer prevention research (Philadelphia, Pa.)2011
Aspirin and low-dose nitric oxide-donating aspirin increase life span in a Lynch syndrome mouse model.
Article in Cancer prevention research (Philadelphia, Pa.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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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.
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Who cites it
29 citing papers in PubMed.
- Trial
- Cancer prevention with aspirin in hereditary colorectal cancer (Lynch syndrome), 10-year follow-up and registry-based 20-year data in the CAPP2 study: a double-blind, randomised, placebo-controlled trial.Lancet (London, England) · 2020Trial
- Chemoprevention in Lynch syndrome.Familial cancer · 2013Trial
- Long-term effect of aspirin on cancer risk in carriers of hereditary colorectal cancer: an analysis from the CAPP2 randomised controlled trial.Lancet (London, England) · 2011Trial
- The Use of Nutritional Interventions to Enhance Genomic Stability in Mice and Delay Aging.Nutrients · 2026Review
- Article
- Advancing translational research for colorectal immuno-oncology.British journal of cancer · 2023Review
- Genetically engineered mouse models for hereditary cancer syndromes.Cancer science · 2023Review
- Article
- Immunology of Lynch Syndrome.Current oncology reports · 2021Review
- Lycorine hydrochloride suppresses stress-induced premature cellular senescence by stabilizing the genome of human cells.Aging cell · 2021Article
- Genome-Protecting Compounds as Potential Geroprotectors.International journal of molecular sciences · 2020Review
- A Chinese family affected by lynch syndrome caused by MLH1 mutation.BMC medical genetics · 2018Article
- Mutation of TGFβ-RII eliminates NSAID cancer chemoprevention.Oncotarget · 2018Article
- Microsatellite Instability in Mouse Models of Colorectal Cancer.Canadian journal of gastroenterology & hepatology · 2018Article
- Different in vivo and in vitro transformation of intestinal stem cells in mismatch repair deficiency.Oncogene · 2017Article
- Chemoprevention of hereditary colon cancers: time for new strategies.Nature reviews. Gastroenterology & hepatology · 2016Review
- Hereditary cancer syndromes as model systems for chemopreventive agent development.Seminars in oncology · 2016Review
- Mouse models of DNA mismatch repair in cancer research.DNA repair · 2016Review
- Manipulation of DNA Repair Proficiency in Mouse Models of Colorectal Cancer.BioMed research international · 2016Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Nonsteroidal anti-inflammatory drugs (NSAID) appear to be effective cancer chemopreventives. Previous cellular studies showed that aspirin (acetylsalicylic acid: ASA) and nitric oxide-donating ASA (NO-ASA) suppressed microsatellite instability (MSI) in mismatch repair (MMR)-deficient cells linked to the common cancer predisposition syndrome hereditary nonpolyposis colorectal cancer or Lynch syndrome (LS/HNPCC), at doses 300- to 3,000-fold less than ASA. Using a mouse model that develops MMR-deficient intestinal tumors that appear pathologically identical to LS/HNPCC, we show that ASA (400 mg/kg) and low-dose NO-ASA (72 mg/kg) increased life span by 18% to 21%. We also note a trend where ASA treatment resulted in intestinal tumors with reduced high MSI (H-MSI) and increased low MSI (L-MSI) as defined by the Bethesda Criteria. Low-dose NO-ASA had a minimal effect on MSI status. In contrast to previous studies, high-dose NO-ASA (720/1,500 mg/kg) treatments increased tumor burden, decreased life span, and exacerbated MSI uniquely in the LS/HNPCC mouse model. These results suggest that MMR-deficient tissues/mice may be specifically sensitive to intrinsic pharmacokinetic features of this drug. It is likely that long-term treatment with ASA may represent a chemopreventive option for LS/HNPCC patients. Moreover, as low-dose NO-ASA shows equivalent life span increase at 10-fold lower doses than ASA, it may have the potential to significantly reduce the gastropathy associated with long-term ASA treatment.
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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.