ArticlePLoS genetics2013
NSAIDs modulate clonal evolution in Barrett's esophagus.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
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.
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Who cites it
48 citing papers in PubMed, 66 citations in OpenAlex.
- The biology and therapeutic implications of heterogeneity in Barrett oesophagus and oesophageal adenocarcinoma.Nature reviews. Clinical oncology · 2026Review
- The evolutionary theory of cancer: challenges and potential solutions.Nature reviews. Cancer · 2024Review
- Tumor Promoters and Opportunities for Molecular Cancer Prevention.Cancer discovery · 2024Review
- Resolving tumor evolution: a phylogenetic approach.Journal of the National Cancer Center · 2024Review
- A war on many fronts: cross disciplinary approaches for novel cancer treatment strategies.Frontiers in genetics · 2024Review
- Unboxing the molecular modalities of mutagens in cancer.Environmental science and pollution research international · 2022Review
- Game of clones: Battles in the field of carcinogenesis.Pharmacology & therapeutics · 2022Review
- Evolutionary dynamics in Barrett oesophagus: implications for surveillance, risk stratification and therapy.Nature reviews. Gastroenterology & hepatology · 2022Review
- Within-patient phylogenetic reconstruction reveals early events in Barrett's Esophagus.Evolutionary applications · 2021Article
- Effects of aspirin on the gastrointestinal tract: Pros vs. cons.Oncology letters · 2020Review
- Review
- Beyond a chemopreventive reagent, aspirin is a master regulator of the hallmarks of cancer.Journal of cancer research and clinical oncology · 2019Review
- Energy oversupply to tissues: a single mechanism possibly underlying multiple cancer risk factors.Evolution, medicine, and public health · 2019Article
- The Cytotoxicity and Synergistic Potential of Aspirin and Aspirin Analogues Towards Oesophageal and Colorectal Cancer.Current clinical pharmacology · 2019Article
- Is Barrett's-Associated Esophageal Adenocarcinoma a Clonal Disease?Digestive diseases and sciences · 2018Review
- NSAID use and somatic exomic mutations in Barrett's esophagus.Genome medicine · 2018Article
- Evolution of Barrett's esophagus through space and time at single-crypt and whole-biopsy levels.Nature communications · 2018Article
- The metaplastic mosaic of Barrett's oesophagus.Virchows Archiv : an international journal of pathology · 2018Review
- From Colitis to Cancer: An Evolutionary Trajectory That Merges Maths and Biology.Frontiers in immunology · 2018Review
- Advances in antitumor effects of NSAIDs.Cancer management and research · 2018Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
Cancer is considered an outcome of decades-long clonal evolution fueled by acquisition of somatic genomic abnormalities (SGAs). Non-steroidal anti-inflammatory drugs (NSAIDs) have been shown to reduce cancer risk, including risk of progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA). However, the cancer chemopreventive mechanisms of NSAIDs are not fully understood. We hypothesized that NSAIDs modulate clonal evolution by reducing SGA acquisition rate. We evaluated thirteen individuals with BE. Eleven had not used NSAIDs for 6.2±3.5 (mean±standard deviation) years and then began using NSAIDs for 5.6±2.7 years, whereas two had used NSAIDs for 3.3±1.4 years and then discontinued use for 7.9±0.7 years. 161 BE biopsies, collected at 5-8 time points over 6.4-19 years, were analyzed using 1Million-SNP arrays to detect SGAs. Even in the earliest biopsies there were many SGAs (284±246 in 10/13 and 1442±560 in 3/13 individuals) and in most individuals the number of SGAs changed little over time, with both increases and decreases in SGAs detected. The estimated SGA rate was 7.8 per genome per year (95% support interval [SI], 7.1-8.6) off-NSAIDs and 0.6 (95% SI 0.3-1.5) on-NSAIDs. Twelve individuals did not progress to EA. In ten we detected 279±86 SGAs affecting 53±30 Mb of the genome per biopsy per time point and in two we detected 1,463±375 SGAs affecting 180±100 Mb. In one individual who progressed to EA we detected a clone having 2,291±78 SGAs affecting 588±18 Mb of the genome at three time points in the last three of 11.4 years of follow-up. NSAIDs were associated with reduced rate of acquisition of SGAs in eleven of thirteen individuals. Barrett's cells maintained relative equilibrium level of SGAs over time with occasional punctuations by expansion of clones having massive amount of SGAs.
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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.