ReviewInternational journal of molecular sciences2013
Colorectal carcinogenesis: a cellular response to sustained risk environment.
Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Association between allergic conditions and colorectal cancer risk/mortality: a meta-analysis of prospective studies.Scientific reports · 2017Pooled it
- Review
- Article
- Exploring the immunometabolic potential of Danggui Buxue Decoction for the treatment of IBD-related colorectal cancer.Chinese medicine · 2024Review
- Modulation of the Tumor Microenvironment by Microbiota-Derived Short-Chain Fatty Acids: Impact in Colorectal Cancer Therapy.International journal of molecular sciences · 2023Review
- Dietary fiber pectin: challenges and potential anti-inflammatory benefits for preterms and newborns.Frontiers in nutrition · 2023Review
- The Modulation of Chaihu Shugan Formula on Microbiota Composition in the Simulator of the Human Intestinal Microbial Ecosystem Technology Platform and its Influence on Gut Barrier and Intestinal Immunity in Caco-2/THP1-Blue™ Cell Co-Culture Model.Frontiers in pharmacology · 2022Article
- Evaluation of graded levels of Bacillus coagulans GBI-30, 6086 on apparent nutrient digestibility, stool quality, and intestinal health indicators in healthy adult dogs.Journal of animal science · 2021Article
- Gut Microbiota: Influence on Carcinogenesis and Modulation Strategies by Drug Delivery Systems to Improve Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- The GenusFrontiers in immunology · 2020Review
- Risk Factors for Colorectal Cancer in Korea: A Population-Based Retrospective Cohort Study.Annals of coloproctology · 2019Article
- Microbial Fermentation of Dietary Protein: An Important Factor in Diet⁻Microbe⁻Host Interaction.Microorganisms · 2019Review
- Therapeutic effects of antimicrobial peptide on malignant ascites in a mouse model.Molecular medicine reports · 2018Article
- Article
- Atopic allergic conditions and colorectal cancer risk in the Multiethnic Cohort Study.American journal of epidemiology · 2015Article
- Colorectal carcinogenesis--update and perspectives.World journal of gastroenterology · 2014Review
- Trends in dietary patterns, alcohol intake, tobacco smoking, and colorectal cancer in Polish population in 1960-2008.BioMed research international · 2013Article
- Intake ofEuroasian journal of hepato-gastroenterologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The current models for colorectal cancer (CRC) are essentially linear in nature with a sequential progression from adenoma through to carcinoma. However, these views of CRC development do not explain the full body of published knowledge and tend to discount environmental influences. This paper proposes that CRC is a cellular response to prolonged exposure to cytotoxic agents (e.g., free ammonia) as key events within a sustained high-risk colonic luminal environment. This environment is low in substrate for the colonocytes (short chain fatty acids, SCFA) and consequently of higher pH with higher levels of free ammonia and decreased mucosal oxygen supply as a result of lower visceral blood flow. All of these lead to greater and prolonged exposure of the colonic epithelium to a cytotoxic agent with diminished aerobic energy availability. Normal colonocytes faced with this unfavourable environment can transform into CRC cells for survival through epigenetic reprogramming to express genes which increase mobility to allow migration and proliferation. Recent data with high protein diets confirm that genetic damage can be increased, consistent with greater CRC risk. However, this damage can be reversed by increasing SCFA supply by feeding fermentable fibre as resistant starch or arabinoxylan. High protein, low carbohydrate diets have been shown to alter the colonic environment with lower butyrate levels and apparently greater mucosal exposure to ammonia, consistent with our hypothesis. Evidence is drawn from in vivo and in vitro genomic and biochemical studies to frame experiments to test this proposition.
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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.