ArticleMolecular cancer research : MCR2016
High-Fat Diet-Induced Complement Activation Mediates Intestinal Inflammation and Neoplasia, Independent of Obesity.
Article in Molecular cancer research : MCR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- Chronic High-Fat Diet Does Not Alter Overall Cancer Incidence in Trp53R270H/+ Mice.Cancer research communications · 2026Article
- Demonstrating trends for early colorectal cancer incidence: a retrospective analysis of patients in Northwest Ohio.Frontiers in oncology · 2026Article
- Docosahexaenoic Acid Consumption Early in Life Improves Immune Dysfunction in High-Fat Diet-Fed Wistar Rats in a Sex-Specific Manner.Molecular nutrition & food research · 2026Article
- The antimicrobial metabolite nisin Z reduces intestinal tumorigenesis and modulates the cecal microbiome in ApcMicrobiology spectrum · 2025Article
- The complement system in intestinal inflammation and cancer.The Journal of clinical investigation · 2025Review
- Upregulation of HOTTIP and Its Potential Role in Monitoring Exercise Adaptation.International journal of molecular sciences · 2025Article
- Association of the energy-adjusted dietary inflammatory index and Sjögren's syndrome: a cross-sectional study.The British journal of nutrition · 2025Article
- Modulation of adipose inflammation and mitochondrial pathways by a yeast-derivedFrontiers in nutrition · 2025Article
- Machine learning-based clustering identifies obesity subgroups with differential multi-omics profiles and metabolic patterns.Obesity (Silver Spring, Md.) · 2024Article
- Differences in tumor-associated T-cell receptor repertoires between early-onset and average-onset colorectal cancer.Journal of the National Cancer Institute · 2024Article
- Article
- The Degree of Inulin Polymerization Is Important for Short-Term Amelioration of High-Fat Diet (HFD)-Induced Metabolic Dysfunction and Gut Microbiota Dysbiosis in Rats.Foods (Basel, Switzerland) · 2024Article
- The Killer's Web: Interconnection between Inflammation, Epigenetics and Nutrition in Cancer.International journal of molecular sciences · 2024Review
- Article
- Altered lipid metabolism in APC-driven colorectal cancer: the potential for therapeutic intervention.Frontiers in oncology · 2024Review
- Epigenetic effects of high-fat diet on intestinal tumorigenesis in C57BL/6J-Journal of translational genetics and genomics · 2023Article
- Obesity accelerates acute promyelocytic leukemia in mice and reduces sex differences in latency and penetrance.Obesity (Silver Spring, Md.) · 2022Article
- Article
- Dietary fat promotes antibiotic-induced Clostridioides difficile mortality in mice.NPJ biofilms and microbiomes · 2022Article
- Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Obesity and related metabolic disturbances are closely associated with pathologies that represent a significant burden to global health. Epidemiological and molecular evidence links obesity and metabolic status with inflammation and increased risk of cancer. Here, using a mouse model of intestinal neoplasia and strains that are susceptible or resistant to diet-induced obesity, it is demonstrated that high-fat diet-induced inflammation, rather than obesity or metabolic status, is associated with increased intestinal neoplasia. The complement fragment C5a acts as the trigger for inflammation and intestinal tumorigenesis. High-fat diet induces complement activation and generation of C5a, which in turn induces the production of proinflammatory cytokines and expression of proto-oncogenes. Pharmacological and genetic targeting of the C5a receptor reduced both inflammation and intestinal polyposis, suggesting the use of complement inhibitors for preventing diet-induced neoplasia. IMPLICATIONS: This study characterizes the relations between diet and metabolic conditions on risk for a common cancer and identifies complement activation as a novel target for cancer prevention. Mol Cancer Res; 14(10); 953-65. ©2016 AACR.
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