Observational studyCancer medicine2020
Epistatic effect of TLR3 and cGAS-STING-IKKε-TBK1-IFN signaling variants on colorectal cancer risk.
Observational study in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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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Who cites it
10 citing papers in PubMed, 45 citations in OpenAlex.
- cGAS/STING pathway and gastrointestinal cancer: Mechanisms and diagnostic and therapeutic targets (Review).Oncology reports · 2025Review
- Genetic polymorphisms in cGAS-STING-mediated type I interferon innate immune signaling pathway are associated with DLBCL.Frontiers in immunology · 2025Article
- The role of cGAS in epithelial dysregulation in inflammatory bowel disease and gastrointestinal malignancies.Frontiers in pharmacology · 2024Review
- TBK1 is paradoxical in tumor development: a focus on the pathway mediating IFN-I expression.Frontiers in immunology · 2024Review
- STING pathway contributes to the prognosis of hepatocellular carcinoma and identification of prognostic gene signatures correlated to tumor microenvironment.Cancer cell international · 2022Article
- Genetic variants involved in the cGAS-STING pathway predict outcome in patients with metastatic colorectal cancer: Data from FIRE-3 and TRIBE trials.European journal of cancer (Oxford, England : 1990) · 2022Article
- Dexmedetomidine and Ketamine Attenuated Neuropathic Pain Related BehaviorsFrontiers in synaptic neuroscience · 2022Article
- Toll-like receptor 4 is a master regulator for colorectal cancer growth under high-fat diet by programming cancer metabolism.Cell death & disease · 2021Article
- Genetic interactions effects for cancer disease identification using computational models: a review.Medical & biological engineering & computing · 2021Review
- Epistatic effect of TLR3 and cGAS-STING-IKKε-TBK1-IFN signaling variants on colorectal cancer risk.Cancer medicine · 2020Observational
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe TLR3/cGAS-STING-IFN signaling has recently been reported to be disturbed in colorectal cancer due to deregulated expression of the genes involved. Our study aimed to investigate the influence of potential regulatory variants in these genes on the risk of sporadic colorectal cancer (CRC) in a Czech cohort of 1424 CRC patients and 1114 healthy controls.
methodsThe variants in the TLR3, CGAS, TMEM173, IKBKE, and TBK1 genes were selected using various online bioinformatic tools, such as UCSC browser, HaploReg, Regulome DB, Gtex Portal, SIFT, PolyPhen2, and miRNA prediction tools.
resultsLogistic regression analysis adjusted for age and sex detected a nominal association between CRC risk and three variants, CGAS rs72960018 (OR: 1.68, 95% CI: 1.11-2.53, P-value = .01), CGAS rs9352000 (OR: 2.02, 95% CI: 1.07-3.84, P-value = .03) and TMEM173 rs13153461 (OR: 1.53, 95% CI: 1.03-2.27, P-value = .03). Their cumulative effect revealed a threefold increased CRC risk in carriers of 5-6 risk alleles compared to those with 0-2 risk alleles. Epistatic interactions between these genes and the previously genotyped IFNAR1, IFNAR2, IFNA, IFNB, IFNK, IFNW, IRF3, and IRF7 genes, were computed to test their effect on CRC risk. Overall, we obtained nine pair-wise interactions within and between the CGAS, TMEM173, IKBKE, and TBK1 genes. Two of them remained statistically significant after Bonferroni correction. Additional 52 interactions were observed when IFN variants were added to the analysis.
conclusionsOur data suggest that epistatic interactions and a high number of risk alleles may play an important role in CRC carcinogenesis, offering novel biological understanding for the CRC management.
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