SynthesisImmunogenetics2021
Rs-10889677 variant in interleukin-23 receptor may contribute to creating an inflammatory milieu more susceptible to bladder tumourigenesis: report and meta-analysis.
Synthesis in Immunogenetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Association of Tumor Necrosis Factor Alpha Gene Polymorphism (TNF-α 308 G/A) with Enhanced Severity of Metal-Induced Chronic Kidney Disease via Upregulation of Transmembrane Protein Expression.Biological trace element research · 2025Article
- Emerging immunologic approaches as cancer anti-angiogenic therapies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- The IL-23R and Its Genetic Variants: A Hitherto Unforeseen Bridge Between the Immune System and Cancer Development.Cancers · 2024Review
- The Urinary Microbiome in Health and Disease: Relevance for Bladder Cancer.International journal of molecular sciences · 2024Review
- Article
- Identifying stage-associated hub genes in bladder cancer via weighted gene co-expression network and robust rank aggregation analyses.Medicine · 2022Article
- The Urinary Microbiome: Role in Bladder Cancer and Treatment.Diagnostics (Basel, Switzerland) · 2022Review
- Cytokine-driven positive feedback loop organizes fibroblast transformation and facilitates gastric cancer progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder cancer (BLC) is a recurrent high-risk malignancy typified by an inherent localised chronic inflammation. IL-23-receptor (IL-23R), as a positive regulator in the priming of T helper-17 cells, is regarded a principal coordinator of inflammation-propelled neoplasia. In this article, we indented firstly to scrutinise the influence of rs10889677"A/C" SNP located in IL-23R-gene on BLC development and progression among Egyptians. Findings revealed that the rs10889677"C" allele was significantly associated with the increased BLC risk and its higher frequencies were plainly noticeable in high-grade and invasive tumours when applied the dominant/homozygous/allelic genetic models. Under the same genetic models, elevated serum levels of IL-23R protein in BLC patients were pertinently correlated with the rs10889677"A/C" polymorphism. As a corollary, the frequent up-regulation of IL-23R exerts a subsequent activation of the IL-23/17 inflammatory axis. That is experienced as a drastic increase in IL-23 and IL17 levels under the dominant/homozygous/heterozygous/recessive models. Second, study further described how the rs10889677 variant confers its pro-tumoural influences on IL-23R-bearing immune cells, involving tumour-associated macrophages (TAMs), natural killers (NKs) and CD4
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