<scp>MDSC</scp> suppresses T cell antitumor immunity in <scp>CAC</scp> via <scp>GPNMB</scp> in a <scp>MyD88</scp>‐dependent manner

Wang, Bo; Wang, Lu; Shang, Runshi; Xie, Lin

doi:10.1002/cam4.6887

Cited by 2 publications

(1 citation statement)

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“…Prevents colorectal cancer development associated with colitis [53] Inhibits cell proptosis Prevents liver ischemia-reperfusion injury [116] Blocks MyD88 signal transduction Prevents the development of CAC as well as downregulating GPNMB mRNA [117] Provides neuroprotection after experimental traumatic brain injury in mice [118], inhibits HCC cell proliferation [94] and relieves lymphoma and leukemia [96] 2016, 2017…”

Section: Inhibits Myd88 Homologous Dimerizationmentioning

confidence: 99%

MyD88 and Its Inhibitors in Cancer: Prospects and Challenges

Song,

Li,

et al. 2024

Biomolecules

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The interplay between the immune system and cancer underscores the central role of immunotherapy in cancer treatment. In this context, the innate immune system plays a critical role in preventing tumor invasion. Myeloid differentiation factor 88 (MyD88) is crucial for innate immunity, and activation of MyD88 promotes the production of inflammatory cytokines and induces infiltration, polarization, and immune escape of immune cells in the tumor microenvironment. Additionally, abnormal MyD88 signaling induces tumor cell proliferation and metastasis, which are closely associated with poor prognosis. Therefore, MyD88 could serve as a novel tumor biomarker and is a promising target for cancer therapy. Current strategies targeting MyD88 including inhibition of signaling pathways and protein multimerization, have made substantial progress, especially in inflammatory diseases and chronic inflammation-induced cancers. However, the specific role of MyD88 in regulating tumor immunity and tumorigenic mechanisms remains unclear. Therefore, this review describes the involvement of MyD88 in tumor immune escape and disease therapy. In addition, classical and non-classical MyD88 inhibitors were collated to provide insights into potential cancer treatment strategies. Despite several challenges and complexities, targeting MyD88 is a promising avenue for improving cancer treatment and has the potential to revolutionize patient outcomes.

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Section: Inhibits Myd88 Homologous Dimerizationmentioning

confidence: 99%

MyD88 and Its Inhibitors in Cancer: Prospects and Challenges

Song,

Li,

et al. 2024

Biomolecules

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Notable correlation between serum epidermal growth factor values and inflammatory status in patients with COVID‐19

Pérez,

Crombet

2024

Immunity Inflam & Disease

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IntroductionDespite its crucial role in Epidermal Growth Factor Receptor (EGFR) activation, and the resulting impact on the health‐disease process, epidermal growth factor (EGF) is an underexplored molecule in relation to how its serum concentrations relate to other analytes and clinical variables in pathological contexts.ObjectiveTo clarify the possible correlation between EGF and clinical and analytical variables in the context of COVID‐19.MethodsCross‐sectional observational and analytical study, in patients with virological and clinical diagnosis of COVID‐19, selected by simple random sampling, admitted between August and September 2021. UMELISA‐EGF commercial kits were used.ResultsDifferences in overall EGF values were observed between groups (566.04 vs. 910.53 pg/ml, p = .0430). In COVID‐19 patients, no notable correlations were observed for neutrophil, platelet, triglyceride or liver enzyme values (p > .05). Significant correlations were observed with the neutrophil‐lymphocyte indicator (r = 0.4711, p = .0128) as well as with the platelet‐lymphocyte index (r = 0.4553, p = .0155). Statistical results of multivariate regression analysis suggest NLR (β = .2232, p = .0353) and PLR (β = .2117, p = .0411) are predictors of inflammation in patients with COVID‐19.ConclusionsSerum EGF concentrations in COVID‐19 correlate positively with prognostic inflammatory markers of severity and could presumably act as an independent risk factor for the development of inflammation in response to new severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2).

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MDSC suppresses T cell antitumor immunity in CAC via GPNMB in a MyD88‐dependent manner

Cited by 2 publications

References 40 publications

MyD88 and Its Inhibitors in Cancer: Prospects and Challenges

MyD88 and Its Inhibitors in Cancer: Prospects and Challenges

Notable correlation between serum epidermal growth factor values and inflammatory status in patients with COVID‐19

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