S100A9 (S100 Calcium Binding Protein A9)

This finding suggests that tasquinimod, an S100A9 inhibitor, could be a viable therapeutic option. Furthermore, the interaction between MMP11 and COL16A1 in stroma-rich regions suggests that cancer-associated fibroblasts may contribute to improved outcomes. Our study underscores the critical role of spatial gene expression analysis in elucidating the tumor microenvironment and its impact on prognosis in patients undergoing E+L treatment, thereby opening new avenues for targeted interventions.

Furthermore, E171-induced secretion of S100A8 and S100A9 in macrophages was suppressed by specific inhibitors, including N-acetylcysteine (NAC, ROS inhibitor), MCC950 (NLRP3 inhibitor), Z-YVAD-FMK (caspase 1 inhibitor), disulfiram (GSDMD inhibitor), and transfection of NLRP3 small interfering ribonucleic acid (siRNA). These results indicate that dietary E171 promotes CAC development by activating macrophages, with S100A8 and S100A9 serving as key mediators, and the NLRP3/caspase 1/GSDMD pathway acting as a critical mechanism.

BALB/C mice were randomized into an NA group, a dexamethasone intervention group (DI, 1 mg/kg), and a Fasudil intervention group (FI, 40 mg/kg). Fasudil ameliorates NA via regulating M1 macrophage polarization, inhibiting the NF-κB/TLR-2/RPS3 pathway, and reducing pro-inflammatory cytokines, with S100A8/A9 and CXCL2 as potential biomarkers. These findings support Fasudil as a promising NA therapy, warranting further clinical translational research.

WWOX2 serves as a tumor suppressor, whereas FUT1 functions as a promoter of malignancy. The interplay between tumor inducers and suppressors may serve as a survival mechanism for cancer cells, a subject that has received limited research attention.

In patients with IBC, high serum levels of S100A8/A9 are an independent prognostic factor for brain metastasis and poor clinical outcomes. These findings support the potential of S100A8/A9 as predictive biomarker for identifying increased risk of brain metastasis and unfavorable prognosis in patients with IBC.

Blocking S100a9 with tasquinimod rescues the defects of Sucnr1 knock-out mice, and combined with a potent Sucnr1 agonist shows therapeutic value in AML mice...Together, Sucnr1 signaling restricts hematopoiesis at least partially through HSPC and via control of S100a8/S100a9. Its dysregulation emerges as contributor to malignancy that opens therapeutic avenues for AML patients.

P1/2, N=18, Active, not recruiting, Cantex Pharmaceuticals | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2024 --> Dec 2026

P=N/A, N=400, Not yet recruiting, The Second Affiliated Hospital of Shandong First Medical University; The Second Affiliated Hospital of Shandong First Medical University

These findings offer preliminary clues for future risankizumab-based combination strategies in psoriasis.

AFP (Alpha-fetoprotein) and GFAP (Glial Fibrillary Acidic Protein) emerged as potential biomarkers from the primary lesion for BM onset, while network analysis identified MET (MET Proto-Oncogene, Receptor Tyrosine Kinase), GDF15 (Growth Differentiation Factor 15), and S100A9 (S100 Calcium Binding Protein A9) as candidate mediators of tumour-brain crosstalk. These results offer new insights into EOC brain tropism, highlighting potential targets for therapeutic intervention and personalized patient management in the precision oncology era.

These findings reveal that HF exerts anti-leukemic effects by modulating the p-eIF2α-S100A8/A9-Ca2⁺ signaling axis in AML cells. HF represents a promising therapeutic candidate for AML, particularly for patients with IDA-resistant disease.

E2F5 is highly expressed in LSCC and is associated with the regulation of NETs-related genes. It may contribute to tumor proliferation and immune evasion by reshaping the tumor microenvironment, highlighting E2F5 as a potential therapeutic target that warrants further functional validation.