FCGR2A (Fc fragment of IgG receptor IIa)

Furthermore, following phagocytosis, CAR-monocytes induced antigen-specific CD8+ T cell activation via antigen presentation. Collectively, these findings highlight CD32a-based and combinatorial ICD designs as a framework for functionally tuned CAR-M platform for solid tumor immunotherapy and anti-viral applications.

High-risk patients were more sensitive to drugs such as Dasatinib. FCGR2A overexpression promoted proliferation, migration, and invasion in vitro. The 15-gene ICD-based model effectively predicts COAD prognosis, reflects immune microenvironment heterogeneity, and offers insights for individualized treatment planning.

Furthermore, polarization of CAR-Ms into a proinflammatory state significantly enhanced tumor-killing efficacy, particularly in FCGR2A CAR-Ms. These findings highlight the potential of FCGR2A as an optimal signaling domain for CAR-M design and underscore the therapeutic promise of proinflammatory polarized CAR-Ms in solid tumor immunotherapy.

Notably, Fc fragment of IgG receptor IIa (FCGR2A, or CD32) was identified as a promising biomarker for ATC, implicating a functional link between immune evasion and tumor aggressiveness. Our findings provide a comprehensive molecular and immunological characterization of thyroid cancer subtypes, offering novel insights into the pathogenesis of ATC and PDTC, and identifying potential targets for diagnosis and precision therapy.

Moreover, CXCL9 inhibited the activation of the ERK and AKT signaling pathways, further inhibiting tumor cell proliferation and invasion. CXCL9 inhibits the proliferation, migration, metastasis and invasion of lung cancer cells by inhibiting M2 macrophage polarization and function, indicating that CXCL9 may serve as a potential therapeutic target for lung cancer.

Drug sensitivity analysis indicated that H-R patients were more sensitive to Staurosporine and Sabutoclax, whereas L-R patients were more sensitive to dihydrorotenone and osimertinib. RT-qPCR validated differential mRNA expression between KIRC and normal cells. This six-LRPMR-based prognostic model provides valuable insights for prognosis assessment and personalized treatment selection in KIRC.

FCGR2A acts as both a prognostic biomarker and an immune regulatory hub in HCC, anchoring a broader gene network that defines immune subtypes and predicts therapeutic responsiveness. Incorporating FCGR2A-based stratification may optimize immunotherapeutic strategies for HCC.

A low-dose combination therapy of fostamatinib, Aducanumab, and acetylsalicylic acid (aspirin) may control TEP effects. In conclusion, our preclinical in silico approach revealed FDA-approved drugs that allow therapeutic targeting of metastasis-promoting TEPs and target NSCLC at the same time.

The optimized machine learning model (glmBoost+Stepglm) generated a parsimonious 14-gene signature demonstrating exceptional cross-cohort accuracy (mean AUC=0.991), while pharmacological screening prioritized kinase inhibitors (e.g., dasatinib, p=2.1×10⁻⁸) and immunomodulators as therapeutic candidates. Our study establishes FCGR2A-mediated myeloid reprogramming as a critical interface between metabolic dysfunction and ccRCC progression, serving as both a prognostic biomarker and therapeutic target. This dual-disease modeling paradigm provides actionable insights for precision management of obesity-associated malignancies.

S1P1 contributes to the immunosuppressive phenotype of microglia. Inhibiting the S1P/S1P1 axis impairs viability and crosstalk between melanoma cells and tumor-activated microglia, offering a potential therapeutic strategy for melanoma brain metastases.

Overall, our findings delineate the kinetics of systemic and mucosal myeloid cell expansion, activation and trafficking achieved by subQ GM-CSF administration in RM. These findings will inform the use of GM-CSF as an adjuvant in clinical applications where myeloid cell mobilization is advantageous.

Despite these modifications, the mutated antibodies effectively restored IFN-γ production, which had been suppressed by PD-1/PD-L1 signaling in stimulated lymphocytes, to levels comparable to those of the original antibody. These findings reveal that the engineered antibodies have potential for future clinical applications in feline oncology.