ARG1 (Arginase 1)

Arginine metabolism stratifies MCs into pro-tumorigenic HAS and quiescent LAS subsets; ASL-high MCs constitute a metabolically wired, highly communicating population that fuels TNBC progression and furnishes an exploitable prognostic signature. OAT, a key HAS-associated gene, promotes breast cancer aggressiveness through proliferation, survival, and invasion.

Mechanistically, lactate-induced histone lactylation upregulates TET2, which, using STAT3 as a bridge, modulates ARG1 promoter methylation to upregulate its expression and ultimately enhance the immunosuppressive function of MDSCs. This research reveals that the histone lactylation-mediated alteration of TET2 presents a novel therapeutic target for cancer treatment.

Our findings suggest that infection natural with L. infantum in dogs may induce dysregulation of the HPA axis, leading to elevated serum cortisol levels and modulation of the immune response, as it is associated with immunological markers involved in disease pathogenesis. These results contribute to a better understanding of the pathogenic mechanisms of the disease.

Molecular docking predicted a strong binding affinity (-7.1 kcal mol-1) for L-arginine, with ligand enzyme complex stabilized by a dense network of hydrogen bonds and electrostatic interactions within the active site. These findings elucidate the structural basis of the enzyme's function and underscore its potential for future experimental validation and therapeutic applications.

Furthermore, a heterozygous missense variant in the ALK gene (p. Arg1275Gln) was identified.

Combination therapy with BBR and anti-PD-L1 antibody synergistically inhibited H22 tumor growth. These findings suggest that BBR can reduce the M2 polarization of tumor-associated macrophages (TAMs) by targeting the IL-4-JAK1-STAT6 axis, and combining with anti-PD-L1 antibody may represent a promising therapeutic strategy to enhance BBR's antitumor efficacy.

The blended phenotype, with early marrow fibrosis, could not be explained by either condition alone. Such dual diagnoses underscore the critical role of molecular testing in atypical pediatric cytopenias.

Despite an early dominance of M1-like macrophage genes (e.g., IL-12α/β), persistent expression of arginase 1 (ARG1) and other M2-associated genes indicated a stable tolerogenic niche. The temporally coordinated immune shifts, such as progressive decline in transcripts associated with T cell functions, TCRs, APCs, and sustained macrophage-driven immunosuppression, suggest tumor-driven adaptation toward immune evasion and identify potential windows for stage-specific immunotherapeutic intervention.

SSG may exert its inhibitory effect on lung cancer by increasing the polarization of macrophages to M1-type TAMs and reducing the polarization to M2-type TAMs. The analysis of the pharmacodynamic components of SSG provides a basis and reference for subsequent research on pharmacokinetics.

Further experiments revealed that the expression of polarization-related markers in M1-type macrophages was significantly suppressed after treatment with the SUCNR1-neutralizing antibody or the PI3K inhibitor LY294002. These findings suggest that succinate may activate the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway via SUCNR1 to promote the polarization of NEC macrophages toward the M1 phenotype, thereby accelerating NEC progression.

NOD1 is an effective predictor of preoperative glioma grade and prognosis. It facilitates glioma progression by promoting microglial M2 polarization through the NOD1/RIP2 pathway.

These polarized macrophages further enhance tumor cell proliferation and invasion, thereby forming a tumor-immune feedback loop. In conclusion, this study clarifies how IL7R signaling mediates crosstalk between ovarian cancer cells and macrophages to maintain the homeostasis of the immunosuppressive tumor microenvironment (TME).