Interferons (IFNs) are a family of cytokines that orchestrate a wide range of antiviral, immunoregulatory, and antitumor activities. This review provides a comprehensive overview of the molecular mechanisms underlying IFN signaling, including both canonical JAK (janus kinases)-STAT (signal transducers and activators of transcription) pathways and non-canonical branches such as MAPK (mitogen-activated protein kinase) and PI3K (phosphoinositide 3-kinase)-AKT (protein kinase B)-mTOR (mechanistic target of rapamycin). The intricate interplay between these signaling modules and transcriptional, epigenetic, and post-transcriptional regulators is essential for maintaining immune homeostasis and tailoring context-dependent immune responses. Under physiological conditions, IFNs are essential for host defense, driving antiviral gene expression, activating innate immune cells, and shaping adaptive immune responses, including T and B cells. Conversely, dysregulation of IFN signaling contributes to the development of autoimmune diseases, neuroinflammation, cardiovascular disorders, and cancer. Tumor cells can exploit IFN-induced suppressive molecules to evade immune attack. The currently emerging therapeutic strategies of IFN signaling have evolved into a dual strategy: replacement therapy in immunodeficient states, and pathway inhibition in autoimmune conditions. Additionally, IFN-based combination therapies with immune checkpoint blockade and radiotherapy have demonstrated synergistic potential but require precise control of dosing and timing to avoid immune exhaustion. Advances in single-cell transcriptomics, proteomics, and metabolomics are providing novel insights into IFN heterogeneity, enabling the development of personalized IFN-based treatments. This review highlights the clinical implications and emerging strategies to harness or restrain IFN signaling for therapeutic benefit.

Although surgical lobectomy with systematic mediastinal lymph node evaluation is considered as the “gold standard” for management of early stage non–small cell lung cancer (NSCLC), image‐guided percutaneous thermal ablation has been increasingly used for medically inoperable patients. Radiofrequency ablation (RFA) is a research‐based technique that has the most studies for medically inoperable early‐stage NSCLC. Other thermal ablation techniques used to treat pulmonary tumors include microwave ablation (MWA), cryoablation and laser ablation. MWA has several advantages over RFA including reduced procedural time, reduced heat‐sink effect, large ablation zones, decreased susceptibility to tissue impedance, and simultaneous use of multiple antennae. This review article highlights the most relevant updates of MWA for the treatment of early‐stage NSCLC, including mechanism of action, clinical outcomes, potential complications, the existing technique problems and future directions.

Background Targeting lactate metabolism represents a promising therapeutic strategy to enhance anti-tumor immune responses. In this study, we developed a novel model based on lactate metabolism-related genes (LRGs) to predict survival, characterize the immune microenvironment, and assess immunotherapy response in gastric cancer (GC), with the potential to identify new biomarkers. Methods Data sets of GC patients were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. LRGs were sourced from the MSigDB database. Five key prognostic LRGs (MMP11, MMP12, HBB, VSIG2, and SERPINE1) were identified using univariate COX regression and least absolute shrinkage and selection operator (LASSO) Cox regression analyses. Patients were classified into high-risk and low-risk groups based on a median risk score. We conducted prognostic analysis, gene set enrichment analysis (GSEA), immune microenvironment analysis, immunotherapy responsiveness evaluation, and drug screening in these groups. Results The high-risk group exhibited poorer prognosis compared to the low-risk group, as predicted by our nomogram for overall survival. Notably, the high-risk group, marked by higher stromal cell infiltration and RNA stemness scores (RNAss), showed increased susceptibility to immune evasion. In contrast, the low-risk group demonstrated better responses to immunotherapy and greater sensitivity to chemotherapy. Single-cell analysis revealed that SERPINE1 is predominantly positively correlated with immune checkpoint expression, while VSIG2 exhibits a negative correlation. Conclusions We have developed and validated a novel lactate metabolism-associated model, providing new insights into the prognosis and immunotherapy of GC patients. The five identified LRGs offer potential as prognostic biomarkers and therapeutic targets in GC.

Technetium 99 conjugated with methylene diphosphonate, which is an anti-inflammatory drug, can inhibit macrophage infiltration and downregulate a number of proinflammatory cytokines, such as tumor necrosis factor-α and interleukin-1β. Recently, numerous studies have indicated that it could improve rheumatoid arthritis (RA) activity by upregulating the frequency of peripheral γδ T cells and cluster of differentiation CD4+CD25+Foxp3+ Tregs, affecting the serum cytokine environment, inhibiting osteoclast formation and reducing the concentrations of rheumatoid factor-immunoglobulin M (IgM)/IgG/IgA. As well, it may have a therapeutic role for choroidal neovascularisation (CNV) and Graves' ophthalmopathy (GO). Therefore, it will be a valuable choice in the treatment of RA, CNV and GO.