CD74 (CD74 Molecule)

Exemplified by CHEK1, these findings establish MIGs as dual therapeutic targets capable of simultaneously disrupting tumor-intrinsic fitness and remodeling the immunosuppressive niche. This work proposes a novel paradigm for selectively targeting MIGs to eliminate aggressive tumor subclones while minimizing toxicity to normal cells.

Immunohistochemistry demonstrated higher CD74 and C1QB expression in jaw osteosarcoma compared to long bone osteosarcoma in both rats and humans (P < 0.05). The expression levels of CD74 and C1QB were significantly higher in jaw osteosarcoma than in long bone osteosarcoma, suggesting that this differential expression may have clinical relevance for patient survival and warrants further investigation.

This study highlights subtype-specific epithelial signatures, identifies key signaling pathways (e.g., MIF), and pinpoints candidate therapeutic targets (CD44, CD74). These discoveries shed new light on the distinct pathogenic mechanisms of LUSC and LUAD and provide actionable insights to facilitate the clinical translation of subtype-specific personalized immunotherapies.

Differential gene expression confirmed elevated levels of MIF, CD74, CD44, and SPP1 in tumor tissues, while pathway enrichment analyses highlighted cytokine signaling, antigen presentation, and chemokine-regulated immune modulation as key biological processes. Collectively, our study provides a high-resolution map of CRC intercellular communication and identifies MIF-CD74-associated signaling as a central immunoregulatory hub with potential relevance for therapeutic targeting and biomarker development.

In this study, we successfully constructed NGR peptide-modified Exos derived from CAFs for the targeted delivery of Res. This work innovatively proposes a novel immunotherapeutic strategy that targets tumor-associated MDSCs rather than directly killing tumor cells. Mechanistically, we identify and validate CXCR2 as a previously unrecognized functional target of resveratrol in MDSCs, through which resveratrol suppresses NF-κB signaling and reprograms MDSC function. Collectively, NGR-Exos@Res represents a precise and efficient delivery platform capable of reversing the immunosuppressive microenvironment in LC and provides a promising combinatorial strategy to overcome immunotherapy resistance by targeting immunosuppressive myeloid cells.

Our findings highlight the potential of another M-GB-ADC as a targeted therapy for overcoming rituximab resistance and treatment failure in DLBCL. This strategy enhances therapeutic efficacy and represents a preclinical proof-of-concept treatment option by directing a cathepsin-inhibitor payload specifically to malignant B cells.

GNAL regulates the spatiotemporal immune remodeling of ER+ breast cancer via calcium signaling and stem-like cell differentiation. The multi-omics risk model offers clinical prognostic value and highlights GNAL as a potential target for precision immunotherapy.

Our findings elucidate the functional alterations of CCT and precursor cells within the context of HCC. The novel prognostic framework provides actionable insights for stratifying patients likely to benefit from combinatorial immunotherapy and chemotherapy.

This analysis has identified and characterized the proliferation-related B cells in DLBCL, which may provide some ideas for the treatment strategies in immune-oncology and cellular therapies.

Our multifaceted approach identified key tumor-immune interactions in medulloblastoma. Among these, MIF-CD74 was validated as a targetable interaction, demonstrating the utility of our integrative approach for identifying novel therapeutic targets across multiple tumor types.

These findings highlight the therapeutic potential of targeting the MIF-CD74 pathway and underscore the importance of integrating immunomodulatory strategies for the treatment of glioma. Mutant IDH1 gliomas exhibit fewer Mo-TAMs and increased Mg-TAMsMutant IDH1 gliomas have less MIF expression via epigenetic reprogramming.Mesenchymal wtIDH1 glioma cells are main source of MIF.MIF inhibition plus immune stimulatory gene therapy extends survival wtIDH1 glioma.

P=N/A, N=20, Not yet recruiting, The First Affiliated Hospital of Soochow University; The First Affiliated Hospital of Soochow University