MIF (Macrophage Migration Inhibitory Factor)

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.

Notably, TLR1 may serve as a drug target, with compounds such as Doxorubicin and Etoposide identified as potential candidates. In conclusion, ADCY3, CASP8, GRHL1, HELQ, and TLR1, as genetic susceptibility genes for breast cancer, hold significant value in understanding tumor development and advancing therapy.

While TNF-α and HGF/IL-12p40 showed promise, most inflammatory biomarkers demonstrated limited accuracy, specifically for outcome prediction in CD; however, this does not preclude their potential usefulness for other clinical or experimental applications. Current evidence does not support the clinical use of this approach and further studies are needed.

These initial observations point to a possible association between gut microbiota imbalance and the inflammatory aspects of endometriosis-associated infertility. Consequently, microbial modulation merits further investigation as a potential strategy to alleviate inflammation and potentially enhance reproductive outcomes.

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.

This indicates that the multistep molecular process of M-MDSC induction from PBMCs by the co-presence of HDBCLs begins with a transient early hyper-inflammatory phase and transitions into a post-inflammatory immunosuppressive phase. Our study demonstrates that treatments that target specific molecular phases regulated by cytokines could reduce M-MDSC induction and improve the effectiveness of immune cell therapy.

Collectively, the present study demonstrates for first time a WISP1/Src/MIF axis as well as its ability to induce an invasive phenotype in MCF7 cells and highlights novel cellular and molecular processes involved in the epithelial-to-mesenchymal transition and the development of invasive breast cancer. This suggests that specific cues from the tumor microenvironment can activate a migratory/invasive phenotype in a subpopulation of cells residing within the heterogeneous breast tumor.

This review synthesizes emerging evidence that CD74 functions as a "master regulator" of antigen presentation in cancer, integrating its canonical chaperone role with its noncanonical role in transcription regulation and in signaling via macrophage migration inhibitory factor. We explore how tumor microenvironmental contexts redefine CD74 biology, influencing antitumor immunity and therapeutic outcomes.

MIF also engages the mechanistic target of rapamycin complex 1 (mTORC1)/activating transcription factor 4 (ATF4) module to reprogram metabolic processes...The review critically assesses current small-molecule classes targeting the catalytic pocket or trimer/interface to identify design principles for next-generation, receptor-focused modulators suitable for combination therapy. Finally, it proposes an imaging- and flux-based translational approach to select patients, confirm on-target action, and rationally pair MIF-axis blockade with metabolic or immunotherapeutic strategies-aiming to transform correlative data into mechanism-based clinical trials.

Validation in patient samples revealed elevated hepatic MIF and CD44 expression in MASLD-associated PDAC liver metastases. This study highlights the MIF-CD44 axis as a promising therapeutic target and underscores the importance of tailoring treatments for PDAC patients with concurrent MASLD.

In the current review, we summarize recent findings about the oncovirus activation of MIF signaling pathways, their functional roles in viral oncogenesis, and the development of MIF-targeted therapies. We also discuss future directions in this interesting field.

More importantly, ligand macrophage migration inhibitory factor (MIF) and receptor CD44 were predicted as a central signaling axis within HNSCC tumor microenvironment, suggesting their potentials as therapeutic targets . CELLetter is freely available at https://github.com/plhhnu/CELLetter.