CSF1 (Colony stimulating factor 1)

Our study identified SIRT expression in macrophages of the DLBCL environment and specifically the importance of SIRT1 in the DLBCL M1 macrophage immune microenvironment. This opens an avenue for the potential translational exploitation of SIRT1 modulation as therapeutic target in this hematological malignancy.

In burn-injured mice, brain neuroinflammation and disrupted brain metabolic switch were concomitant with systemic inflammation. Mice exhibited neurobehavioral changes even after burn wounds had healed.

No treatment-related fatalities were observed. This trial is registered with www.chictr.org.cn (ChiCTR2400081835) on 13 March 2024.

P1/2, N=47, Recruiting, Encoded Therapeutics | N=22 --> 47 | Trial completion date: Apr 2031 --> Jan 2033 | Trial primary completion date: Apr 2027 --> Jan 2028

These findings suggest that dysregulated gene expression may contribute to the activation of stromal cells and macrophages within the spleen, facilitating malignant transformation. Overall, these findings deliver novel transcriptomic insights into canine splenic tumorigenesis that may improve diagnostic precision, inform prognostic assessment, and support the development of targeted therapeutic strategies in veterinary oncology.

IFN-gamma emerges as a critical biomarker for prognostic assessment and therapeutic monitoring in advanced GC immunotherapy, and its composite model incorporating PD-L1 Combined Positive Score (CPS) demonstrated superior predictive efficacy, highlighting the necessity for validating additional biomarkers in future clinical studies.

In external transcriptomic validation (TCGA-CRC), GSEA indicated enrichment of interferon/inflammatory programs in TIGIT-high tumors, while CD155-high tumors preferentially showed proliferation-related MYC/E2F/G2M signatures. Together, these findings support tumor-wide upregulation of the TIGIT/CD155 axis in CRC and suggest that TIGIT, more than CD155, tracks with MSI/BRAF-associated immune activation, providing a rationale for patient stratification in checkpoint-directed immunotherapy.

The findings reveal that the infiltration of CD163+ macrophages in meningioma may be mediated by the IL-17/CSF1 axis through SMARCB1 regulation.

Macrophages from Il1α⁻/⁻ tumors exhibited activated immune gene signatures similar to human macrophages. These findings reveal that IL-1α drives an immunosuppressive TME partly through PGE2 signaling, highlighting IL-1α as a potential therapeutic target in breast cancer.

A higher CD103+ Tfh to IGFL2high Tfh ratio, together with the selective clonal expansion of the CD103+ subset, was strongly associated with improved tumour immunity and superior responses to anti-PD-1 checkpoint blockade, surpassing the predictive value of exhausted CD8 T cells. These findings integrate Tfh and CD4 with cytotoxic potential in breast cancer, offering new insight into anti-tumor immunity and response to checkpoint blockade.

This study underscores the dual role of CSF1 in regulating both tumor survival and M2 macrophage activation in HNSCC. Targeting the DKK1/CSF1 axis may represent a promising strategy to overcome chemoresistance by disrupting tumor-macrophage crosstalk and reprogramming the immunosuppressive microenvironment.

Paclitaxel-induced translational upregulation of NOTCH2 enables immediate juxtacrine activation by JAG1-positive macrophages, coupling tumor cell survival with immune remodeling in the tumor microenvironment to drive chemoresistance. Our results suggest NOTCH2 is a viable biomarker for paclitaxel resistance and that combining NOTCH2 inhibitor with taxane is an effective therapeutic strategy to selectively disrupt tumor-macrophage interaction and overcome macrophage-mediated taxane resistance in NOTCH2-positive tumors.