LGALS9 (Galectin 9)

We defined a novel ISG signature in iCCA and identified EGR1 as a critical driver of senescent tumor cells in iCCA.These findings offer new insights into senescent tumor cells and the immunosuppressive microenvironment.

CSF TIM-3 and galectin-9 represented additional diagnostic biomarkers for PCNSL alongside B-cell-associated factors.

Ferroptosis downregulated the transcription of CD155 and galectin-9 in glioma cells, but inhibition of extracellular acetyl-HMGB1 reversed the effect of ferroptosis on the downregulation of galectin-9 transcription. In conclusion, ferroptosis downregulates galectin-9 transcription via extracellular acetyl-HMGB1, thereby inhibiting the biological behavior of glioma cells.

Upon R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) treatment, mesoderm-originating ENI (ENI-mesoderm) was significantly associated with inferior progression-free survival and overall survival, as compared to ectoderm-originating ENI (ENI-ectoderm) and endoderm-originating ENI (ENI-endoderm). Regarding immune checkpoints, ENI-ectoderm, ENI-endoderm, and ENI-mesoderm exhibited significant upregulation of LGALS9, PD-L1, and B7-H3, respectively. Our findings thus contributed to a better understanding of crosstalk between lymphoma progression and embryonic development, providing new insights into targeted approaches against germ layer-dependent invasion in cancer treatment.

The machine learning model established based on multimodal MRI parameters can potentially facilitating personalized therapeutic stratification predict the expression of Galectin-9 in rectal cancer.

Galectin-9 and SHH are lowly and highly expressed, respectively, in CRC. Their expression levels are associated with tumor differentiation, invasion, and metastasis, and hold predictive value for the risk and prognosis of CRC patients.

Meanwhile, MTT diminished the interactions between DCs and Tregs through LGALS9-CD45 axis, leading to a reduction in peripheral Tregs. These findings reveal the mechanism by which MTT promotes antitumor immunity in patients with HCC and warrant further investigation in large-scale clinical studies.

Collectively, our findings establish TSPAN6 as a migrasome-related regulator driving adverse immunotherapy outcomes and responses. Targeting TSPAN6, potentially with mitoxantrone, presents a potential strategy to enhance immunotherapy efficacy.

LAG3 expression is an independent prognostic biomarker of mCRC. The distinct Galectin-9-TIM-3 signaling in LAG3⁺CD8⁺ T cells may contribute to limited therapeutic efficacy of LAG3 blockade, suggesting potential combinational immunotherapy strategies.

Concurrently, IL30 suppresses T cell function by reducing CD25 and HLA-DR expression on CD4⁺ and CD8⁺ T cells, inhibiting their activation and proliferation, decreasing TNF-α and IFN-γ production, and boosting LAG-3 expression, which strongly correlates with IL30 levels in clinical samples. Collectively, these findings identify IL30 as a critical driver of melanoma dissemination and T cell exhaustion, providing a mechanistic link to immune resistance and failure of combination immunotherapies.

This in silico immune network highlights checkpoint centered hubs and coordinated immune programs with prognostic relevance in endometrial cancer, providing a rationale for biomarker guided immunotherapy development and patient stratification. Validation in independent cohorts and correlation with clinicopathologic and treatment response data are needed to support clinical translation.

The potential for using these findings in real-world clinical settings is backed by models showing that combining A2AR expression with adenosine pathway activity and immune profiling greatly improves the accuracy of risk assessment compared to standard prognostic markers, while earlier studies show that targeting this pathway could be a viable treatment option. These results collectively position A2AR as a master regulator of prostate cancer immunosuppression and a promising biomarker-guided therapeutic target, particularly for combination immunotherapy approaches in advanced disease settings where current treatment options remain limited.