CD93 (CD93 Molecule)

Moreover, we identified the GALNT10 inhibitor Luteolin, which effectively suppresses ovarian cancer metastasis, modulates the immunosuppressive tumor microenvironment through tumor vascular-immune crosstalk, and exhibits synergistic effects with anti-PD1 therapy. Collectively, our findings indicate that GALNT10 facilitates ovarian cancer metastasis through the induction of tumor cell EMT and tumor vascular dysfunction, suggesting that GALNT10 inhibitors represent a promising avenue for the development of novel therapeutic strategies in ovarian cancer.

More importantly, CBP-D8 peptide combined with radiotherapy significantly abrogated tumor growth and elicited systemic antitumor immune response. Our study identified a novel peptide blocking CD93/IGFBP7 interaction to normalize tumor vascular function, as well as revealed an approach to promote a favorable tumor microenvironment for the therapeutic intervention.

At markedly reduced intravenous doses, IGFBP7-sEVs efficiently concentrated temozolomide (TMZ) within glioma and elicited pronounced tumor growth inhibition...Our data suggest that IGFBP7-modified sEVs represent a novel platform that enables highly efficient, glioma VECs-targeted delivery of therapeutics into glioma, and are adaptable to a broad spectrum of agents, especially immunomodulators. It is a novel and effective strategy for treating gliomas.

Vector optimization retained the efficacy of DC-based therapy, achieving curative responses in pancreatic tumor models. These findings support the clinical development of this 2nd Gen DC immunotherapy for pancreatic and potentially other tumors.

Our study highlights the predictive significance of efferocytosis in assessing chemotherapy sensitivity, emphasizing the pivotal role of the immune microenvironment in mediating drug resistance. Moreover, we identified potential targets for immunotherapeutic strategies in the treatment of TNBC.

Targeting the CD93 signaling pathway has the potential to improve tumor vascular function and enhance the efficacy of immunotherapy, making it a promising therapeutic target. This review summarizes the current understanding of CD93's structure, function, and disease mechanisms, providing a framework for further research and clinical translation in related fields.

Our study establishes CD93 as a key NETs-related biomarker in AK, mechanistically linking neutrophil-driven inflammation to angiogenesis. The CD93-Gö6976 interaction provides a translational basis for developing novel targeted therapies against AK.

Our findings support previous studies which confirm that MCC is unlikely to be derived from Merkel cells and instead from multiple or divergent cell types, including those of B-cell lineage. Our work highlights the need for a more personalized approach to diagnosis/characterization and treatment of MCCs, given the documented variability of novel potentially targetable pathways.

Critically, anti-CD93 mAb treatment prolongs survival in RIP1-Tag2 mice with late-stage, sunitinib-resistant PanNETs. Our results support CD93 blockade as a promising therapeutic approach for advanced PanNETs.

In vivo, treated humanized mice showed increased CD4+, CD8+, and NK cell frequencies in peripheral blood and within tumors, correlating with reduced tumor burden. Our data shows that the antigen-pulsed, engineered DCs have the potency to activate immune cells, which leads to a significant reduction in pancreatic tumors and therefore could potentially provide an effective therapeutic opportunity for the treatment of pancreatic cancer and other solid tumors.

Finasteride significantly enhanced doxorubicin efficacy ex vivo and in vivo by reprogramming the TME, reducing M2 macrophage infiltration while promoting an M1 phenotype. Our findings establish ZBTB20 as a key regulator of macrophage polarization in TNBC and introduce finasteride as a clinically viable agent to reverse TME immunosuppression. Targeting macrophage polarization via ZBTB20 modulation, particularly by repurposing finasteride, offers a promising therapeutic strategy for TNBC with immediate translational potential.