CD96 (CD96 Molecule)

These effects are observed with CAR-T cells targeting CD25 or CD96 as AML-associated targets. Our results indicate that CXCR4 strengthens CAR-T cell memory and durability, offering a strategy to improve immunotherapy outcomes in AML and beyond.

Incorporating these markers in combination with established aberrant markers can enhance the identification of LSCs and help distinguish them from HSCs in both CD34 + and CD34- AML. Our findings support the use of an expanded combinatorial marker panel and warrants its further evaluation in a larger AML cohort, particularly in the context of measurable residual disease (MRD) assessment, prognostication and correlation with treatment response and survival outcomes.

Importantly, CD96-CAR T cells did not inhibit colony formation by HSPCs during manufacturing. These findings indicate that CD96 is a promising target for AML immunotherapy, and the combination of CD96-CAR and CD33-CCR may represent a potent strategy for patients with CD96-positive AML while preserving normal hematopoiesis.

Our findings suggest that TIGIT and CD96 could be markers of the clinical stage and treatment response of HNSCC. Therefore, administering anti-TIGIT and anti-CD96 after radiotherapy may provide a novel approach for incorporating immunoradiotherapy into HNSCC treatment.

Collectively, our data provide novel molecular insights into the immunoregulatory role of CD155 and establish epitope-specific mAbs as valuable tools for studying immune checkpoint pathways. This study provides a framework for developing CD155-targeted immunotherapies and enhances the understanding of immune escape mechanisms in cancers.

Recent therapeutic advances, particularly Nectin-4-targeted ADCs, anti-TIGIT ICIs, and bispecific antibodies (BsAbs), underscore their clinical promise. This review integrates current understanding of Nectin family members in oncogenesis and immunoregulation, focusing on their biological functions, mechanisms of immune modulation, therapeutic strategies, and remaining challenges in clinical translation.

The PVR-TIGIT/CD96/CD226 axis is a critical immune checkpoint in glioma. Targeted disruption of this pathway offers a promising strategy to overcome resistance and improve clinical outcomes.

Notably, Sig27IMG stratified patients with a poor prognosis risk in these 17 cancer types. In summary, Sig27 and its derivative panel, Sig27IMG, offer a robust assessment of PC recurrence, highlighting immunosuppressive features mediated by TAMs, dendritic cells, and endothelial cells across multiple cancer types.

The CD155-CD226/TIGIT/CD96 immune checkpoint complex expressed on both TME TC and TILs, and interacted with TILs to exhibit diverse prognosis effect on BC. The immunotherapy against these checkpoint proteins should check the expression on both TC and TILs and further studies should explore the molecule complex collectively for comprehensive prediction of BC prognosis.

However, a specific combination of tumoral cells expression of CD226(≥4%), CD155(≥40%), and CD96(≥35%), coupled with TIGIT expression on tumoral (<35%) and stromal cells (<12.5%), was able to identify patients with G1 response to NAC.ConclusionExpression levels of TIGIT/CD155/CD226/CD96 on tumoral and stromal cells might collectively serve as predictive biomarkers for NAC response in TNBC. This implied that CD155-TIGIT axis could be prospectively applied clinically to identify NAC-resistant TNBC patients.

This study established a novel prognostic tool for BC by combining TME markers with clinicopathological factors. The developed nomograms enabled accurate individualized risk stratification and demonstrated clinical utility, offering a framework for precision oncology to survival prediction.

This study elucidates the synergistic mechanisms and identifies key resistance pathways underlying chemo-immunotherapy combinations in patients with ESCC, providing a scientific basis for refining future combination therapeutic regimens.