EFNB2 (Ephrin B2)

In conclusion, our results highlight that a subset of EPHs and EFNs may be associated with worse clinical outcomes (EPHA4, EPHA5, EPHA7, EPHA8, EPHB2, EFNA2, and EFNB2), and an aggressive histological subtype (EPHA2, EPHA4, EPHA8, EPHB4, EFNA1, EFNA3, EFNA4, and EFNB2). The potential correlation of these genes with clinicopathological parameters of UVM need to be evaluated and validated with bioinformatic and experimental approaches in well-characterized cohorts of UVM patients.

Knockdown of CD109 and EFNB2 significantly suppressed CCA cell proliferation, migration and invasion while it promoted disulfidptosis under glucose deprivation. The present study established an association between DRGs and CCA prognosis/immune dynamics, provided a robust four‑gene prognostic signature, and identified CD109 and EFNB2 as potential therapeutic targets, positioning disulfidptosis as a promising focus for precision medicine in CCA.

These results were further validated in vivo using cell‑derived xenograft models, which confirmed the key role of Wnt/β‑catenin pathway activation in EFNB2‑induced tumor progression. Collectively, these results suggested that EFNB2 represents a promising molecular target for therapeutic intervention in GC.

Critically, tumor suppressor SH3BP1 (a key regulator) correlates with reduced tumor progression and enhanced CD8+ T cell anti-tumor immunity when highly expressed. These findings underscore that SH3BP1 may represent a promising therapeutic target for precise intervention in GMS-immune interactions in GC.

In cervical DRG of patients with acute or chronic pain (N = 12), scRNA-seq data from neuronal or non-neuronal cells were enriched for chronic pain-associated genes (e.g., EFNB2, GABBR1, NCAM1, SCN11A). This cell-type-specific genetic architecture of chronic pain across central and peripheral nervous system circuits provides a foundation for targeted translational research.

The advantage of AP8901 is that it is expected to prevent T cell exhaustion and maintain its anti-tumor effect. This phase 1 study of AP8901 will provide new evidence for the application of this novel CAR-T cell therapy in patients with solid tumors, including Ewing sarcoma.

In cervical DRG of patients with acute or chronic pain ( N = 12), scRNA-seq data from neuronal or non-neuronal cells were enriched for chronic pain-associated genes (e.g., EFNB2 , GABBR1 , NCAM1 , SCN11A ). This cell-type-specific genetic architecture of chronic pain across central and peripheral nervous system circuits provides a foundation for targeted translational research.

Expression of Trop-2 and ephrin B2 may demonstrate therapeutic possibilities for patients with SH/DD, who usually have limited treatment options, particularly in small cell carcinoma, in which few targets have been identified. Clinical trials to investigate the efficacy of these novel treatments are warranted.

Conclusion. These results demonstrated a hierarchical network of gut injury mechanisms differentially regulated in the course of the emergence of 5-FU-induced mucositis.

ST from LSCC showed that spots with high-risk scores were colocalized with TGF-β and the proliferating malignant cells, additionally, the risk scores have a negative correlation with TCR signaling but positive association with LAG3 transcription. The CDRscore model could be utilized as a powerful prognostic indicator for HNC.

Our study suggests that DHA treatment affects the functions of DU145 and PC-3 cells by regulating the expression of NR2F2 and its potential target genes, and NR2F2 may serve as a potential therapeutic target for prostate cancer.

Overall, we aim to uncover the mechanism in TAMs induced CRD which promotes liver metastasis of GC and provide novel ideas for therapeutic strategies.