EPHA7 (EPH Receptor A7)

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.

Altogether, these findings were insufficient to establish a diagnosis of pcGDTCL. We review the clinical, histopathologic, and molecular sequencing data pertaining to our rare patient as well as the recent literature on indolent CD30+LPD with gamma-delta T-cells.

Using a tree-based classification algorithm, we also predicted ADAM28 as a possible mechanistic marker. The results of this study have potential implications for patients who have been diagnosed with B-ALL by providing improved mechanistic understanding and information on possible diagnostics and repurposed therapeutics for B-ALL.

ARN509 and finasteride also showed pro-apoptotic effect in patient-derived AML cells and in a humanized AML model in NSG mice. These data support a drug repurpose effort to use anti-androgen therapy to improve the efficacy of AML treatments.

MiR-3613-3p negatively regulated EphA7 expression levels, and overexpressing miR-3613-3p reversed the reduction of the apoptosis rate and increase of cell proliferation caused by overexpression of EphA7. In this research, we identified that high expression levels of miR-3613-3p were associated with a better prognosis and EphA7 was negatively regulated by miR-3613-3p to inhibit the development of glioma.

In vivo, chidamide treatment reduced EPHA7 protein expression by regulating METTL3, leading to inhibited tumor growth. Collectively, these findings identified the METTL3/EPHA7 axis as a key mediator of chidamide's anti-tumor effects, suggesting chidamide's potential as a novel therapeutic strategy for NSCLC.

We show that in hRMS ephrin-A5 binds and signals to EphA8 and EphA7 binds and signals to ephrin-A2, and that Fc chimeras of both molecules are potent inhibitors of hRMS proliferation. These results identify key differences between hRMS and normal muscle cells and support further research into Eph: ephrin signaling as potential differentiation therapies.

This is the first report of CAPNON progression to glioblastoma and of molecularly characterized glioma occurring decades after head trauma. A multifactorial etiology including genetic predisposition and posttraumatic repair is hypothesized. The discussion presents possible roles of EPH RTKs in posttraumatic repair and CAPNON, and of POT1 and PDGFRα in subsequent progression to glioblastoma. https://thejns.org/doi/10.3171/CASE25152.

This study clarifies the specific role of tRFAla-AGC-3-M8 in AD pathology and offers a promising target for therapeutic interventions.

Sema7A is involved in glial scar formation and may influence serotonin channel remodeling, thereby affecting motor coordination. Given these findings, the local or systemic application of neuronal guidance proteins represents a promising avenue for spinal cord injury treatment.

Furthermore, our findings highlight the clinical potential of targeted drug inhibitors, including vandetanib, dabrafenib, and selumetinib, for improving treatment outcomes. Future efforts should focus on including underrepresented populations, developing population-specific prevention strategies, and fostering global collaboration to ensure equitable access to pharmacogenomic testing and innovative therapies. These initiatives have the potential to transform thyroid cancer care and align with the broader goals of personalized medicine.

In addition, EphA7 demethylation reduced the half-maximal inhibitory concentration (IC50) of cisplatin and paclitaxel. Pooled analysis revealed that EphA7 promoter hypermethylation was positively correlated with tumor purity but negatively correlated with immune cell infiltration, cytotoxic T lymphocyte (CTL) and immune checkpoint (IC) activity, and the expression of EphA7 was significantly positively correlated with tumor mutational burden (TMB), microsatellite instability (MSI) and the presence of single nucleotide variant (SNV) neoantigens, suggesting a better prognosis for patients with EphA7 promoter hypomethylation and high expression. Collectively, these findings indicate that targeted demethylation of the EphA7 promoter and restoration of endogenous EphA7 expression by dCas9-Tet1 are promising therapeutic approaches and are favorable for the prognosis of CC patients.