VOPP1 (VOPP1 WW Domain Binding Protein)

Additionally, the IME subtype exhibited higher immune checkpoint activity and a higher frequency of DYNC2H1 mutation, with patients benefiting from immunotherapy. These findings provide critical insights into LUAD treatment optimization.

VOPP1 reduced ovarian tumor cell migration and PTX resistance via regulation of NOTCH and WNT mediated EMT process. Therefore, it can be suggested as a novel therapeutic target in OC patients following further animal studies and clinical trials.

This study identifies VOPP1 as a novel gene associated with rheumatoid arthritis susceptibility. VOPP1 may contribute to disease progression by elevating X-23,587 metabolite levels and activating the p38 MAPK signaling pathway.

The failure of phase III clinical trials on the NEDD8-activating enzyme (NAE) inhibitor, MLN4924, has increased the demand for sensitive biomarkers for efficient patient selection...Our data suggest that the VOPP1-E2F1-CDT1 axis regulates the NAE inhibitor sensitivity of NSCLC cells. Furthermore, our findings provide important insights for further evaluation of VOPP1 as a potential NAE inhibitor sensitivity biomarker in clinical settings.

Furthermore, we provide histological and epigenetic findings and clinical outcome. The case expands the known molecular spectrum of oncogenic drivers in glioneuronal tumors and provides a link to potentially prognostic and therapeutically relevant alterations.

Plumbagin exhibits an inhibitory effect on the growth of the PDX model of TSCC. Moreover, plumbagin enhances the inhibitory effects of cisplatin.

To investigate the mechanisms of acquired resistance to BET inhibitor (BETi)s, we generated a series of drug resistant sublines by exposing non-small cell lung cancer (NSCLC) NCI-H1975 cells to the BETi ABBV-075...Through combined treatments with BETis and BCL-2 inhibitors (BCL-2is), we demonstrated that BCL-2is synergistically sensitized the resistant cells to BETis. Implications: Based on these results, for the first time, we establish a causal link from VOPP1 loss to BCL-2 gain and then to BETi resistance, which provides new insights into BETi resistance and paves the way for further testing to circumvent BETi resistance.