PTEN (Phosphatase and tensin homolog)

Furthermore, static magnetic fields have been reported to increase apoptosis, inhibit proliferation, and may offer a complementary treatment with low toxicity. These findings suggest that magnetic-field-based approaches offer an innovative strategy for GBM treatment.

TRIM37-triggered post-translational modification of PTEN via ubiquitination may have a vital function in promoting HCC progression. These findings suggest that targeting the TRIM37/PTEN/AKT/GSK-3β/β-Catenin axis may offer a promising therapeutic approach for the management of HCC.

Future integration with multi-omics data, radiomics, and artificial intelligence (AI) promises to enhance its clinical utility. Overcoming current hurdles through standardization and technological innovation is essential for its routine clinical adoption.

These net costs amount to $0.88 per-member-per-month. While introduction of capivasertib could reduce adverse event and follow-up costs, it may result in an overall increase in payers' budget.

A transcriptional signature associated with SARM sensitivity was identified, primarily driven by proliferation-related processes, consistent with a significant decrease in S-phase cell cycle proteins upon treatment in EP0062-sensitive models. In some EP0062-resistant tumors, the combination with palbociclib enhanced the antitumor effect of EP0062, suggesting a potential strategy for metastatic patients with acquired ET resistance.

P2, N=96, Completed, M.D. Anderson Cancer Center | Active, not recruiting --> Completed

Gross examination of the colectomy specimen revealed more than 20 large polyps measuring up to 4 cm. Histopathological analysis demonstrated colonic serrated polyposis without evidence of invasive malignancy, wall infiltration, or lymph node involvement, with clear surgical margins.

Notably, low-dose Capivasertib, an AKT inhibitor targeting tumors with PIK3CA/AKT1/PTEN mutation(s), induced senescence selectively in FUCA2-high LUAD irrespective of PIK3CA/AKT1/PTEN/TP53 mutational status, and its combination with the nutraceutical senolytic procyanidin C1 achieved potent and low-toxicity suppression of LUAD across multiple preclinical models. Together, our results uncover the FUCA2-ErbB3 fucosylation-AKT pathway as a central regulator of senescence and propose a FUCA2-guided drug repurposing strategy for LUAD.

Our data suggest that all mentioned treatments significantly reduce cell migration by downregulating MMP-2 and MMP-9 and decrease clonogenicity by downregulating SOX2 and OCT4 in SK-MEL-3 cells, with these effects being more evident after combination treatment. In conclusion, our findings highlight the potential of PDT pre-treatment to enhance DTIC sensitivity in SK-MEL-3 cells and suggest that the combination therapy is a promising strategy for further research in melanoma treatment.

P1, N=23, Recruiting, Deborah Doroshow | Trial completion date: Dec 2027 --> Jul 2028

By targeting tumor suppressors, miR-21 facilitates epithelial-to-mesenchymal transition (EMT), invasion, and metastasis of HCC cells. Understanding the molecular mechanisms regulated by miR-21 not only sheds light on the pathogenesis of HCC but also highlights potential therapeutic targets for combating this aggressive cancer.

SOX2 promotes HCC progression by negatively regulating FOXJ3, thereby activating the PI3K/AKT signaling pathway and inducing autophagy and mitophagy. The potential SOX2-FOXJ3-PI3K/AKT axis may serve as a novel regulatory pathway underlying HCC development and represents a potential target for therapeutic intervention.