Farydak (panobinostat)

Samples with low stemness and elevated pyroptosis showed enhanced inferred drug resistance, particularly to LBH589...CONCLUSION‌: This study highlights the molecular heterogeneity of gastric cancer, demonstrating how distinct cell death patterns and PTM features shape prognosis and drug sensitivity. The identified biomarkers and resistance profiles may provide valuable guidance for personalized therapeutic strategies.

Our study demonstrates that LBH589 not only directly induces apoptosis, inhibits proliferation, migration, and invasion, but also enhances the anti-tumor immune response through improving tumor immunogenicity. These findings not only broaden the mechanistic understanding of HDACi in TNBC, but also provide a theoretical basis for combining epigenetic therapy with immunotherapy, supporting LBH589 as a potential immunotherapy sensitizer for triple-negative breast cancer.

Decreased expression of stemness-related genes upon KDMi treatment in FaDu cells was associated with decreased binding of KDM4A and/or KDM6B at SOX2 and POU5F1 gene promoters. The suppression of stemness-associated phenotype, and the concurrent promotion of apoptosis by the studied combinations of chemicals, suggest their potential as a novel therapeutic strategy in HNSCC.

We therefore characterized the impact of pan-HDAC inhibitor, panobinostat, and class I HDAC inhibitor, nanatinostat, on the growth, survival, and lytic reactivation of four EBV-positive cell lines: P3HR1-ZHT BL, Jijoye BL, IBL-1 immunoblastic lymphoma, and de novo infection derived lymphoblastoid cell lines (LCL). Functional validation through a Cas9-RNP approach revealed that the CD137 receptor is indeed involved in preventing successful lytic reactivation. These data have important implications for how we approach oncolytic therapies for EBV-associated malignancies.

Ve combined with Pa exerts a synergistic inhibitory effect on the growth and metastasis of FRO and ARO cells, while promoting apoptosis and cellular redifferentiation. This combination may provide a potential therapeutic strategy for ATC.

Importantly, combined treatment with panobinostat and the anti-angiogenic agent anlotinib resulted in superior inhibition of tumor growth and vascularization compared with either monotherapy in patient-derived organoid xenograft models. Together, these findings uncover an enzymatic activity-independent RNA regulatory function of NQO1 in ESCC and provide a mechanistic rationale for targeting the NQO1/AGRN axis.

These findings reveal a novel cytoplasmic function of WEE1 in sustaining MYC stability and chemoresistance. Targeting WEE1 destabilizes MYC and enhances therapeutic response, supporting the combination of MK-1775 and Panobinostat as a promising treatment strategy for EAC.

In search of the molecular mechanism underlying a potentially intrinsic panobinostat resistance, we identified up-regulation of the HDAC8-transforming growth factor-β (TGFβ)-epithelial-to-mesenchymal transition (EMT) axis in the TO model, whereas subsequent HDAC8 depletion increased the sensitivity to panobinostat. These data highlight the utility of personalized drug screenings on TOs to identify suitable drug targets and inhibitors for more effective treatment of clinically aggressive meningiomas and to help advance our understanding of counteracting resistance mechanisms.

Our study identified IL3RA as novel biomarker and therapeutic target for ER+ breast cancer. Further validation and mechanistic studies are warranted to advance precision oncology strategies for ER+ breast cancer management.

P1/2, N=49, Active, not recruiting, Erasmus Medical Center | Recruiting --> Active, not recruiting

Viability, cytotoxicity, and caspase-3/7 activity were assessed following single-agent treatment with asciminib, ponatinib, bortezomib, or panobinostat. Co-inhibition of proteasomes and histone deacetylases eliminates TKI-refractory BCR::ABL1-driven leukaemia cells by inducing mitochondrial apoptosis and loss of clonogenic potential. These findings indicate a clinically actionable, TKI-independent strategy for the salvage treatment of multidrug-resistant CML.

Furthermore, panobinostat downregulated a network of oncogenes and cell cycle regulators, including c-Myc and key cyclins. These findings indicate that panobinostat can enhance 5-FU cytotoxicity by targeting TS expression and reprogramming oncogenic transcriptional networks, supporting its potential as a complementary strategy for overcoming fluoropyrimidine resistance in GC therapy.