Unfortunately, the preliminary bioactivity test showed low activity and selectivity toward breast cancer cell lines. Structural optimization or a more appropriate selection of the bioactive group to be conjugated would be required.

Translational studies in human NSCLC-derived PC9 cells further demonstrated that SAHA enhances osimertinib antitumor efficacy while alleviating cardiotoxicity. Collectively, these findings define HDAC-dependent epigenetic repression as a key mechanism underlying osimertinib-induced cardiotoxicity and identify HDAC inhibition as a therapeutically actionable strategy to improve both cardiac safety and cancer treatment efficacy.

P2, N=120, Not yet recruiting, BeBetter Med Inc

The patient achieved complete remission (CR) after 6 cycles of chidamide plus CHOP chemotherapy, with no evidence of recurrence at 6 months. This case broadens the recognized cutaneous spectrum of AITL and underscores the importance of considering lymphoma in the differential diagnosis of unexplained subcutaneous nodules.

Treatment of human sarcoma lines with decitabine and entinostat induced similar gene expression changes, including shared antigen targets, and increased MHC I expression. These findings demonstrate that epigenetically upregulated antigens can serve as effective tumor-specific targets and broaden immunotherapy strategies for low-mutation sarcomas.

In a recent clinical study, the combination of an orally administered histone deacetylase (HDAC) inhibitor, nanatinostat (NSTAT) with valganciclovir (GCV), showed promise as a lytic induction therapy for EBV-positive lymphoma. In addition, NSTAT treatment also promoted global histone acetylation and suppressed c-MYC and BCL2 expression, leading to cell cycle arrest and cell death in the EBVaGC tumor cells. Importantly, this study demonstrated the potent antitumor efficacy and safety of combined NSTAT and GCV treatment in both in vitro and in vivo preclinical EBVaGC models.

Cumulatively, these therapies illustrate both the progress and the ongoing challenges of biomarker-driven treatment in NHL, including resistance mechanisms, toxicity management, optimal therapeutic sequencing, and variability in evidence maturity across targeted strategies. While pirtobrutinib and brentuximab vedotin are supported by increasingly robust clinical evidence in selected lymphoma subtypes, the role of belinostat remains constrained by modest response rates and limited randomized data, underscoring the continued need for biomarker refinement and more precisely individualized therapeutic approaches in NHL precision medicine.

The clinical use of the anticancer drug doxorubicin (Dox) is limited by irreversible cardiotoxicity...Therefore, we comparatively investigated the response of murine embryonic stem cells (mESC), endothelial progenitor cells (EC d4) and terminally differentiated endothelial-like cells (EC d6) following exposure to Dox and selected pharmacological inhibitors of DNA repair/DNA damage response (DDR) (RAD51i B02; HDACi entinostat (EST))...Notably, drug treatment of EPC (EC d4) causes multiple dysfunctions in differentiated EC d6. Hence, pharmacological measures aiming to specifically protect EPC from Dox-induced damage are suggested to foster the maintenance of healthy endothelial functionality during regeneration, thereby lowering the risk of detrimental late cardiotoxicity resulting from Dox-based anticancer regimen.

This pan-cancer analysis establishes APOC1 as a context-dependent biomarker and a TAM-derived modulator of adaptive immune resistance, with prognostic and therapeutic implications across malignancies. APOC1-expressing TAMs represent a potential target for combination immunotherapy strategies.

Entinostat-BPD achieved tumor-specific HDAC inhibition while displaying potent efficacy and reduced systemic toxicity. These findings reveal an HDAC-dependent DDR vulnerability and offer combinational and precision targeting strategies to facilitate clinical translation and improve PDAC patient outcomes.

Notably, SHN7 exerted strong in vivo anti-tumor effects relative to napabucasin and SAHA, with minimal toxic effects. Therefore, SHN7 may be a promising NQO1/STAT3/HDAC triple-target agent that can decrease the resistance of TNBC to HDAC inhibitors and can be developed as a candidate anti-TNBC drug.

Patients with high RCDI exhibited higher sensitivity to several targeted therapies, including Vorinostat and Trametinib. The RCDI model effectively stratifies HCC patients based on RCD-related molecular features, providing a valuable tool for predicting survival and therapeutic responses. The identification of key genes offers new insights into the molecular mechanisms of HCC and potential therapeutic targets.