P=N/A, N=30, Not yet recruiting, Sun Yat-sen University

P2, N=118, Completed, Chipscreen Biosciences, Ltd. | Active, not recruiting --> Completed

P2, N=30, Active, not recruiting, Sun Yat-sen University

P1, N=20, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Apr 2026 --> Apr 2027

P1, N=24, Recruiting, University of Nebraska | Trial completion date: Mar 2027 --> Jul 2029 | Trial primary completion date: Mar 2026 --> Jul 2027

This trial adopted a Simon two-stage design: eligible patients received tucidinostat plus metronomic capecitabine together with either an aromatase inhibitor (Cohort 1) or fulvestrant (Cohort 2), selected according to prior ET. In addition, exploratory analyses of biomarkers indicated that the baseline TP53 mutation status (Wild type vs. mutated, 7.64 months vs. 3.55 months) and circulating tumor cell (CTC) status (CTC-negative vs. CTC-positive, 7.59 months vs. 3.78 months) were associated with the median PFS. Our study demonstrated that tucidinostat combined with mCAP and ET is efficacious and well-tolerated in patients with HR-positive HER2-negative ABC previously treated with CDK4/6i.

P1, N=30, Recruiting, New York Medical College | Trial completion date: Dec 2024 --> Dec 2027 | Trial primary completion date: Dec 2023 --> Dec 2026

P=N/A, N=7, Completed, Prisma Health-Upstate | Active, not recruiting --> Completed

Exploratory drug-response modeling with pRRophetic suggested lower estimated half-maximal inhibitory concentration (IC50) values for agents including MS-275 (entinostat), PF-4708671, and roscovitine in the high-risk group. The TIDE algorithm carries prognostic information in NSCLC beyond immunotherapy settings. The proposed TIDE-informed gene signature reproduced prognostic stratification across cohorts, suggesting potential applicability to a broader NSCLC population and supporting future personalized risk stratification.

Although pancreatic ductal adenocarcinoma (PDAC) is generally considered an immunologically "cold" tumor, approximately 20% of cases can be classified as immune-hot. Single-cell RNA sequencing revealed that the Gemcitabine-SAHA combination remodels the tumor microenvironment by enhancing CD8+ T cell function and depleting cancer-associated fibroblasts. Clinically, we defined a CD8high/FASNhigh/PARP9high signature that identifies an IE patient subgroup with poor survival, representing those most likely to benefit from the "Gemcitabine-Nivolumab-SAHA" triple-combination therapy.

This study aimed to investigate the regulatory effect of suberoylanilide hydroxamic acid (SAHA) on HLA-E expression via the PERK/ATF4/CHOP pathway in NB...Moreover, SAHA inhibited the expression of ERS pathway proteins, including PERK and CHOP, in NB cell lines. This study demonstrated that SAHA downregulates HLA-E expression by inhibiting the PERK/ATF4/CHOP pathway, offering new insights into the regulation of tumor proliferation, migration, and immune evasion in NB.

Taken together, these results indicated that SAHA inhibition of FOXM1 oncogenic signaling may be mediated by MYCN in RB. Although the current data provide a preclinical rationale for the consideration of SAHA either as a single agent or in combination with other therapies, for the treatment of metastatic RB with MYCN-amplified RB1-/RB1-molecular phenotype, further research is warranted to gain greater insight into FOXM1-MYCN interaction in response to SAHA, in this molecular subtype of RB.