P2, N=132, Active, not recruiting, National Cancer Institute (NCI) | Suspended --> Active, not recruiting

EBF1 presented a promoter hypermethylation pattern in COAD cell lines, in which its expression was restored upon treatment of the methylation inhibitor 5-azacytidine. In conclusion, this study highlights that the hypermethylation of EBF1 leads to transcription activation of DEPDC1B, which promotes cell cycle progression, EMT, and malignant progression in COAD. Restoring EBF1 levels or suppressing DEPDC1B expression may be promising strategies for COAD management.

P2, N=132, Not yet recruiting, National Cancer Institute (NCI) | Initiation date: Feb 2026 --> May 2026

These nanoparticles release hyaluronidase (HAase) and decitabine (DEC) in acidic tumor microenvironments, promoting stroma degradation and C-C motif chemokine ligand 5 (CCL5) secretion, while retaining αPD-1 on TILs to prevent exhaustion...This approach increases TIL infiltration by 12-fold in immunodeficient mice and, in immunocompetent settings, mobilizes both exogenous TILs and endogenous CD8+ T cells, enabling tumor eradication and metastasis suppression with 10-fold lower TIL doses than conventional therapies. Collectively, this nanoengineered TIL therapy offers a potential strategy for addressing immune-resistant tumors, showing distinct benefits in stromal-rich settings.

Leukemic stem cells (LSCs) in acute myeloid leukemia (AML) depend on oxidative phosphorylation (OXPHOS) sustained by fatty acid oxidation (FAO) and mitochondrial fusion (mitofusion). In vivo, miRisten potentiated the VEN/azacitidine (AZA) regimen, an FDA-approved therapy for older or unfit AML patients, significantly prolonging survival in patient-derived xenograft models. VEN/miRisten combination also reduced LSC burden and restored VEN sensitivity, establishing miR-126 inhibition as a transformative therapeutic strategy in AML.

Moreover, SOX5 was associated with genomic instability, susceptibility to medicines such as azacitidine and distinct mutation patterns. SOX5 suppression in NSCLC cells in vitro impeded proliferation, migration and invasion. These findings collectively emphasize the key function of SOX5 in tumor biology and highlight its potential as a biomarker for cancer diagnosis, prognosis and therapeutic targeting.

P1/2, N=36, Active, not recruiting, Groupe Francophone des Myelodysplasies | Recruiting --> Active, not recruiting

P2, N=57, Completed, Sidney Kimmel Cancer Center at Thomas Jefferson University | Active, not recruiting --> Completed

P1, N=53, Suspended, National Cancer Institute (NCI) | Recruiting --> Suspended

This study aims to demonstrate that ABC-14 regimen is non-inferior to "3 + 7" regimen in newly diagnosed AML induction therapy while overcoming AB resistance and reducing toxicity associated with "3 + 7". It seeks to provide a broadly applicable alternative induction strategy for AML.

We uncovered 31 potential key genes showing differential early responses to DAC treatment in TP53-mutant versus wild-type cells, which may be associated with resistance development. This study revealed the potential molecular mechanisms of TP53 gene locus mutation in DAC-treated MDS.

P1/2, N=101, Active, not recruiting, Taiho Oncology, Inc. | Trial completion date: Dec 2025 --> Dec 2026