decitabine

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, N=6, Active, not recruiting, Thomas Jefferson University | Phase classification: P1/2 --> P1

P2, N=152, Recruiting, Ruijin Hospital | Not yet recruiting --> Recruiting

P1, N=54, Recruiting, City of Hope Medical Center | Trial completion date: Nov 2025 --> Feb 2026 | Trial primary completion date: Nov 2025 --> Feb 2026

Overall, addition of DAC to the conditioning regimen was associated with favorable immunomodulatory effects on NK and T cells post-alloSCT in AML patients. These findings suggest that DAC may enhance donor NK and T cell-mediated graft-versus-tumor responses supporting its further clinical evaluation as an adjuvant prior to alloSCT.

While the patient failed high-risk T-LBLL induction therapy, blinatumomab followed by decitabine and venetoclax induced a morphologic remission. This case illustrated the importance of integrating MFC analysis with NGS data to provide individualized patient treatment. The authors have confirmed clinical trial registration is not needed for this submission.

Among the pathways disrupted, retinoic acid signaling is of particular interest, as retinoid receptors such as RARα and RARβ are frequently hypermethylated and repressed in EBVaGC. Our findings indicate that DNMT inhibition can partially reverse RA receptor silencing, supporting further investigation of DNMTi-RA combination strategies as a novel therapy for EBV + gastric cancer.

Additionally, decitabine treatment induced a reduction in SEPT9 methylation levels, which affects microtubule stability, suggesting a potential mechanistic link to tumor invasion. These findings indicate that SEPT9 methylation is a promising biomarker for distinguishing invasive breast cancer from DCIS and for identifying high-risk DCIS lesions with greater potential for progression.

P2, N=20, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Nov 2025 --> Nov 2026 | Trial primary completion date: Nov 2025 --> Nov 2026

P2, N=40, Recruiting, Beijing 302 Hospital

The hypomethylating agents (HMAs) 5-azacytidine (vidaza-AZA) and 5-aza-2'-deoxycytidine (decitabine-DAC) are part of the standard of care for the treatment of myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). In the intent of deciphering the regulation of DNMT3B expression, we found that DAC significantly increased the level of H3 acetylation at the DNMT3B promoter. These preliminary data shed light on DAC-mediated methylation dynamics at satellite 2 repeats, suggesting that satellite 2 remethylation could limit the genomic-destabilizing effects mediated by HMAs in tumor cells and, thus, the future evaluation of strategies to impair this methylation regain and to improve HMAs activity against tumor cells.

This study aims to investigate the genetic characteristics of Acute Myeloid Leukemia (AML) patients and identify which patients derive the greatest benefit from a low-intensity regimen of decitabine combined with modified Cytarabine + Aclarubicin + Granulocyte Colony-Stimulating Factor (D-CAG) or intensive chemotherapy (IA regimen). Notably, older patients with complex or monosomal karyotypes exhibited longer median OS than their younger counterparts (P < 0.05). In conclusion, D-CAG may represent a more suitable therapeutic option for AML patients with high-risk karyotypic profiles.