We also demonstrated that, compared with that with each drug used as single agents, the combined 5-aza and HDAC3i treatment induced the epigenetic remodeling of DLBCL cells, which resulted in a more potent reexpression of differentiation genes, including XBP1 and ATF4. Our results highlight the importance of specifically targeting multiple layers of the epigenome to maximize the efficacy of epigenetic-based therapies.

Azacitidine/venetoclax is the standard treatment for patients with acute myeloid leukemia (AML) unfit for intensive chemotherapy. The potentiated antileukemic activity positions cobicistat as a promising complementary agent in AML therapy. This trial was registered at www.clinicaltrials.gov as NCT06014489.

He was initially treated with azacitidine and venetoclax but demonstrated disease progression. In the setting of a KMT2A::ELL fusion, therapy was transitioned to the menin inhibitor revumenib, resulting in short-term clinical stability and tolerability under continued supportive care.

Previously, we showed that ex vivo priming with decitabine (DAC) enhances CAR T persistence and efficacy. Single-cell sequencing indicates that DAC priming enriches for memory-like progenitors, which maintain cytotoxic and memory signatures, and upregulates genes associated with T cell fitness and engagement of endogenous immunity. These data establish DAC-priming as a clinically feasible epigenetic reprogramming strategy enhanceing CAR T durability and efficacy, offering a generalizable paradigm for engineered cell therapies in malignant tumors.

This case may preliminarily suggest ATRA's potential in AML1-MTG16⁺ AML, offering translational clues for ultra-rare leukemia subtypes, pending further validation.

Decitabine was predicted as a potential agent targeting these genes, with DUSP13 showing strong binding affinity (-6.9 kcal/mol)...Their expression patterns may provide supplementary molecular evidence to support the early identification and dynamic risk monitoring of high-risk patients. However, the clinical translational potential of these findings requires further validation through large-scale, multicenter prospective studies.

After eight years and treatment with lenalidomide with excellent clinical response, she developed progressive cytopenias and transformation to acute myeloid leukemia, myelodysplasia-related (AML-MR)...The patient was treated with combination azacitidine and venetoclax and an investigational immunotherapy within a clinical trial...Our findings expand the spectrum of dmin-associated oncogenic amplifications in myeloid neoplasms and highlight FLI1 and ETS1 as recurrent targets of 11q24-derived ecDNA amplification. Recognition of such rare events underscores the importance of integrative cytogenomic profiling for uncovering novel mechanisms of leukemic transformation and potential therapeutic targets.

ASTX727 plus talazoparib produces significant myelosuppression without other adverse events. Modest methylation changes in PBMCs were detected. There were no objective responses, but some heavily pretreated patients had stable disease for >4 months despite the attenuated doses.

Disease-modifying activity with decreases in mutated clones is rare. Although the exact mechanism behind our findings remains undetermined, they are in line with the proposed effects of HMA on epigenetics in leukemia cells.

Age, bone marrow blasts, iron overload, and high-risk cytogenetics are key prognostic factors. Incorporating clinical, cytogenetic, and mutational variables into new prognostic models may enhance individualized treatment decision-making for high-risk MDS patients.

The CLL-1 targeted NPs loaded with MDP5 and AZA demonstrated superior AML control and targeting of LSCs in TP53-mutant mice models, while sparing normal hematopoiesis in healthy NSG mice. These promising results highlight a potential efficacy of our novel CLL-1 targeted NP combination approach to treat AML, particularly those harboring TP53 mutation.

Post-transcriptional regulation by 5-azacytidine (5-Aza) and synergy with doxorubicin (ADM) were assessed via DNA damage repair and apoptosis assays. AA@Tf-Lip enhanced cellular uptake and tumor specificity, achieving higher tumor inhibition and reduced cardiotoxicity versus free drugs. Indirect RDM1 inhibition via post-transcriptional regulation combined with targeted co-delivery effectively enhances HCC chemosensitivity, offering a safe, precise therapeutic strategy.