This study provides genetic and functional evidence linking breast cancer to meningioma risk through DNA repair and hormonal pathways, supporting early risk assessment and targeted therapies to improve patient outcomes.

Decitabine restores gasdermin E expression to couple oxidative stress with caspase-3-mediated pyroptosis, while chlorogenic acid repolarizes tumor-associated macrophages toward a pro-inflammatory phenotype. This coordinated multimodal cell-death cascade establishes a self-amplifying immunogenic circuit that suppresses tumor growth, sensitizes CRC to ICB, and elicits systemic antitumor immunity.

Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Oncology Reports 35: 1375‑1384, 2016; DOI: 10.3892/or.2015.4492].

The LPMD algorithm effectively captured DNMT3A mutation-associated epigenetic instability (Cohen's d = 0.8, p < 0.001), with the strongest effects observed in the 5'UTR-Exon1 region (d = 0.74) and a gradient pattern from CpG islands to shores (d: 0.59→0.54→0.43). The 5-DMDR panel offers a practical tool for azacitidine response prediction, while dynamic LPMD monitoring provides a potential biomarker for therapeutic guidance. These findings establish methylation disorder as a clinically actionable dimension of epigenetic dysregulation in myeloid malignancies.

Therapeutic strategies including activation of NK cells via chemotherapeutics (bortezomib, decitabine), blockade of inhibitory receptors (NKG2A, CD161), and combinatorial approaches with immune checkpoint inhibitors are under active investigation. Notably, chimeric antigen receptor (CAR)-engineered NK cells targeting EGFR, HER2, GD2, and CD133 show promise in preclinical glioma models due to their enhanced specificity and reduced toxicity compared to CAR-T cells. This review summarizes the multifaceted roles of NK cells in glioma immunity and highlights novel immunotherapeutic strategies to restore NK cell function and improve clinical outcomes.

P2, N=170, Suspended, Alliance for Clinical Trials in Oncology | Trial completion date: Jun 2026 --> May 2027 | Trial primary completion date: Jun 2026 --> May 2027

Not available.

Venetoclax (Ven) in combination with hypomethylating agents (HMA) (azacitidine or decitabine) is the standard of care for elderly or unfit patients with acute myeloid leukemia (AML) and is being explored in high-risk myelodysplastic syndrome (HR-MDS). Neutropenic fever occurred in 15%, there were no therapy-related fatalities, and the 100-day mortality was 7.5%. A non-cytotoxic metronomic dosing schedule of decitabine/Ven has a low toxicity profile in TP53-mutated myeloid malignancies.

Silencing p53 also failed to affect simvastatin-induced cell cycle arrest or impact the sensitivity of MB cells treated with simvastatin in combination with hypoxia, X-ray or azacitidine, an epigenetic therapy with DNA methyltransferase inhibition. Collectively, our findings indicate that MVP function is independent of p53 in MB.

Decitabine and GSK3685032 reduced histone lysine acetylation and methylated-lysines whereas GSK3685032 had minimal effects on histone modifications in cells. Our results suggest that some doses of DNMT inhibitors may increase p16 expression making them potentially effective in gastric cancer, while higher doses will decrease p16 expression possibly reducing efficacy.

Among the three patients who received at least three cycles of decitabine, improvements in anemia and thrombocytopenia were observed in those with elevated NKT-like cell levels. These findings suggest that low-dose decitabine may enhance the NKT-like cell population, which may be associated with therapeutic responses in chronic myeloid neoplasms.

Furthermore, BIS-LNPs@DCA-siTNF attenuated osteoclastogenesis, restored bone integrity, and improved locomotor performance. These results establish BIS-LNPs@DCA-siTNF as a programmable nanoplatform that overcomes both pharmacological and microenvironmental barriers, offering a promising approach for enhanced AML therapy.