The combined treatment of syngeneic LLC lung cancer with C36 and a PD-1 antibody significantly enhances anti-tumor efficacy. Our study identifies a new allosteric mechanism of PRC2 inhibition and paves the way for the development of highly selective EZH2/PRC2 inhibitors for combination therapy.
18 hours ago
Journal • PD(L)-1 Biomarker • IO biomarker
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
Mutations in ASXL1, SRSF2, EZH2 and NRAS were significantly more frequent in RUNX1-mutated patients compared with those without RUNX1 mutations (adjusted p < 0.05). RUNX1-mutated patients exhibited poorer overall survival (median OS 18 months vs. 51 month, p < 0.001), while U2AF1 co-mutations were associated with a relatively better prognosis (median OS 34 months vs. 17 months, p = 0.003), indicating a potential modifying effect of U2AF1 on the outcome of RUNX1-mutated patients.
In addition, tumor cells exhibited a type II EBV latency pattern (LMP1+/EBNA2-) in 84.6% of cases, and LMP1 expression correlated with larger tumor size (p=0.021). Taken together, these findings support a role for EBV-driven activation of the cyclin D1 pathway and suggest that EBV-LMP1-CCND1 signaling may contribute to the pathogenesis of IFDCS.
Although limited by its retrospective character, small sample size and incomplete molecular data, this study shows that long-term survival after allo-HCT is achievable in patients with MDS/MPN with Neutrophilia, particularly in younger individuals with low disease burden. However, relapse and NRM remain major challenges underscoring the need for optimized post-transplant strategies.
Flow cytometry antibody indicators can suggest that MDS patients are prone to gene mutations related to chromatin regulation, transcriptional regulation, poor prognosis and leukemia transformation. The proportions of CD25+ T cells and lymphocytes were both closely related to the T-bet and GATA3 gene mutations.
The protective effects of six curcumin compounds were examined using molecular docking with AutoDock 4.2.6 to assess protein dynamics and binding interactions. Optimal complexes were selected for dynamics simulation using GROMACS, and potential strategies for long-term cancer prevention related to arsenic exposure were identified.
Before conditioning, 20 patients received intensive induction chemotherapy, 1 received decitabine plus venetoclax, and 3 proceeded directly to transplant. In conclusion, our results suggest that achieving remission before alloHSCT in BP-MF is associated with favorable outcomes. The adverse impact of TP53 or EZH2 mutations supports early post-transplant strategies to prevent relapse.
Valemetostat, which inhibits EZH1/2, as well as tazemetostat in combination with other drugs have been subject of recent research. The purpose of this article is to review the role of EZH2 in normal B cell differentiation and in the pathogenesis of B-Cell lymphomas.
21 days ago
Review • Journal • IO biomarker
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
We identified a novel ACSS2-H3K9ac-HK2 signaling axis that is characteristically activated in EZH2-non-mutant solid tumors and drives metabolic reprogramming and resistance to EZH2 inhibition.
1 month ago
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • ACLY (ATP Citrate Lyase) • ACSS2 (Acyl-CoA Synthetase Short Chain Family Member 2)
In selected postoperative or frail patients, rituximab monotherapy can serve as an effective bridge to full chemotherapy, facilitating recovery and improving outcomes. Early diagnosis and targeted treatment remain essential to prevent complications from lymphatic loss and to optimize prognosis in lymphoma-associated chylous ascites.
Pharmacological inhibition of EZH2 using DS-3201 reproduced some of the molecular effects of viral infection, including increased mutp53 stability...Indeed, the inhibition of SIRT1 with EX-527 reversed mutp53 accumulation but restored c-Myc expression and increased extracellular IL-6 release...These results establish a mechanistic link between viral infection, epigenetic remodeling, and oncogenic dependency. They also suggest that targeting IL-6 signaling could represent a therapeutic vulnerability in HHV-6A-associated thyroid cancer, particularly in combination with SIRT1 inhibitors.