EP300 (E1A binding protein p300)

This study provides a theoretical framework for exploring the molecular mechanisms through which DEP may contribute to CRC development, emphasizing the value of network toxicology in cancer research. These findings may inform future investigations into the risks of DEP exposure and support public health policy and the development of targeted therapeutic strategies.

These findings suggest that ASEO has great potential as a natural anti-inflammatory agent, its key compositions and multiple anti-inflammatory mechanisms make it a promising candidate for further research and development for clinical applications.

NGS revealed that a common progenitor cell with BCL2-IgH translocation and mutations in TP53, KMT2A, KMT2C, and KMT2D gave rise to two distinct subclones: one (CD5 + CD23+CD200+) CLL driven by mutations in TNFAIP3 and BCORL1, and the other (CD5-CD23-CD200-) driven by mutations in EP300, NOTCH1, and BCL2. This case highlights the significance of clonal heterogeneity in CLL and underscores the crucial role of MFC, flow sorting, and molecular genetics in diagnosing and understanding the complex evolution of this disease.

Our work reveals new therapeutic vulnerabilities in synovial sarcoma and suggests broader relevance for targeting coactivator-dependent transcription in fusion-driven cancers. BAF degradation does not alter SS18::SSX-activated transcriptional programsDirect SS18::SSX transcriptional activation is independent of BAF interactionThe SS18 C-terminus engages the co-activator EP300 to promote gene expressionSmall molecule degraders of EP300/CREBBP abolish SS18::SSX-mediated transcription.

Collectively, our findings identify NARF as stiffness-responsive driver that is transcriptionally regulated by YAP protein in HCC. By activating LEF1-mediated Wnt signaling in an EP300 dependent manner, NARF promotes HCC growth and metastasis, highlighting its potential as a prognostic biomarker and therapeutic target for HCC.

Critically, in patient-derived organoids (PDOs), A485 selectively attenuated tumor organoid growth and reduced MKI67+ and CD44+ cell populations, sparing adjacent normal tissue organoids. Collectively, EP300 promotes bladder cancer progression by sustaining proliferation through MYC regulation, and its inhibitor A485 represents a promising targeted therapeutic candidate.

These findings uncover a previously unrecognized EP300-H2BK5ac-HSPA1A regulatory pathway that links environmental exposure to biomechanical and epigenetic remodeling in lung cancer. Targeting this axis may offer new strategies to mitigate B(a)P-driven metastasis.

Given their indolent course after local excision alone, the noncommitted term EP300::VGLL3-fused rhabdomyoblastic tumor might be more appropriate for these tumors than the original RMS terminology to avoid overprognostication/overtreatment that the "rhabdomyosarcoma" label would imply. Reporting more cases is mandatory to elucidate the full anatomic and biological spectrum of this morphologically, anatomically, and genetically unique entity.

Pharmacological restoration of histone acetylation with the HDAC inhibitor Trichostatin A (TSA) effectively suppressed tumor growth. Collectively, our findings identify KMT2C as a key epigenetic regulator linking promoter histone acetylation, NF2-Hippo pathway activity, and ferroptosis susceptibility. These results provide mechanistic insights into high-grade meningioma progression and highlight ferroptosis induction and epigenetic modulation as promising therapeutic strategies for NF2-wild-type, KMT2C-deficient meningiomas.

Our data highlights mutational variation across demographic cohorts. These patterns are vital to future studies into identifying diagnostic markers or therapeutic targets.

Thymoma-associated multilineage cytopenias are heterogeneous, frequently relapsing, and driven by complex T-cell-mediated immune dysregulation. Comprehensive evaluation and individualized immunosuppressive therapy are essential for management.