CREBBP (CREB binding protein)

AITL with HRS-like cells is prone to misdiagnosis as CHL due to overlapping morphological and immunophenotypic features. Integration of EBER, TCR/IG clonality assessment, and molecular profiling, particularly the identification of TET2 and RHOA mutations is essential for accurate classification. Recognizing this entity is critical for avoiding diagnostic pitfalls and guiding appropriate therapeutic strategies.

Importantly, we identified novel single nucleotide variants in DUX4, CSF3R and CREBBP, and fusion transcripts. This study not only reports transcriptional heterogeneity in our Latin American cohort but also supports the implementation of open-source bioinformatic pipelines in resource-limited settings to enhance precision diagnosis and guide personalized treatment.

Intriguingly, administration of the histone deacetylase inhibitor trichostatin A resulted in the upregulation of CYP3A5 expression...Because ESCC develops, CYP3A5 suppression promotes tumor metastasis and invasion. CYP3A5 is a potential biomarker and therapeutic target for ESCC.

In the gastric cancer validation cohort, all tumors with PTVs demonstrated a partial response to anti-PD-1 therapy. We report CREBBP and EP300 coding mutations as novel potential surrogate biomarkers for hypermutation in gastroesophageal adenocarcinomas and demonstrate their association with favorable immunotherapy outcomes, supporting their potential clinical utility for patient stratification.

In conclusion, CBP deficiency is a rare event in many different tumor types. Reduced or absent CBP expression is linked to aggressive cancer phenotypes.

Conversely, ACAT2 decrotonylation triggers ER stress and promotes the apoptosis of PDAC cells. This study reveals the roles of GCDH in controlling cholesterol metabolism and PDAC progression and suggests that GCDH is a new target for therapeutic intervention in patients with PDAC.

The 4 MRGs may contribute to the understanding on UPRmt in LUAD and the development of relevant medicine in clinical practice.

Through an integrated multi-omics strategy combining whole-exome sequencing, transcriptome profiling, and histone modification analysis in a Chinese HPSCC cohort, we identified recurrent loss-of-function mutations in EP300/CREBBP. These mutations reduced H3K27 acetylation and downregulated PPARγ, thereby activating the ANGPT4/Tie2 oncogenic signaling axis. Functional assays confirmed enhanced proliferation, invasion, and immune evasion, characterized by a regulatory T cell-dominant immune phenotype. Treatment with daidzein restored PPARγ expression, suppressed ANGPT4/Tie2 signaling, and reversed these malignant features, both in vitro and in vivo. Compared with previous studies, our work not only elucidates the functional consequences of EP300/CREBBP mutations in HPSCC but also proposes a novel therapeutic strategy targeting this axis. Importantly, we reveal a previously unrecognized EP300/CREBBP-PPARγ-ANGPT4/Tie2 axis and identify daidzein as a dual agonist of EP300 and PPARγ, providing mechanistic insights and translational potential for HPSCC therapy.

HAD/ACED demonstrated higher TP53 mutation accumulation and TP53-related cancer stemness gene overexpression, including LIN28B, IGF2BP1, and HMGA2. Therefore, TP53 and these cancer stemness genes might be involved in the occurrence of HAD/ACED.

These clinically actionable genes, aberrantly expressed before treatment, may serve as early biomarkers for risk stratification. Further validation in PARPi-sensitive and -resistant ovarian cancer cohorts is needed.

The findings suggest that RD has the potential to mitigate OP by modulating the IR microenvironment through the ER/PI3K-EP300 signaling axis. Through the integration of dose-effect weighted network pharmacology and metabolomic analysis, our study advances beyond existing descriptive research on RD and pioneers the elucidation of the ER/PI3K-EP300 axis, thereby offering a novel mechanistic explanation.

Gene Ontology and KEGG pathway analyses suggested potential mechanisms involving HIF-1 signaling, TNF signaling, and calcium signaling pathways. Our findings suggest a significant association between exposure to certain OCPs and increased mortality risks among diabetic populations, emphasizing the need for public health strategies to mitigate environmental pollutant exposure in diabetes management.