TNFAIP3 (TNF Alpha Induced Protein 3)

SOX9 and TNFAIP3 emerge as key mediators linking persistent epigenetic alterations with immune remodeling in HCV-related HCC, and as potential non-invasive biomarkers for evaluation of HCC risk and post-DAA surveillance.

Transcriptomic analyses of Egr1-deficient tumors suggested immune dysregulation, including heightened inflammation and potential markers of T cell exhaustion in the tumor microenvironment. These findings indicate that Egr1 may play a role in suppressing tumor growth through modulating immune dynamics, offering new insights into the interplay between tumor progression and immune regulation in lung adenocarcinoma.

In summary, the TNFAIP3, IRAK1, and TLR4 gene polymorphisms are associated with RA susceptibility.

This multicenter study showed the features of small bowel lesions among VEOIBD by VCE. Safety of VCE in VEOIBD patients have also been demonstrated.

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.

Through MR analysis, this study systematically identified 10 hub genes associated with AD and predicted 5 potential drug candidates. These findings offer novel insights into the molecular mechanisms underlying AD and may contribute to improved strategies for clinical diagnosis and targeted therapy.

Comparative genomic analyses of populations in cold and arid environments identified several candidate genes related to energy and water homeostasis, as well as hair development (TP53 [Tumor Protein P53], ATG101 [Autophagy Related 101], ATP12A [ATPase H+/K+ Transporting Non-Gastric Alpha2 Subunit], KRT80 [Keratin 80], KRT7 [Keratin 7]). Additionally, Tibetan sheep in the high-altitude arid deserts exhibit stronger adaptive selection for energy homeostasis and water utilization; meanwhile, the HIF-1 [Hypoxia Inducible Factor 1] signaling pathway helps counteract oxidative stress induced by extreme water scarcity in the plateau environment. Our study supports the hypothesis that Tibetan sheep originated in northern China and identifies distinct adaptive features in the Tibetan sheep genome corresponding to their habitats.

Clinically, newly diagnosed patients, most treated with venetoclax based regimens, achieved high remission rates. Our data delineate the structural diversity of BCL11B rearrangements identified by OGM and show that BCL11B activation cannot be reliably inferred from partner gene identity alone. BCL11B immunohistochemistry as a practical surrogate for assessing BCL11B activation is recommended in routine practice.

This study provides a comprehensive genomic profile of T-LGLL, identifying recurrent somatic mutations and commonly affected pathways. Notably, frequent alterations were observed in the FAS-FASL signaling pathway, underscoring its potential as a target for therapeutic development.

Further investigations revealed that BAP ultimately enhances NETs formation by acting on CXCR4, PADI4, and TNFAIP3. In summary, this study provides potential theoretical guidance for the prevention and management of asthma.

Our findings suggest a role of TNFAIP3 as a critical regulator of BRCA progression and tumor immunity. The TNFAIP3-LINC01096 axis represents a promising therapeutic target, particularly for immunotherapy-resistant cases. These results provide a rationale for developing TNFAIP3-based prognostic tools and immunomodulatory strategies in BRCA management.

RNA sequencing demonstrated a novel TNFAIP3::GLI1 gene fusion in the liver lesion, which had higher mitotic activity but showed similar pure epithelioid morphology and immunophenotype as the original small bowel lesion. In addition to expanding the spectrum of GLI1-associated gene fusions, this case highlights the potential for misdiagnosis of epithelioid GLI1-altered mesenchymal tumors as adenocarcinoma (particularly given the variable immunoreactivity for cytokeratin), and the need for long-term follow up of these typically slowly growing neoplasms.