P1/2, N=40, Recruiting, Cocrystal Pharma, Inc. | Not yet recruiting --> Recruiting | Initiation date: Nov 2025 --> Mar 2026 | Trial primary completion date: Jun 2026 --> Oct 2026
5 days ago
Enrollment open • Trial initiation date • Trial primary completion date
High POFUT2 expression in CRC regulates JUP fucosylation, increasing JUP and VEGFA levels, which promotes angiogenesis. These findings suggest POFUT2 could serve as a prognostic marker for colorectal cancer, and targeting it may inhibit angiogenesis and aid in treatment.
The analyzed variants in the PTPN22, CD226, and INS genes were overrepresented in pediatric patients with T1D, suggesting potential therapeutic targets for modulating the autoimmune process. Their associations with specific clinical and autoimmune profiles can be applied in the identification of high-risk patients and help optimize their follow-up.
1 month ago
Journal
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CTLA4 (Cytotoxic T-Lymphocyte Associated Protein 4) • SH2B3 (SH2B Adaptor Protein 3) • FUT2 (Fucosyltransferase 2) • PTPN22 (Protein Tyrosine Phosphatase Non-Receptor Type 22)
Preclinically, combining RT with LCN2-neutralizing antibodies elicited synergistic anti-tumor immunity. These results unveil FUT2 as a regulator of PDAC radiosensitivity via the FUT2-FBXO2-NR2F2-LCN2 axis, offering a promising therapeutic target to overcome RT resistance.
These host responses were accompanied by a selective enrichment of mucin-associated bacteria, particularly Akkermansia, suggesting a potential interaction between epithelial remodeling and microbiota composition induced by P. clypearia. Notably, malic acid alone reproduced the protective effects of P. clypearia by inducing epithelial fucosylation, reinforcing barrier integrity, and modulating gut microbial communities.
FUT2 variants are associated with the development of pancreatic IPMNs. FUT2 and rs601338 have important functions in mucin synthesis, biliopancreatic duct homeostasis, carcinoembryonic antigen, and cancer antigen 19-9 regulation, which provide a biologically plausible role in IPMN pathogenesis.
This review focuses exclusively on protein-centric glycosylation and highlights current studies on the roles of glycosylation in CRC, encompassing molecular mechanisms, diagnostic biomarkers, and emerging therapeutic strategies targeting glycosylation enzymes or glycan epitopes. Understanding glycan dysregulation provides new perspectives for biomarker development and targeted interventions in precision oncology.
The GRG profile serves as a prognostic biomarker for STAD, offering new insights into therapeutic approaches and potential applications in other gastrointestinal cancers.
Mechanistically, FUT2 mediates the fucosylation of β-catenin, which maintains its activity and promotes its nuclear translocation, thereby increasing the expression of glutathione peroxidase 4 (GPX4) and cancer stemness-associated proteins. Our study uncovers a previously unrecognized function of FUT2 in ferroptosis and chemoresistance, offering a novel therapeutic target for LUAD.
This study identified novel genetic variants for pancreatic PDFF and confirmed related genes functions in the pancreas. These findings emphasize the need for regular surveillance of pancreatic fat deposition in the population with a high genetic risk based on FUT2 polymorphism, which could facilitate risk stratification and tailored therapeutic approaches for the primary prevention of CP.
Genetic testing is ready for prime time in PDAC screening. It stratifies patients into low-risk (no surveillance) and high-risk (surveillance warranted) groups, improving early detection, outcomes, and cost-effectiveness, thus transforming PDAC prognosis through targeted intervention.
7 months ago
Journal • BRCA Biomarker • PARP Biomarker
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BRCA2 (Breast cancer 2, early onset) • FUT2 (Fucosyltransferase 2) • FUT3 (Fucosyltransferase 3) • CA 19-9 (Cancer antigen 19-9)
HPV6-induced gene expression signature in infected epithelial cells may play a role in RRP pathogenesis. Further molecular investigations are necessary to determine whether controlling these genes and related factors can control the progression of RRP.