TCF7L2 (Transcription Factor 7 Like 2)

Compared with 5-fluorouracil (5-FU), UnSap exhibited a strong antioxidant capacity, excellent safety (in PBMCs), and a higher selectivity index (SI) with a lower IC₅₀ against HepG-2 cells...Across all investigated parameters, UnSap demonstrated superior anticancer efficacy compared with 5-FU. These findings highlight the potential of UnSap as a promising natural therapeutic candidate and provide a foundation for future studies on its bioactive constituents for the development of novel anticancer agents.

Consistent with its role as a Wnt/β-catenin effector, TCF7L2 displayed significant effect on lung adenocarcinoma cell growth. Our data highlighted context-specific susceptibility genes, especially from alveolar cells of lung, contributing to lung cancer etiology.

H3K27ac-marked enhancers were enriched near adipocytic marker genes in WDLPS and mesenchymal markers in DDLPS. Together, these findings reveal the cellular heterogeneity of tumor and immune compartments across liposarcoma subtypes and identify regulatory programs driving their differentiation states.

We show that in a Tcf4 -haploinsufficient background, the Tcf4 Lin-, but not the Tcf4 Lin+, cell population represents the cell of origin for colon tumors driven by deletion of Apc . Our results provide a foundation for understanding Apc -allele-specific differences during colon tumorigenesis and identify a new stem-cell population that may prove valuable in the treatment of diseases caused by intestinal barrier homeostasis defects.

Adipose tissue LYC concentration displays high interindividual variability, which can be explained in part by genetic variants in genes involved in carotenoid and lipid metabolism. Clinical trial registry: ClinicalTrials.gov registration number NCT02100774.

P4, N=300, Recruiting, The University of Texas Health Science Center, Houston | Trial completion date: Jul 2026 --> Oct 2026 | Trial primary completion date: Nov 2025 --> Oct 2026

The results of this small-scale retrospective cohort study indicate a significant association between type 2 diabetes mellitus and colorectal adenomas. The clinical sample experimental evidence in this study indicates that the increased activity and expression of Wnt/β-catenin/TCF7L2 is one of the mechanisms of type 2 diabetes mellitus and colorectal adenomas.

Results obtained with a preclinical TNIK inhibitor in human colorectal cancer cells show efficient abrogation of MYC expression and consequently impaired dimerization with its interaction partner MAX. The antagonistic BASP1 effect on MYC and the MYC dependency on TNIK could enhance the development of strategies to interfere with oncogenic functions of the cancer driver MYC.

Taken together, our findings identify MASLD as a modifiable risk factor for neurodegeneration, with systemic inflammation playing a pivotal role in the liver-brain axis. This study highlights key genes and pathways underlying MASLD-induced cognitive impairment, advances understanding of metabolic-neural cross talk, and offers potential therapeutic targets for mitigating cognitive decline through intervention in the liver-brain axis, developing intervention strategies and highlight the therapeutic promise of targeting the liver-brain axis.

Functionally, TCF7L2 maintained proliferation via the MAPK signaling axis in this subtype of CRPC. Together, these data provide a mechanistic rationale for interventions that perturb DNA binding of the pro-proliferative transcription factor TCF7L2 and/or direct MAPK signaling inhibition in the CRPC-WNT subclass of advanced prostate cancer.

Overall, our results provide genetically-underpinned molecular mechanism through which promising treatments for PD may work.