LEF1 (Lymphoid Enhancer Binding Factor 1)

Therefore, in the differential diagnosis between SCT and LCT, our results suggest LEF1 is a highly sensitive and specific immunohistochemical marker and may represent a robust alternative to β-catenin, offering clearer nuclear staining and easier interpretation. The detection of IL13Rα2 in a subset of LCTs is a novel finding and suggests potential biological and therapeutic relevance, warranting further investigation in larger and clinically aggressive cohorts.

Combined use of LEF1 and β-catenin improved sensitivity (90%) but resulted in a medium specificity (93%). In conclusion, the proposed immunohistochemical panel can improve diagnostic accuracy in basaloid tumors of the salivary glands.

Cyclin D1 can be used as a complementary marker in WNT-AG detection. ROR2 negativity may indicate G3 tumors, though further studies are warranted to confirm its prognostic value.

Our results suggest that LEF1 inhibits ferroptosis in CRC cells by promoting SLC7A11 transcription, potentially serving as a therapeutic target for CRC. This study reveals that the promotion of CRC by LEF1 is associated with activating SLC7A11 transcription and inhibiting cellular ferroptosis, providing a new direction for clinical targeted therapy of CRC.

Female C57BL/6N mice were subjected to hair cycle synchronization through depilation, followed by cyclophosphamide (CYP) administration to induce hair loss and graying...Moreover, propolis upregulated expressions of Lef1 and melanogenic genes (Tyr, Tyrp1, Dct) at 30 days of treatment. These findings suggest that Philippine stingless bee propolis promotes hair follicle regeneration and melanocyte function, offering a potential natural therapeutic approach for CIA.

These findings indicate that miRNA-133a and miRNA-452 downregulation, coupled with CLNK and LEF1 upregulation, may drive CLL pathogenesis, with age-related differences highlighting their potential as diagnostic biomarkers. Further validation in larger cohorts and functional studies are warranted to elucidate their mechanistic roles.

By emphasizing the significance of LEF-1 in the processes of carcinogenesis, the discussion aims to shed light on the potential implications of these findings for developing innovative treatment strategies. Understanding the function of LEF-1 not only enhances our comprehension of tumor biology but also opens pathways to novel therapeutic interventions.

These transcription factors are also expressed in human chronic lymphocytic leukaemia B cells and in a B-1-like population that is abundant in pleural fluid and circulation of some patients with pleural infection. Our findings define a TCF1-LEF1-driven transcriptional program that integrates stemness and regulatory function in B-1a cells.

The expression of CTNNB1, LEF1/TCF7, and cyclinD was significantly increased in cells of the epithelial-mesenchymal phenotype with stemness features in patients with refractory tumor. The duration of the relapse-free period is associated with the level of CTNNB1 expression in cells of the epithelial-mesenchymal phenotype with stemness features and the level of LEF1 expression in cells of the epithelial-mesenchymal phenotype.

Our study shows consistent changes in genes involved in EMT in gliomas of different grades. Additional research is needed to confirm the knowledge brought by this study.

Our findings suggest that BCAs with abundant S100 protein-positive stroma are tumors that morphologically display tricellular differentiation into inner (luminal) ductal epithelial cells, outer (abluminal) basaloid myoepithelial cells, and spindle-shaped stromal S100-positive cells (stromal abluminal). According to our investigation, BCAs with S100 protein-positive stroma represent a distinctive triphasic subset of BCA, which is substantially different from PA, both in immunoprofile and molecular underpinnings.

We identified genetic subtypes of γδ T cells with distinct genotypic and clinical characteristics in DLBCL patients. Expression levels within these subgroups emerged as potential indicators for patient outcomes and as crucial factors in shaping therapeutic strategies. These insights significantly advance our understanding of intricate relationships among cellular subgroups and their roles in influencing disease progression and patient prognosis.