TCF7 (Transcription Factor 7)

Additionally, we validate cTR-T's phenotypic changes following PD-1 blockade therapy in mouse tumor models with artificial antigen. These findings suggest that the phenotypic state and transition of cTR-Ts may reflect their functional potential after tumor infiltration and are associated with therapeutic outcomes of ICIs.

Mechanistically, bryostatin upregulated CD20 expression in tumor cells via the MEK/ERK pathway and enhanced c‑JUN/TCF7 levels in CAR‑T cells, promoting their tumor infiltration. Bryostatin enhances CD20 CAR‑T efficacy by counteracting trogocytosis‑driven antigen loss and upregulating CD20 expression, providing a promising strategy to overcome antigen escape in lymphoma therapy.

EA of BL40 and BL23 can significantly up-regulate the expressions of Pax7, MyoD, MyoG and MyHC in the injured multifidus muscle, and promote the regeneration and repair of lumbar multifidus muscle, which may be related to its functions in promoting the release of exosomes in the acupoint area.

Immune-related gene expression patterns are associated with response to nCRT in rectal cancer. High expression levels of S100A8, SPINK5, ANXA1, FOXJ1, and CLEC7A were indicative of favorable treatment response, and S100A8 and SPINK5 were associated with prognosis. A machine learning-based model composed of immune-related genes showed strong predictive potential. Our results support the use of immune gene signatures to guide personalized therapy in rectal cancer.

The present study suggested that MFAP2 could be involved in the carcinogenic progression of UCEC via the β-catenin/TCF7L1 axis. MFAP2 overexpression may contribute to immunosuppression in UCEC patients.

Additionally, Western blot and experiments employing the PI3K inhibitor LY294002 have demonstrated that TCF7L2 activates the PI3K/AKT signaling pathway, thereby facilitating the proliferation of CRC cells...Spearman correlation analysis confirmed a positive relationship between the expressions of TCF7L2 and HIF-1α, while Kaplan-Meier survival analysis demonstrated that their co-expression was predictive of reduced overall survival. Collectively,these findings position TCF7L2 as a critical downstream effector of HIF-1α in hypoxic CRC, and its mechanistic role in promoting malignancy and correlation with poor prognosis provide a theoretical basis for exploring TCF7L2 as a potential therapeutic target in future studies..

These findings suggest the presence of the Th7R-Tpex axis. Th7R, which reflects antitumor T-cell immunity, is a useful predictive marker for treatment efficacy in ES-SCLC.

Any potential difference in observed expression values across the paired samples could be related to the different cell type proportions across the samples. The sample size was small, and each study used different sequencing technologies, so any interpretation should be confirmed with additional studies.

These findings established a robust experimental foundation for advancing magnesium alloy-mineralized collagen composite scaffolds as next-generation biodegradable adjunctive therapeutic materials for cervical cancer treatment. The synergistic combination of biocompatibility and tumor-targeted activity positions this material as an innovative platform for circumventing shortcomings in existing clinical regimens.

Overexpression of TCF-1 confers resistance to apoptosis, limits excessive activation, and promotes a less differentiated phenotype, collectively enhancing CAR-T cell persistence and long-term efficacy. These findings suggest that TCF-1 modulation represents a promising strategy to improve durability and safety of CAR-T cell therapy in relapsed or refractory hematologic malignancies.

Furthermore, we developed a risk stratification model based on EMT continuum signatures, providing a novel tool for prognostic assessment. Our findings contribute to a comprehensive understanding of EMT-driven tumor evolution and open new avenues for prognostic stratification and targeted therapies in LUAD.

Bhlhe40 is essential in CD8 T cells for anti-PD-1 ICT, but dispensable for anti-CTLA-4 due to compensatory CD4 T cell function CD8 T cell-intrinsic Bhlhe40 drives effector/exhausted states over TCF-1 + naïve and progenitor-exhausted like phenotypes Bhlhe40 sustains T cell metabolic fitness, supporting glycolysis under both therapies and OXPHOS primarily during anti-PD-1CD8 T cell-intrinsic Bhlhe40 is required for full ICT-driven macrophage remodeling In human cancers, Bhlhe40 is enriched in tumor-reactive CD4 and CD8 T cells, positively linked to TOX / IFNG and inversely to TCF7 (TCF-1).