TBX21 (T-Box Transcription Factor 21)

Moreover, CRE editing of PDCD1 and HAVCR2 repressed PD-1 and TIM-3 expression in human tumor-infiltrating lymphocyte CD8 T cells, highlighting regulatory role of these CREs in disease relevant exhausted T cells. Together, this approach offers a compact CRISPRi platform that enables high-throughput dissection of functionally relevant non-coding genomic regions in T cells, providing insights for mechanistic studies and precision genome engineering of advanced cellular therapies.

CHOP or CHOP-like regimens have long been the standard frontline therapy; however, the addition of brentuximab vedotin has improved overall survival and established a new standard of care for CD30-positive PTCL...Epigenetic modulators, including histone deacetylase inhibitors and an EZH1/2 inhibitor, have demonstrated particularly high activity in TFH-derived subtypes, supporting the integration of biomarker-driven patient selection as a path toward precision medicine in PTCL. This review summarizes current insights into the genetic landscape, recent clinical advances in novel agents, and future perspectives on therapeutic stratification, highlighting the need to translate molecular insights into durable clinical benefits for patients with PTCL.

Co-culture experiments showed that TBX21-deficient tumor cells reduced the induction of CD25+Foxp3+ Treg cells from activated CD4+ T cells. TBX21 is associated with tumor progression and an immunosuppressive microenvironment in PCa, underscoring its potential role in modulating the tumor-immune balance.

These chromatin-associated features were accompanied by increased nitric oxide production and enhanced cytotoxicity in functional assays. Collectively, these findings suggest that variation in CTCF levels is linked to coordinated epigenetic and immune-associated changes in NSCLC, supporting its potential relevance as an immuno-epigenetic factor in shaping anti-tumor immune responses.

Overall, these findings demonstrate the ability of BPP to influence dendritic and T-cell responses in NSCLC via coordinated transcriptional and chromatinremodelling activities.

Although previous research focuses on the direct impact of TSA on tumor cells, in our study, we exclusively highlight TSA ability to reprogram the immune cells epigenetically in a more inflammatory tumor-reactive phenotype. The findings justify the possibility of TSA as an epigenetic adjunct of low toxicity in immuno-oncology and form a basis to continue in vivo and translational study in CRC immunotherapy.

Importantly, vitC-CAR19-Ts outperformed CAR19-Ts in long-term antigen stress assays and 3D multicellular spheroid models, indicating a potentially improved in vivo functionality and tumor infiltration capacity. In summary, vitC conditioning represents a promising strategy to enhance CAR T-cell yield, cytotoxic potential and durability, complementing existing approaches to overcome the limitations of CAR T cells in the treatment of hematological malignancies and solid tumors.

Besides, patients in the high-risk group exhibited lower IC50 values for vorinostat, elesclomol, OSI-906, pyrimethamine, thapsigargin, and doxorubicin, but a higher IC50 value for cisplatin, compared to those in the low-risk group, indicating differential drug sensitivities. In summary, we established a robust DRGs signature comprising BTN3A1, CEBPA, KCNAB2, TBX21, and MYC, which showed strong prognostic value and predictive potential for immune status and drug sensitivity in OS. Notably, functional experiments confirmed that BTN3A1 acted as a tumor suppressor in OS, highlighting it as a promising therapeutic target.

In line with this, pathway enrichment analysis revealed immunosuppressive effects related to T cell regulation, similar to UV radiation-induced response. This study provides the first evidence of the efficacy of radon treatment, including the underlying mechanisms in a preclinical mouse model.

In vivo, RIN1 promoted the expression of IL-17 and IFN-γ in CD4+ TILs while suppressing PD-1 expression and reducing the frequency of Treg cells, exhibiting tumor growth inhibition. These findings suggested that RIN1 enhances CD4+ T cell-mediated antitumor immunity in HCC by modulating gene transcription and cell subset differentiation, highlighting its potential as an immunostimulatory agent (Graphical abstract).

The antitumor effect induced by the combinational therapy was abolished by administration of an anti-VCAM-1 neutralizing antibody. Our findings demonstrate that combining metformin with fasting exerts a synergistic antitumor effect by recruiting CD8+ T cells-relocated to the BM during fasting-back to the tumor during refeeding, facilitated by enhanced VCAM-1 expression on normalized tumor vasculature.

Partial hepatectomy disrupts antitumor immunity and limits adjuvant ICI efficacy. Neoadjuvant anti-PD-1 immunotherapy offers a superior strategy compared to adjuvant immunotherapy in enhancing immune responses and reducing HCC recurrence.