DPP4 (Dipeptidyl Peptidase 4)

Moreover, DPP4 knockdown recapitulated the antiproliferative effects of quercetin. Collectively, these findings identify DPP4 as a functional therapeutic target for thyroid cancer and demonstrate that quercetin inhibits thyroid cancer cell proliferation through a DPP4-dependent mechanism.

This study presents an integrative pan-cancer framework linking CD26 expression to immune infiltration, together with in vitro observations in breast cancer cells, offering a comprehensive pan-cancer and experimental characterization of CD26. CD26 might be a novel prognostic biomarker candidate and therapeutic target to counteract tumor development in highly aggressive cancer.

Inhibiting the enzymatic activity of sCD26 with Sitagliptin significantly mitigated aGVHD and improved survival in late-infused female mice. Our study indicates that scheduling UCB transplantation in the early morning could be a simple and effective prophylactic strategy for aGVHD and that inhibiting sCD26 could be a promising therapeutic approach for late infusions.

CAR-intrinsic features, notably co-stimulatory domain choice, define the tonic NF-κB activation tone in resting CAR T cells. Metabolic refueling boosts these baseline states without overstimulation, suggesting it may be especially valuable for weaker CAR constructs. These findings provide a framework for tuning CAR T cell function through combinatorial design strategies targeting signaling and metabolism.

P1/2, N=118, Active, not recruiting, AstraZeneca | Recruiting --> Active, not recruiting | Trial completion date: Jul 2026 --> Mar 2027 | Trial primary completion date: Jul 2026 --> Mar 2027

In vitro, treatment with vildagliptin reduced the expression of Vimentin and the capacity for colony formation in H460 and LLC cell lines. The correlation of CD26 expression in lung adenocarcinomas and better patient survival, the antiproliferative effect on tumor cells by CD26 inhibition, and an altered EMT status give rise to the hypothesis that CD26 inhibitors impact the biology and clinical course of lung adenocarcinomas.

Monomethyl auristatin E (MMAE) is used as the cytotoxic payload for enfortumab vedotin (EV) in the treatment of locally advanced and metastatic bladder cancer (BC). In addition, the DPP4 inhibitor sitagliptin suppressed the proliferation, migration, and invasion of BC cells, and cotreatment with MMAE effectively induced cell apoptosis, arrested cells in the G2M phase of the cell cycle, increased reactive oxygen species production by inhibiting the AKT pathway, and significantly inhibited the in vivo growth of MMAE-resistant cells. This study provides insights into the use of DPP4 inhibitors as a treatment strategy for MMAE-resistant BC.

Including TRBC1 antibodies in a routine flow cytometry panel facilitates the identification of T-cell neoplasms. The analysis must be interpreted within its clinical context since T-cell lymphomas with a small and sometimes surface CD3-negative neoplastic T cell population, may display normal patterns of TRBC1-expression with a background of reactive T cells. Conversely, monotypic T-cells can be found in the absence of T-cell neoplasm.

These findings suggest that LKB1 loss suppresses DPP4 expression, contributing to the immunosuppressive characteristics of the TME in KL-NSCLC cells, whereas restoring DPP4 expression promotes NK cell recruitment, facilitates immune activation, and enhances the effects of anti-PD-1 therapy. These results suggest that DPP4 is a key immune modulator and a promising therapeutic target, providing a novel strategy to overcome immune resistance and improve immunotherapy outcomes in this challenging subset of lung cancer.