DUSP4 (Dual Specificity Phosphatase 4)

These findings suggest that mesalazine differentially modulates DUSP gene expression in normal and malignant colon epithelial cells, potentially contributing to its antiproliferative and pro-apoptotic effects through the regulation of MAPK signaling. These results provide new insights into the molecular mechanisms underlying the anticancer effects of mesalazine in colorectal cancer.

Although MAPK alterations are pervasive in CRC, their distribution varies meaningfully by ancestry, age, and treatment exposure. These findings highlight NF1, MAPK3, RPS6KA4, and PDGFRB as potential biomarkers in EOCRC and H/L patients, supporting the need for ancestry-aware precision oncology approaches.

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.

Collectively, this study shows that direct stimulation of TILs with anti-CD3 mAb and CD28 co-stimulation achieves efficient expansion of tumor-reactive TILs. Genetic engineering of cytokine signaling in TILs may further enhance TIL functions and replace cytokine administration after TIL infusion.

Lineage-informed classification highlights subtype-dependent oncogene activity and supports new therapeutic strategies. A context-specific association between RAS mutation and expression of the dual-specificity phosphatase gene DUSP4 may have therapeutic potential.

DUSP5 silencing-induced growth suppression was partially due to G1 cell cycle arrest, associated with p21 upregulation. Collectively, our findings highlight DUSP5 as a potential therapeutic target for lung cancer.

DUSP4 acts as a negative regulator of ferroptosis and a positive regulator of CD8+ T cell infiltration in MSI CRC.

Our findings provide clues for prognosis evaluation in BM patients. They also establish a theoretical basis for predicting immunotherapy efficacy.

DUSP4/NLRP3/caspase-1/GSDMD-mediated pyroptosis is demonstrated to be the therapeutic mechanism of plumbagin in CCA.

We establish FENDRR as a tumor-suppressing gene that plays a significant role in suppressing the advancement and metastatic spread of COAD. These findings underscore its diagnostic and prognostic utility in COAD.

Our study elucidates clonal evolution in gastric cancer peritoneal metastasis, identifies mutational drivers, and highlights potential therapeutic targets. These findings provide valuable insights for developing precise treatment strategies for gastric cancer patients with peritoneal metastasis.

The classic OSF-inducing molecule arecoline significantly increases the expression of INHBA (p < 0.0001) in vitro experiments stimulating THP-1 cells...The increased INHBA+Mac and iCAF in ODSCC are associated with the observed more severe TISME. The upregulated INHBA in ODSCC and its interaction with INHBA-ACVR1/ACVR2A/ACVR2B may mediate the modulation effect of INHBA+ Mac and iCAF on Treg differentiation and functionality.