DUSP4 (Dual Specificity Phosphatase 4)

Western blotting and qRT-PCR analyses confirmed that STAT3 and DUSP4 expression was significantly upregulated after AMI (P < 0.001). In summary, STAT3 and DUSP4 are key biomarkers of acute myocardial infarction and may hold promise as targets for personalized therapeutic strategies in AMI.

Pharmacological activation of the p38 MAPK/MK2 pathway abolished the cardioprotective effects mediated by DUSP4 overexpression. Collectively, these findings demonstrate that DUSP4 alleviates DOX-induced cardiotoxicity by suppressing the p38 MAPK/MK2 signaling cascade, highlighting the DUSP4 axis as a potential therapeutic target to improve cardiac safety during DOX-based chemotherapy.

A novel EGFR mSig that captures the transcriptional footprint of EGFR activation revealed a subset of EGFR WT LUADs with "mt-like" features. mSig refines LUAD taxonomy beyond mutation-only pie-chart models by incorporating lineage and co-mutation context. Lineage-directed stratification with co-alteration identifies clinically relevant groups across EGFR and RAS states and highlights new treatment opportunities for patients currently considered "oncogene-negative.".

Targeting KDM5B and USP7 synergistically represses tumor progression and increases sensitivity to cisplatin. Overall, we propose two new UPS-associated proteins, USP7 and FBXW7, which are responsible for abnormal KDM5B protein regulation, and suggest a novel mechanism to overcome cisplatin resistance in OVC by targeting the KDM5B-DUSP4 axis.

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.