Lactate derived from CAFs mediates H3K18la in stemness gene promoters, which promotes tumor malignant phenotype formation

METTL1/USP48 Axis Stabilizes LCN2 Expression to Promote the Malignant Phenotypes of Cutaneous Squamous Cell Carcinoma.

M2 macrophage-derived exosomal EHF transcriptionally activates FGFR1 to promote malignant phenotypes and glycolysis in NSCLC

In vivo experiments demonstrated that exosomes from EHF-silenced M2 macrophages inhibited tumor growth and downregulated proliferation markers, and highlighted the EHF/FGFR1 axis as a novel molecular link between macrophages and NSCLC cells.

CAF-derived BHB modulates FXR1-Kbhb and NK-cell lipid metabolism in osteosarcoma

Osteosarcoma (OS) is the most common primary malignant bone tumor in children and adolescents and is characterized by high aggressiveness and poor prognosis. Although surgery and chemotherapy have improved overall survival, outcomes for relapsed or metastatic disease remain extremely poor, thus underscoring the urgent...

HDAC4 Promotes Cancer Stemness in Nonsmall Cell Lung Cancer by Upregulating SLC38A2 Expression via HIF‐1α to Enhance Glutamine Metabolism

Background and Purpose The malignant progression of nonsmall cell lung cancer (NSCLC) is closely related to cancer stemness. Histone deacetylase 4 (HDAC4) plays a regulatory role in lung cancer, but its effect on NSCLC stemness remains unclear. This study aimed to investigate the role and mechanism of HDAC4 in NSCLC st...

HIST1H4L promotes small cell lung cancer tumorigenesis by regulating the PI3K/Akt pathway and serves as a potential diagnostic biomarker

HIST1H4L was significantly upregulated in SCLC tumors versus normal tissues and enriched in DNA transcription-related pathways and correlated with poor patient survival; critically, high HIST1H4L expression correlated with poor patient survival.

Abstract A062: SFRP2 Silencing Restrains Pancreatic Cancer Growth and Enhances Survival Through Remodeling of the Tumor Microenvironment

Findings identify SFRP2 as a key regulator of PDAC progression and support the development of SFRP2-targeted therapies as a novel treatment strategy for pancreatic cancer.