Colorectal cancer (CRC) remains a predominant cause of global cancer-related mortality, largely due to the high incidence of systemic metastasis driven by the epithelial-mesenchymal transition (EMT). Although diagnostic and therapeutic advances have reduced mortality, approximately 20%–30% of patients are still diagnosed with metastatic disease, resulting in a poor 5-year survival rate of less than 15%. Understanding the genetic alterations underlying initiation, progression, and metastasis of CRC may help in the development of targeted therapies.

Driven by complex genetic and epigenetic dysregulation, colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide. The limitations of current targeted therapies necessitate the identification of novel molecular targets to overcome challenges associated with established treatment regimens.

Breast cancer progression is increasingly recognized as being shaped not only by protein-coding oncogenes but also by long non-coding RNAs (lncRNAs) that regulate gene expression across multiple cellular compartments. While many lncRNAs have been linked to tumor growth, how their subcellular localization contributes to coordinated oncogenic signaling remains incompletely understood.

A novel study using a mouse model has found that the absence of the angiopoietin-like 4 (ANGPTL4) protein during development triggers a long-lasting reprogramming of the immune system that protects against intestinal inflammation. The findings from the study in The American Journal of Pathology, published by Elsevier, may have important implications for identifying molecular or cellular signatures that predict disease susceptibility, and for developing therapeutic strategies that enhance protective immune programs in inflammatory bowel disease and inflammation-driven colorectal cancer.