Researchers have developed a new mRNA-based immunotherapy that effectively suppresses colorectal cancer in mice. Using lipid nanoparticles to deliver mRNA encoding anti-PD-L1 nanobodies, the treatment reduced tumor growth in both sporadic and colitis-associated colorectal cancer models. The quadruple nanobody format showed superior efficacy by prolonging therapeutic activity and enhancing anti-tumor immunity. This approach represents a promising alternative to conventional antibody therapies, particularly for cancers resistant to current immunotherapies.

The study involved over 278,000 people who were randomly offered either a primary colonoscopy; two faecal immunochemical tests (FIT), where the patients provided a stool sample, which was followed by a colonoscopy if one of the samples was positive; or no intervention at all, termed usual care. At the end of the follow-up period, the clearest results were seen in the group where the participants had done FITs. There, 0.61 per cent developed colorectal cancer, compared to 0.73 per cent in the control group. 

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.

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.