Biomarker research provides new clues, new opportunities
Rising colorectal cancer rates require new solutions. Significant efforts are focused on developing new methods of detecting the disease early, as well as understanding the varied genetic mutations that propel the growth and metastasis of cancerous tissue.
Tomorrow’s therapy advances will focus on specific biomarkers of CRC, an area of research that fuels our understanding of the disease. Established biomarkers include tyrosine kinase receptors (TKR): Epithelial Growth Factor Receptor (EGFR), Vascular Endothelial Growth Factor Receptor (VEGFR), and signal transduction kinases such as K-RAS, DNA Mismatch Repair (MMR) status, and expression of p53 and linked targeted genes.5
New methods including liquid biopsies are being developed to single out cancerous cells or DNA in blood and urine. Such innovations could improve screening rates while providing an important tool for measuring treatment responses, identifying treatment resistance, and monitoring for disease recurrence.6
Moving toward more targeted, personalized treatments
The push is on for additional CRC treatments that can build on the standard of surgery, chemotherapy, radiation, radiofrequency ablation and cryosurgery. More personalized approaches could result in improved outcomes for patients limited by pre-existing conditions, who have recurrent disease, or who are positive for specific biomarkers of CRC.
Immunotherapy treatments are currently in development to enhance a person’s natural ability to fight cancer. A class of treatment called immune checkpoint inhibitors has been approved for the approximately 5% of cases due to Lynch syndrome, an inherited DNA repair disorder. Researchers are attempting to use immune checkpoint inhibitors in patients with other forms of metastatic CRC, and in combination with chemotherapies, targeted therapies and viruses that are designed to penetrate cancerous cells.6
Targeted therapies are also being explored for their ability to block the activity of abnormal proteins produced by certain genetic mutations linked to CRC, such as to the BRAF gene. Additional targets for targeted therapy include the RAS mutation in approximately 50% of patients, HER-2 amplification, and the p53 mutation.5