Inflammation in Colorectal Cancer: Understanding Its Dual Role and Therapeutic Implications

Abstract

Colorectal cancer (CRC) continues to be a leading cause of cancer-related mortality, significantly influenced by both genetic and environmental factors. Although substantial progress has been made in early detection and treatment, sporadic cases account for over 70% of CRC diagnoses, with certain inherited syndromes further increasing risk. This review emphasizes the complex interplay between inflammation and CRC pathogenesis, examining three types of inflammation—chronic, tumor-elicited, and therapy-induced—and their roles in tumor initiation, promotion, and progression.

Chronic inflammation, particularly in conditions like inflammatory bowel disease, significantly increases the risk of cancer development and mutation accumulation. Additionally, inflammation induced by tumors contributes to immune evasion and fosters tumor growth through intricate intercellular interactions within the tumor microenvironment (TME). Therapy-induced inflammation can have dual effects, either suppressing or promoting recurrence.

Recent advancements in immunotherapy, especially the use of immune checkpoint inhibitors, have shown promising outcomes in specific CRC subtypes; however, challenges persist, particularly in proficient mismatch repair (pMMR) cases. Understanding the role of inflammation in various CRC contexts is crucial for developing targeted therapies and improving clinical outcomes. This comprehensive framework highlights the need for further research to dissect the complexities of inflammation in CRC, ultimately paving the way for more personalized treatment approaches.