In colorectal cancer (CRC), circulating tumour cells (CTCs) employ genetic alterations to dodge the body's immune system. These alterations occur in specific "driver" genes, including KRAS, BRAF, p53, MYC, APC and PTEN. Changes in these genes can control how the tumour interacts with the immune system and influence the expression of immune checkpoint molecules such as PD-1, PD-L1, PD-L2, CTLA-4 and CD47. These molecules help suppress the immune system's response against the tumour, thus promoting tumour growth. However, the precise relationship between driver gene mutations and the expression of immune checkpoint molecules in CTCs, along with their clinical significance, remains incompletely understood. By studying these genetic changes and how they affect the behaviour of CTCs, researchers can gain critical insights into the development and progression of CRC, especially the roles of CTCs, which could improve CTCs' implications in liquid biopsy. Moreover, understanding these alterations can also highlight potential therapeutic targets. This may pave the way for more effective, targeted therapies to delay or prevent CRC progression. Therefore, investigating the genetic alterations in CTCs and their role in immune escape mechanisms is a significant area of study in CRC research.
Aktar et al. (Sun,) studied this question.