Cancer Surveillance

Surveillance against tumors is governed by both intrinsic (non-immune) and extrinsic (immune) surveillance. While research on non-immune surveillance started as early as the 1960s when it was demonstrated that cell environment within and around can induce tumor-suppressing mechanisms, a major part of the progress is missing compared to immune surveillance. Part of the reason could be due to the fact that immune surveillance is seen to have more potential in therapeutic application in curing cancerous tumors compared to non-immune surveillance mechanisms. Many of the non-immune mechanisms are still under investigation as theories, although a few studies have shown their possibility. Contrary to this, there is a plethora of studies on immune surveillance. The immune system has been proven to have a role in the surveillance against tumors, thus conferring a certain degree of protection. However, not all tumor cells are successfully detected by innate immunity, and many of them have developed strategic ways of escaping adaptive immunity. The immunosurveillance in both animal models and humans shows overwhelmingly that cells with immunodeficiencies are more susceptible to tumor development. However, it is confounding that even immune-competent individuals develop tumors, and thus a significant process is responsible. Thus, immunoediting was proposed as a theory to explain why tumors can escape immunosurveillance. This chapter provides detailed evidence from animal and human tumors and analyses the mechanisms, pathways, and components implicated in tumor immune surveillance. The findings suggest that while immune surveillance could be the key to promoting immune function against the development of tumors, there is more research and understanding needed in the various mechanisms and cells implicated. This is because most, if not all, of the therapeutic studies using immune effectors have proved to be poor in preventing, treating, or regulating the development of tumors.