Cancer is characterized as a malignant tumor, defined by its ability to grow progressively, invade surrounding healthy tissues, and spread to distant sites through a process known as metastasis. These malignant cells are essentially altered versions of the body’s own cells, having escaped normal growth-regulating mechanisms and apoptotic signals, which leads to unchecked proliferation.
From an immunological standpoint, the immune system plays a vital role in cancer surveillance as part of its regular maintenance functions. However, cancer cells often develop mechanisms to escape immune detection. The interaction between cancer and the immune system is explained by a dynamic process called immunoediting, which occurs in three phases:
Elimination: The immune system detects and eradicates newly formed cancer cells.
Equilibrium: A state is reached where there is a balance between the immune-mediated destruction of neoplastic cells and the survival of a small population of cancer cells.
Escape: The most aggressive and least immunogenic tumor cells proliferate and spread, often aided by immune pathways, after developing sophisticated strategies to bypass the immune response.
Cancer cells express various tumor antigens that can be recognized by the immune system, which are categorized as follows:
Tumor-specific antigens (TSAs): Unique proteins arising from DNA mutations or viral infections, resulting in novel, non-self peptides.
Tumor-associated antigens (TAAs): Normal cellular proteins with abnormal expression patterns, such as embryonic proteins expressed in adults (oncofetal antigens) or overexpressed self-proteins.
To evade immune responses, transformed cells utilize several strategies, including downregulation of MHC class I expression, resistance to apoptotic signals, and impaired or blocked costimulatory signals necessary for T-cell activation. These factors can contribute to the establishment of an immunosuppressive microenvironment around the tumor. Additionally, chronic inflammation can paradoxically foster a pro-tumor microenvironment by promoting mutation accumulation and enhancing tumor progression.