Figure 1.

A balance between carcinogenesis and cancer immunosurveillance system. Abnormal genetic modifications such as gene mutations, deletions, amplifications, copy-number variations (CNVs), chromosomal abnormalities, or instability and gene fusions can all result in abnormal expression of genes and proteins leading to transformation of a normal cell into a pre-cancer state and/or cancer stage. Similarly, abnormal epigenetics, such as aberrant DNA methylation patterns, histone modifications, and ncRNA expression (e.g., miRNA) levels, also cause tumorigenesis. Recently, abnormal RNA methylation patterns, such as m⁶A RNA post-transcriptional modifications (epi-transcriptomics), have been shown to result in the initiation and progression of cancer. Although these abnormalities in malignancy promote tumorigenesis, the cancer immunosurveillance system acts as a tumor suppressor working against the formation of pre-malignant and cancer cells. The cancer immunosurveillance system comprises the innate and adaptive immune systems that have various components that help to regress or eliminate tumor cells. However, some immune cells can be pro-tumor, which paradoxically help tumor progression in the tumor microenvironment. Cancer can evolve and escape the immune system by developing immunosuppressive escape mechanisms (such as high expression of PD-L1) that allow it to progress. This state can be reversed with immunotherapy, such as immune checkpoint inhibitors (ICPi).