Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression of the cells. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act as the drivers for cancer are termed cancer-critical genes and are categorized into two broad classes – proto-oncogenes and tumor suppressor genes. Tumor suppressor genes under normal conditions slow down cell division, repair errors in DNA, or control cell apoptosis. The loss-of-function mutations in tumor-suppressor genes make cells grow out of control and contribute to the development of cancer. Except for a few mutations in tumor-suppressor genes, which are inherited, most are acquired. Tumor suppressor genes like INK4, p53, and PTEN are very commonly mutated in many cancer types.
The major difference between proto-oncogenes and tumor suppressor genes is that oncogenes result from the overactivation of proto-oncogenes, and tumor suppressor genes cause cancer when they are inactivated.
