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. 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. In their normal state, proto-oncogenes encode for proteins involved in cell cycle regulation that control cellular growth and division. But gain-of-function mutations in proto-oncogenes turn them into overactive forms called oncogenes that make the cells grow out of control, leading to cancer. In most cases, these cancer-causing mutations are acquired and not inherited. Some of the most common examples of proto-oncogenes in humans are Ras, HER2, Myc, and Cyclic D.
The major difference between proto-oncogenes and tumor suppressor genes is that proto-oncogenes lead to cancer upon over-activation, while tumor suppressor genes cause cancer when they are inactivated
