The general feature of cancer is uncontrolled cell division, which leads to a mass of cells called a tumor. A tumor is considered benign until it starts to invade nearby tissues, at which point it is then malignant.

In healthy cells, proliferation is tightly regulated through a complex network of positive and negative regulating factors. These factors make sure that cells divide only when they are supposed to. When genes encoding the positive regulators are mutated to produce over-active proteins, they are called oncogenes. Some viruses cause cancer through inserting their own copies of oncogenes into healthy cells. For example, the viral version of the SRC enzyme, a key molecule involved in cell signaling, is missing the regulatory domain that controls the human version. The lack of this domain triggers uncontrolled division in the host cells.

As opposed to oncogenes, tumor suppressor genes encode proteins that negatively regulate proliferation. When they are mutated, cell division proceeds unchecked. Up to 50% of human tumors have mutations in the tumor suppressor gene coding for p53. This multifunctional protein is essential for cell cycle control and apoptosis. Uncontrolled cell proliferation leads to tumor growth. This means that the cells need more oxygen and nutrients. In a process called angiogenesis, they produce growth factors that promote blood vessels to form in the tumor.

The more the tumor keeps growing, the more the cells keep dividing and changing, the higher the chance that cells can break free from the tumor and spread elsewhere in the body. The spread of cancer cells from the tumor is called metastasis, and is responsible for nearly 90% of cancer-related deaths. A major challenge to the treatment of cancer is the fact that it is not just one disease, each cancer patient has specific gene mutations, and every tumor is composed of a different group of mutated cells.