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For most of the cancers, it cannot be told which event was the initial cause. However, with molecular biology, it is possible to characterize the mutations within a tumor, and to a certain extent predict its behavior. For example, about half of the tumors are deficient in the tumor suppressor gene p53, also known as "the guardian of the genome". This is associated with poor prospects for the patient, since those tumor cells are unlikely to go into apoptosis (programmed cell death) after they are damaged by therapy. There are more mutations that make a tumor more malignant. Telomerase mutations enable a tumor cell to divide indefinitely. Other mutations enable the tumor to grow new blood vessels to feed it, or to detach from the surrounding tissue, spreading to other parts of the body.

Cancer is, ultimately, a disease of genes. Typically, a series of several mutations is required before a cell becomes a cancer cell. We distinguish between oncogenes, which promote cancer when "switched on" by a mutation, and tumor suppressor genes, which prevent cancer unless "switched off" by a mutation. These mutations can have various causes: radiation or chemicals called carcinogens; some inherited predisposition is not uncommon; some viruses that can cause cancer have also been described. Usually, they carry in their genome some oncogene or tumor suppressor inactivating gene. In about 15% of all cancers, viruses seem to play a role; Bacteria, like Helicobacter pylori, also induce carcinogenesis by a process of chronic inflammation. Finally, damage by free radicals, which are a natural by-product of oxygen metabolism, can cause mutations in the DNA.

A cell that degenerates into a tumor cell does usually not acquire all these properties at once, but its daughter cells are selected to build them. This process is called cellular evolution. A first step in the development of a tumor cell is usually a small change in the DNA, often a point mutation, which leads, among other things, to a genetic instability of the cell. The instability increases to a point where the cell loses whole chromosomes, or has double ones. Also, the DNA methylation pattern of the cell changes, activating and deactivating genes more or less at random. Cells that divide at a high rate, such as stem cells, show a higher risk of becoming tumor cells than those which divide less or not at all, for example neurons. If the initial tumor cell (or group of tumor cells) is not removed by the immune system, it will develop into cancer.