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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.

Carcinogenesis (lit.: creation of cancer) is the process of derangement of the rate of cell division.