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Cancers are capable of spreading through the body by two mechanisms: local invasion and distant metastasis. Invasion refers to the direct migration and penetration by cancer cells into neighboring tissues. Metastasis refers to the ability of cancer cells to penetrate into lymphatic and blood vessels, circulate through the bloodstream, and then invade normal tissues elsewhere in the body. Cancer is most deadly when it metastasizes.

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.

In cellular model systems, cells are exposed to carcinogenic influences (chemicals, radiation). In these systems, the first signs of a cell developing into a tumor cell are:

  • Immortality. The usual number of cell divisions for a mammalian cell is 50-60 (cell senescence), then it ceases to divide. Tumor cells keep dividing forever.
  • Altered morphology.
  • Building of cellular clusters (Foci).
  • Loss of contact inhibition.
  • Low or no need for growth factors.

Items 2-4 (above) can sometimes be traced to mutations in genes that result in a disruption of cell adhesion. Some cell adhesion proteins are oncogenes.