Unlike bacteria or viruses, which infect the body from the outside, cancer originates in the body’s own cells. The disease begins deep in the cell nucleus, in the chromosomes that contain our genes.

Of the approximately 22,000 genes in human cells, several hundred are involved in the process of cell division. These genes ensure that division occurs in an orderly, controlled manner—that each step in the process occurs in the right order, at the right time, with the right prompts, and the right pace—and that, after a certain number of divisions, a cell dies.

Sometimes, a gene will acquire an abnormality that interferes with its ability to function. This can take several forms:

  • A mutation, in which the DNA within the gene is misspelled

  • A copying error, in which too many or too few copies of a gene are present

  • A translocation, in which a gene or section of gene gets sewn into the wrong section of the genome.

These errors can occur in a variety of ways. In some cases, they may be inherited from a parent. More often, they arise during one’s life, as a result of exposure to harmful chemicals such as those found in tobacco, exposure to too much ultraviolet light from the sun, or simply bad luck — a mistake made during the process of DNA duplication during cell division.

Most of the time, these non-inherited errors — known as somatic mutations — can be corrected by the cell. Cells have a variety of mechanisms for “proofreading” their DNA, for verifying that the letters of the genetic code are in the proper order and, when they are not, replacing them with the right letters. When the genetic derangements are so extensive that the cell cannot function normally, or that cell division threatens to veer out of control, special genes order that the cell die for the good of the body as a whole.

When these corrections are not made, or when a diseased cell fails to self-destruct, cell growth and division can begin to break free of their constraints. As more mutations occur, affecting more aspects of cell life, a cell may gain the ability to grow without restraint, to invade nearby tissue and drift to other parts of the body, hide from the immune system, and outlive its normal lifespan — to become, in effect, a cancer cell. The process usually occurs over a period of years.

Although these mutations give cancer cells a survival advantage over normal cells, they also create dependency — the cancer cell literally cannot live without them. Targeting such mutations with specially designed drugs remains one of the greatest areas of promise in cancer medicine.

This article was originally published on October 5, 2018, by Dana-Farber Cancer Institute. It is republished with permission.