How Does Cancer Develop?

By Linda L. Isaacs, M.D.

The short answer: we don’t know. Why not? We can’t predict when a cancer will form, either in people or in experimental animals. We can’t be on the scene when an individual cell first goes rogue. It’s microscopically small, and we don’t know where to look.

Descriptions of how cancer starts are not direct observations, but are theories, based on what is known about cancer. Theories in science are useful to guide experiments and develop treatments, but they need to be adjusted as new information comes in. Too often, theories become unquestioned dogma.

The most commonly accepted theory about cancer development is the Somatic Mutation Theory. In this model, cancer develops as a result of damage to the genetic material of adult cells. This theory is more than a century old. With a microscope, scientists back then could see that the nucleus of a cancer cell does not look normal.

The nucleus contains the chromosomes made of DNA, the genetic material that controls the manufacture of different proteins. In the Somatic Mutation theory, alterations to the genetic material change the function of the cell, leading it to divide uncontrollably, invade other tissues, and spread throughout the body.

Over the decades, the Somatic Mutation Theory has expanded, to the point where tumor samples are routinely analyzed for genetic mutations that are thought to promote cancer. These findings have led to the creation of “targeted therapies,” designed specifically to address the altered functions caused by genetic changes in cancer. Some less conventional approaches, such as using pharmaceuticals to “starve” the cancer, are also based in assumptions from the Somatic Mutation Theory.

What if it’s wrong?

Next Section: Problems with the Somatic Mutation Theory

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