How Damaged Genes Cause Cancer

Every person begins life as a single fertilized egg cell. Through a complicated process of growth, division, and specialization, the egg multiplies into the trillions of cells in a healthy body. Every cell contains complex instructions that direct this process. The instructions are chemically coded in long coils of a substance called DNA (deoxyribo nucleic acid). Particular sections of DNA make up genes that control specific cell functions. DNA even contains genes that enable the molecule to repair itself. But as people grow older, damage can build up and destroy DNA's ability to repair itself.

Cancer often results from damage to the genes that control cell growth and division. Two important classes of these genes are called proto-oncogenes and suppressor genes. Proto-oncogenes promote cell growth or division. Damage to a proto-oncogene may transform it into an overactive form called an oncogene. Oncogenes can lead to cancer by directing a cell to multiply excessively. Scientists have identified dozens of oncogenes that contribute to cancers in many sites, including the bladder, breasts, liver, lungs, and colon.

Suppressor genes limit cell growth or division. Damage to a suppressor gene can lead to cancer by destroying that gene's ability to stop cell multiplication.

Scientists think most cancers involve transformation of many proto-oncogenes into oncogenes and inactivation of a number of suppressor genes. In most cases, genetic damage must accumulate for years before a cell becomes cancerous. Once cancer occurs, the disorganized, rapidly dividing cells gradually build up into a mass that compresses and destroys nearby tissue. As the cancer grows, cells can break away and travel through blood or lymph (fluid from body tissues) to invade other parts of the body. This spread of cancer to other sites is called metastasis. The likelihood of curing cancer drops sharply after the tumor has spread.

People acquire the genetic damage that can lead to cancer in two main ways: (1) by inheriting damaged genes; and (2) through exposure to substances in the environment that damage genes.

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