Cancer cells develop as a result of damage to deoxyribonucleic acid (DNA). Located in every cell, DNA is the molecule that directs all cell activities including growth, division and function. Usually the body is able to repair DNA when it is damaged. However, in cancer cells damaged DNA may not be repaired normally.

Damaged DNA can be inherited from a parent, or more commonly, normal DNA can become damaged by environmental factors. Chemicals, radiation, viruses and heredity all play a role in the development of cancer by producing changes, or mutations in DNA. In some cases, DNA mutations occur for no apparent reason.

Genes are made of the chemical bases that form DNA. They contain information that determines an individual’s outward appearance, including hair color, eye color and height. They also contribute to an individual’s risk of developing certain diseases, such as some types of cancer. Genes are carried on chromosomes. Normally, humans have 23 pairs of chromosomes. In each pair, one member is inherited from the person’s father, and the other member is inherited from the person’s mother. Each chromosome contains many genes, hundreds or thousands for some chromosomes.

Mutations can be seen in many types of genes. However, the following types of genes are most often associated with cancer-linked mutations:

• Oncogenes. Genes that promote cell division. Oncogenes develop from the mutation of normal genes (proto-oncogenes). Proto-oncogenes instruct cells to produce proteins involved in growth control. While oncogenes also perform this function, they order a distorted version or excessive amounts of the proteins. As a result, the presence of an oncogene causes a cell to continually grow and divide.
  
  The presence of oncogenes in certain forms and/or overactivity can trigger the development of cancer. In healthy cells, oncogenes can contribute to cancer development by ordering cells to produce proteins that encourage excessive cell growth and division.
  
  
• Tumor suppressor genes. Genes that instruct cells to manufacture proteins responsible for slowing cell growth and division. The absence of tumor suppressor genes has been linked to cancer development.
  
  The p53 gene is a particular type of tumor suppressor gene that produces a protein that causes apoptosis, or cell suicide, which is a normal occurrence. When the DNA in a cell is damaged, the p53 protein normally stops cell growth and division. When the DNA damage cannot be repaired, the p53 protein will initiate apoptosis, thus preventing the damaged cell from growing uncontrollably.
  
  Cancer may develop when a pair of tumor suppressor genes are either lost from a cell or inactivated by mutation. Such an absence would cause cells to uncontrollably grow and divide.    
  
  People who inherit an increased risk of developing cancer are frequently born with one defective copy of a tumor suppressor gene. Because genes come in pairs, an inherited defect in one copy will not lead to cancer because there is another normally functioning copy. Cancer may develop only when the second copy undergoes mutation, and the patient no longer has a normally functioning copy of the gene.
  
  
• DNA repair genes. Genes that instruct cells to produce proteins required to correct errors that may occur when cells duplicate their DNA prior to division. When these genes become mutated they can fail to repair, allowing additional mutations to build up.

Usually multiple mutations must occur for cancer to develop. It may develop as the result of an accumulation of mutations involving oncogenes, tumor suppressor genes and DNA repair genes. Cancer can begin with a defect in one type of gene, such as a tumor suppressor gene, that allows excessive cell production. The cells often acquire additional mutations involving DNA repair genes, other tumor suppressor genes and several other growth related genes. Eventually the accumulating mutations can produce a highly malignant (cancerous) tumor that is able to metastasize (spread).

Genes can be mutated in several ways. Researchers have identified a number of DNA mutations that “turn on” oncogenes and “turn off” tumor suppressor genes, thereby causing cancer to develop. These include:

• Translocations. The transfer of DNA from one chromosome to another.
  
  
• Deletions. The loss of part of a chromosome.
  
  
• Inversions. The rearrangement of DNA in part of a chromosome.
  
  
• Additions. All or part of a chromosome is duplicated and too many copies are found in a cell.

Although these mutations have been identified and connected with cancer, researchers are still unaware of exactly how the mutations happen and why they occur in some people but not in others. While causes are unknown, certain factors have been found to increase the risk of cancer, including tobacco and alcohol use, excessive exposure to ultraviolet rays and unhealthy diet.