Thirty years ago research in areas related to cancer genetics concentrated on the investigation of damage to genetic material, usually damage produced by cancer-causing chemicals. Researchers typically treated cells with a carcinogen, and then they looked for damage to the cells' chromosomes. At M.D. Andersen Cancer Center in Houston, one researcher looked at the cells from hundreds of breast cancer patients.
With the introduction of molecular biology techniques, researchers received a way to look more closely at the connection between DNA damage and the symptoms of cancer. The cancer research that involved molecular biology techniques came to be called cancer genetics. Scientists who had pursued graduate studies in medical genetics stood at the forefront of research on cancer genetics.
By the close of the 20th Century, those scientists had made some important observations.
Discoveries made in the field of cancer genetics had thus become the subject of TV news. In 1994 researchers had announced discovery of a genetic mutation that could cause breast cancer. They called it BRCA1. In 1995 other researchers found a second mutated gene, another gene that could cause breast cancer. They called that gene BRCA2.
Those discoveries helped to explain why some families had many family members with breast cancer. . The patients from those families tended to have an early onset of breast cancer, a cancer in both breasts, cancer of the ovary (in addition to breast cancer) or knowledge of a male family member who had had breast cancer. Research in the field of cancer genetics uncovered more information about such patients.
In February of 2002 a researcher in Australia announced the discovery of BRCA3. Details on that discovery disclosed that molecular biologists had uncovered yet a third mutation that could cause breast cancer. That finding, a benefit of the techniques used in cancer genetics, had reinforced the importance of the family history. Questions about family history thus became standard practice in all oncology clinics.
As genetic testing revealed the presence of BRCA1, 2 or 3 in certain families, the women in those families looked closely at information on the cancer genetics web. Many of those women thus read about Human Epidermal growth factor Receptor 2 (HER-2). Molecular biologists had learned that a healthy breast cell has 2 copies of the HER-2 gene. That gene makes the required HER-2 protein, a protein needed for growth, repair and division.
Information on cancer genetics web disclosed that breast cancer could be produced by an excess of the HER2 gene. The presence of a mutated HER2 gene could lead to production of an abnormally large amount of HER-2 protein. A mutation in the HER-2 gene could lead to erratic and supposedly unchecked cell growth.
One chemical did have the power to control the growth of the dividing breast cancer cells. That chemical was the drug named Herceptin. Herceptin was a monoclonal antibody, i.e. a protein with recombinant DNA Herceptin could bind selectively to cells with the "marker," the HER-2 protein,
Herceptin demonstrated the ability of cancer genetics to spur the development of cancer drugs that targeted only cancer cells.