Oncogene Spawns Further Mutation in Study.(breast cancer)

2001 FEB 22 - (NewsRx.com) -- Researchers at the University of Pennsylvania School of Medicine described how the human myelocytomatosis (MYC) gene can select for spontaneous mutations in other genes - leading to more tumor growth even after the MYC gene is shut off.

Their study, published in the January 2001 issue of Nature Medicine, has implications for the search for therapeutics in cases of MYC-induced breast cancer.

"MYC is an oncogene, a gene that has the potential to cause cells to grow out of control, resulting in tumor growth," said Lewis A. Chodosh, PhD, University of Pennsylvania School of Medicine. "MYC-induced tumors tend to behave more aggressively than other forms of breast cancers, and we were looking to better understand why."

The researchers had primarily set out to study a larger mystery: why women who give birth at a younger age are less likely to develop breast cancer later in life. Part of the difficulty was finding an animal model that could mimic this phenomenon. A transgenic mouse, one whose DNA included a cloned human gene, would over-express the oncogene continually, not just later in life.

Instead, they created a strain of mice that would express human MYC on demand. By mating transgenic MYC mice with a strain of mice that would turn genes on in the presence of an antibiotic, the researchers were able to create mice whose MYC gene would turn on in the presence of a particular antibiotic, doxycycline. As a result, the researchers had a mouse whose MYC gene could be turned on or off at will to simulate MYC-induced breast cancer.

The effort paid off well for the purposes of research: ...