Scientists at the McGill University Health Centre (MUHC) have made an important discovery that will advance our understanding of how the female hormone estrogen causes growth of breast cancer cells. The research, in collaboration with scientists at the Institut de Recherches Cliniques de Montreal (IRCM) identifies 153 genes that respond to estrogen and one in particular that can be used to halt the growth of breast cancer cells.
The study, published in the Proceedings of the National Academy of Sciences (PNAS), will focus future research for a breast cancer cure. "We have known for a very long time that estrogen causes the growth of breast cancer cells," says lead investigator Dr. Vincent Giguère. "This is how oncologists came to use anti-estrogen as drugs to combat the most common forms of breast cancer." What has remained a mystery however, is the molecular mechanism by which estrogen makes breast cancer cells grow. "Until this is solved, we will be no closer to figuring out how to prevent and cure breast cancer," Dr. Giguère noted.
Over the past two decades researchers have identified around 20 estrogen-activated genes that play a role in development of breast cancer. "That's about one gene discovery per year," says Dr. Giguère. "Using cutting edge new technology derived directly from the human genome project, this study adds over hundred additional genes to this total."
The technology used information obtained from the human genome project to create a new type of DNA microchip containing the partial DNA sequences of approximately 19,000 genes. Dr. Giguère's team was able to localize where the estrogen receptor was bound in the genome of breast cancer cells, thereby identifying a large number of genes that respond to this hormone in a single experiment. "This technology, first developed for the study of yeast, now offers the opportunity to rapidly identify, in a genome-wide manner, the genes involved in the response to natural hormones or drugs in normal and cancer cells," says co-author Dr. François Robert from the IRCM.