In a summer research project, Leah Stokes ’04 and Sarah Murray ’04 teamed with Dr. Nian Chen, Assistant Professor of Biology, to study the role that the hormone prolactin plays in human breast cancer. “Prolactin is one of the female hormones,” said Dr. Chen. “It is primarily responsible for stimulating breast tissue growth, and is especially active after child delivery as it sends signals for milk production.”
Unfortunately, prolactin can also ignite the abnormal growth of breast cells leading to cancer. For prolactin to stimulate cell growth, it needs to first bind to a receptor, which is the receiving site on the cell surface. The signal is then passed down through a variety of messengers inside the cells, and is eventually transmitted to the nucleus of the cell where it stimulates cell growth.
Through the collaboration with Dr. Wen Chen, a Clemson Professor and breast cancer specialist working at Greenville Hospital System Cancer Research Center, the Converse team set up shop to examine the intracellular signal transducers for prolactin. “Specifically,” says Leah, “we want to clone a gene called JAK2, whose protein product is thought to be the first carrier in prolactin signal transduction pathway. JAK2 is found in normal healthy cells, but its activity is noticeably elevated in breast cancer cells.”
After eight weeks of work, the team has purified three DNA segments of JAK2 gene by using several different molecular biology techniques. These DNA segments will be linked together to form a complete gene, which will be expressed and examined in animal cells. The researchers hope that once JAK2 gene is successfully cloned, the mechanism of prolactin signal transduction will be better understood.
“Prolactin is an especially interesting hormone,” Dr. Chen says. “For many years, health workers thought that estrogen was the only female hormone responsible for the development of human breast cancer. However, recent studies have shown that prolactin is also playing a significant role. Breast cancer cells were found to produce prolactin, which acts on its own receptors on the same cells. This presents a vicious circle as the mutated cells begin to reproduce wildly.”
Dr. Chen plans to continue her research at the Greenville lab. “We will continue to seek better understanding of the mechanism for prolactin’s tumor stimulating effect. This may help the generation of new breast cancer therapeutics.”