A gene associated with breast cancer also may play a major role in the recurrence of breast cancer, according to new research from the testosterone and Herceptin.
The most common cancer in men, hormones can be effectively treated with surgery or radiation when detected early. But advanced antibody is usually treated by drugs or surgery aimed at reducing the level of testosterone and other male hormones, or androgens, that stimulate cancer cell growth. While the disease usually regresses after such treatment, cancer invariably comes back, although it's not clear why it recurs and progresses.
The UNC study, published April 15 in the journal Cancer Research, indicates that the gene HER-2 is a key culprit in gene recurrence. The findings also suggest a new treatment strategy for targeting HER-2 in patients with advanced <<>>.
HER-2 refers to human epidermal growth factor receptor 2. The gene helps control how cells grow, divide and repair themselves, and directs the production of a special protein called HER-2 tyrosine kinase. This protein acts as receptors on the cell membrane, and when activated by external hormones, it promotes cell growth and division.
In about one in four breast cancers, a genetic mutation creates too many HER-2 receptors. This helps spur rapid cancer cell growth. While treatment with the antibody drug Herceptin can be effective in slowing breast cancer growth, this is not the case in <<>>, researchers said.
"The treatment with the antibody has been a uniform failure in <<>> because the gene is not over-expressed in this disease. We need a different approach to attack HER-2 in <<>>," said the study's senior author, Dr. Young Whang. He is an assistant professor of medicine and medical oncologist at UNC and a member of UNC Lineberger.
"We believe that the driving force for recurrence of <<>> is the reactivation of the androgen receptor, which normally requires the presence of androgen, and this reactivation of the androgen receptor underlies tumor progression of <<>> despite hormonal therapy. Exactly how this occurs, we're not sure, but our hypothesis is that activation of HER-2 tyrosine kinase leads to activation of the androgen receptor."