Lani
05-31-2006, 07:42 PM
Appetite-Inducing Hormone Receptor Found Active in Breast Cancer
A hormone receptor with regulatory roles as diverse as food intake, fear response, and cardiovascular function may also be involved in breast cancer, according to University of Cincinnati researchers.
The UC research team, led by Hassane Amlal, PhD, and Sulaiman Sheriff, PhD, report their laboratory findings on the hormone, neuropeptide Y, and its receptor in the journal Cancer Research.
Earlier studies have shown that neuropeptide Y’s receptor, known as Y1, is overproduced in human ovarian, prostate and breast cancers. This study, however, is the first to demonstrate that the Y1 receptor is actually working in breast cancer cells and can be “turned on” by excessive estrogen—a known cause of about 60 to 70 percent of breast cancers, they say.
“The high incidence and activity of the Y1 receptor in human breast tumor cells suggests that it may play an important role in breast cancer,” explains Sheriff, a UC research assistant professor in the department of surgery.
Pilot data suggests that about 40 percent of all breast cancer patients have increased levels of the Y1 receptor, he says.
“We knew this receptor was overproduced in breast cancer tissue,” adds Amlal, a research assistant professor in the department of internal medicine, “but now the real question is what does it do in breast cancer cells, and how can we use it as a target to fight cancer.”
The UC researchers were able to slow the growth of breast cancer cells with abnormally high levels of the Y1 receptor by treating them with neuropeptide Y hormone produced by chemical synthesis.
“This finding gives us a promising new investigational target in the fight against breast cancer,” the authors report. “If we can find a way to selectively activate the Y1 receptor, we can limit breast cancer growth in the body.”
Further studies of the Y1 receptor’s role, they explain, may ultimately lead to more targeted drug therapy for many breast cancer patients.
SOURCES:
Cancer Research, April 2006
University of Cincinnati Medical Center (http://www.medcenter.uc.edu)
A hormone receptor with regulatory roles as diverse as food intake, fear response, and cardiovascular function may also be involved in breast cancer, according to University of Cincinnati researchers.
The UC research team, led by Hassane Amlal, PhD, and Sulaiman Sheriff, PhD, report their laboratory findings on the hormone, neuropeptide Y, and its receptor in the journal Cancer Research.
Earlier studies have shown that neuropeptide Y’s receptor, known as Y1, is overproduced in human ovarian, prostate and breast cancers. This study, however, is the first to demonstrate that the Y1 receptor is actually working in breast cancer cells and can be “turned on” by excessive estrogen—a known cause of about 60 to 70 percent of breast cancers, they say.
“The high incidence and activity of the Y1 receptor in human breast tumor cells suggests that it may play an important role in breast cancer,” explains Sheriff, a UC research assistant professor in the department of surgery.
Pilot data suggests that about 40 percent of all breast cancer patients have increased levels of the Y1 receptor, he says.
“We knew this receptor was overproduced in breast cancer tissue,” adds Amlal, a research assistant professor in the department of internal medicine, “but now the real question is what does it do in breast cancer cells, and how can we use it as a target to fight cancer.”
The UC researchers were able to slow the growth of breast cancer cells with abnormally high levels of the Y1 receptor by treating them with neuropeptide Y hormone produced by chemical synthesis.
“This finding gives us a promising new investigational target in the fight against breast cancer,” the authors report. “If we can find a way to selectively activate the Y1 receptor, we can limit breast cancer growth in the body.”
Further studies of the Y1 receptor’s role, they explain, may ultimately lead to more targeted drug therapy for many breast cancer patients.
SOURCES:
Cancer Research, April 2006
University of Cincinnati Medical Center (http://www.medcenter.uc.edu)