Archive for February, 2008
Enzyme reinforces tumor-causing role of the nuclear coactivator SRC-3
HOUSTON -- (February 29, 2008) -- High levels of the enzyme atypical protein kinase C (aPKC) increases the activity of the cancer-associated protein steroid receptor coactivator-3 (SRC-3) in cancer cells that depend on estrogen to promote their growth, said researchers at Baylor College of Medicine in Houston in a report that appears in the current issue of the journal Molecular Cell.
"This finding has implications for better understanding diseases such as breast cancer," said Dr. Bert O'Malley, chair of molecular and cellular biology at BCM and senior author of the report that investigated the relationship between SRC-3 and the enzyme.
Results link aPKC with cancer
Atypical protein kinase C is frequently found at high levels in tumors as is SRC-3. In this study by BCM researchers, experiments demonstrated that the enzyme activates and stabilizes (through adding a phosphate molecule) the coactivator SRC-3 in a way that makes it dependent on the presence of a cellular receptor for the hormone estrogen.
"These results link the aPKC with cancer initiation and growth that is dependent on estrogen," said O'Malley, also associate director of basic science research in the Dan L. Duncan Cancer Center at BCM.
Kinases
This activity takes place in an acidic area of the SRC-3 molecule and prevents the coactivator from being degraded, said O'Malley. This is important because SRC-3 is known to induce cancer and to promote its growth. Other studies had already demonstrated that other kinds of kinases could degrade SRC-3.
"Kinases that stabilize SR-3 in cancer cells have not previously been reported," said O'Malley.
"We propose that when aPKC is overexpressed in cancer cells, the consequence is increased SRC-3 function and powerful enhancement of estrogen-receptor target gene transcription and promotion of estrogen-dependent cell growth in cancer cells such as breast," he said.
Others who took part in the study include Ping Yi, Qin Feng, Larbi Amazit David M. Lonard, Sophia Y. Tsai and Ming-Jer Tsai, all of BCM.
Funding for this work came from the National Institutes of Health, the National Institute of Child Health and Human Development and the U.S. Department of Defense Breast Cancer Research Program.
The article is available at http://www.molecule.org/
Added strategy may provide better handle on annual flu epidemic
HOUSTON -- (February 28, 2008) -- Vaccinating school-age kids up to age 18 not only protects youngsters, but the entire community, say flu experts at Baylor College of Medicine in Houston.
This added strategy by the Centers for Disease Control and Prevention’s Immunization Advisory Committee was needed to try to get a handle on the annual flu epidemic, but Glezen says the biggest hurdle now is developing the infrastructure to deliver vaccines to this population.
"If we develop the infrastructure, vaccinating this age group will be a great way to reduce illness in the family and in the entire community," said Glezen. "Having an infrastructure in place will also put us in better shape for the next pandemic."
The indirect effects of vaccinating all school-age children are significant because they are the primary spreaders of flu illness every year. But Glezen says that for these recommendations to work, it will require cooperation between medical groups, public health professionals and the schools.
Read additional flu information at http://www.bcm.edu/news/features/item.cfm?newsID=1066.
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