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New hope for breast cancer research from unlikely source
COLLEGE STATION, TX - There's new hope for breast cancer
research, and it's coming from a very unlikely place.
Researchers at the Texas A&M University College of
Veterinary Medicine & Biomedical Sciences recently published
articles in the journals Molecular and Cellular Biology
and Carcinogenesis which indicate that a protein long
suspected to play a role in Down Syndrome may also contribute to
treating this devastating disease.
It has long been known that Down Syndrome is caused when an
individual has an extra copy of the 21st chromosome, giving them a
total of three instead of the normal chromosome pair. With improved
medical care, people with Down Syndrome are now living longer,
healthier lives. With this advance came the observation that
individuals with Down Syndrome have a significant decrease in risk
for several types of tumors. Most striking is the observation that
women with Down Syndrome are 10-25 times less likely to develop
breast cancer. This effect is thought to be due to the presence of
one or more "tumor suppressor" genes on chromosome 21. However, the
identity of such genes has not been known, until now.
"Years of research into the genetics of Down Syndrome has helped
us to discover a very important gene on chromosome 21," said Dr.
Weston Porter, Associate Professor in the Veterinary Integrative
Biosciences Department. "This gene, called Single-minded 2 or SIM2
is thought to play an important role in Down Syndrome by regulating
neuron growth in the developing brain. Based on its developmental
role, we hypothesized that SIM2 may also be involved in breast
cancer, which is essentially a disease of uncontrolled growth."
For the last five years, Porter and his colleagues, Richard
Metz, Brian Laffin and Elizabeth Wellberg, have been using human
breast cells and mouse models as part of a research grant from the
National Institutes of Health to validate this hypothesis, and what
they have found is very promising. SIM2 is lost or suppressed in a
majority of human breast tumors, and deletion of the SIM2 gene
triggers rapid tumor growth in mice.
However, the process by which SIM2 suppresses breast cancer is
complex and not fully understood. This same protein which may hold
so much promise for breast cancer treatment is also thought to
contribute to the negative effects of Down Syndrome.
"As we move forward," said Porter, "it will be important for us
to understand the circuit of SIM2 and how it is turned on and off.
In light of the available data on breast cancer incidence in the
Down Syndrome population and our experimental data, knowing how to
turn SIM2 expression on and off and identification of down-stream
targets should have great therapeutic value."
While still in the early stages, this research represents a
promising weapon in the fight against breast cancer as it sheds
light on a previously unknown target to shoot for.
"What we are seeing now is a paradigm shift in breast cancer
research" said Porter. "For years we have gone after the wrong
kinds of cells. It was all about getting rid of the tumor itself.
This has led to a dandelion effect where, we didn't get to the root
and the cancers kept coming back and spreading. Now we're looking
at ways to get to the root of breast cancer, and not simply
shrinking the tumor to come back another day."
While it may be years before their research results in a
definitive treatment or cure, it is impacting our approach towards
understanding breast cancer today.
Angela G. Clendenin
Director, Communications & Public Relations
Ofc - (979) 862-2675
Cell - (979) 739-5718
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