For most of his professional career, Dr. Gordon Woods has been an equine reproduction specialist. Known for ground-breaking research in equine cloning, his path seemed well defined – continue his research in equine reproduction at the University of Idaho, retire, and maybe do a little consulting on the side. But then, Dr. Woods had an “aha” moment.
“We were getting very frustrated trying
to produce in vitro-fertilized foals,”
said Dr. Woods, who now is the Director
of the Equine Reproduction Laboratory
and holds the John Alexander Chair in
Large Animal Reproduction. The Equine
Reproduction Laboratory is part of the
Animal Reproduction and Biotechnology
Laboratory, in the Department of Biomedical
Sciences, College of Veterinary
Medicine and Biomedical Sciences at Colorado
State University. “The problem
seemed to be that the embryonic horse
cells were not dividing. There was something
different with horse cells. I stepped
back. I had three graduate students, and
plenty of samples and we just started
looking. When I was attending veterinary
school here, Jim Voss (former CVMBS
dean) told me that for every mistake you
make for not knowing, you’ll make nine
for not looking. Eventually, we found what
we were looking for.”
What the research team found was a connection between calcium levels and cellular activity. In the horse, extracellular calcium (calcium levels outside of the cell) is high, higher than in humans, while intracellular levels are low. Once the team increased the calcium levels inside the cells, the success rate of transferred embryo cloning jumped. In 2003, the first cloned equine was born, Idaho Gem, followed shortly after by Utah Pioneer and Idaho Star. While that made the headlines and garnered national attention, Dr. Woods’ focus was shifting to an intriguing possibility. Cancer cells and embryonic cells share some of the same traits that allow them to rapidly divide. If low calcium levels in embryonic cells resulted in low rates of cell division, wouldn’t it follow that high calcium levels would result in high rates of cell division, similar to what occurs in cancer?
“Horses have a much lower incidence of cancer than humans and even when they do get cancer, the tumors are normally benign,” said Dr. Woods. “We were wondering, might this have something to do with the lower levels of intracellular calcium? In humans, 24 percent of us die of cancer while that number is only 8 percent in horses.”
Dr. Woods
looked at levels
of prostate specific antigen (PSA) in a study
group. Those with higher PSA levels
(which indicate a risk for prostate cancer)
also had higher levels of intracellular calcium.
Dr. Woods decided to try to find out
why. Using venture capital, he helped to
found a small biotech company, CancER2,
which did basic studies on the chemical
differences between stallion and man.
When the ERL chair position opened up
at Colorado State University, the opportunity
to further develop his cancer studies
and work with world-class programs in
calcium channels, oncology and reproduction
was one he couldn’t pass up.
“The environment at Colorado State
University is incredible for collaborative
research,” said Dr. Woods, who came to
CSU in January 2007. “With the Animal
Cancer Center, the Equine Reproduction
Laboratory, all the work in calcium channels
going on in the Department of Biomedical
Sciences, and the Animal
Reproduction and Biotechnology Laboratory,
there are just an amazing number of
extremely talented people here pushing
toward common goals. I also plan to work
with the Denver Medical Center, which
will enable us to enhance our studies in
human diseases using horse models.”
Dr. Woods now has two research applications in progress. The first focuses on determining why reproductive performance is not optimal in horses today. His research team will develop the potential to identify horses with low intracellular calcium levels and investigate what regulates those levels, as well as best methods for correcting imbalances giving the horse the opportunity to optimize reproductive success. His second study is a continuation of the high PSA/high calcium connection in prostate cancer, particularly with regard to calcium regulation.
