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The research team, which included U of
I pathobiology professor Anne Barger, examined the homeostatic role
of an enzyme, a receptor activator of nuclear factor kappa-B, known
as RANK, and two key modulators of its activity: RANK ligand, known
as RANK-L, and osteoprotegrin, known as OPG. RANK is one of a family
of receptors that regulates bone and immune homeostasis. In health,
RANK, RANK-L and OPG together keep the continual process of bone
growth and resorption in balance.
Bone tumors presumably derail this homeostatic process, however,
by upregulating RANK-L expression. RANK-L binds to RANK, stimulating
the production and activation of osteoclasts, which are bone cells
that increase the breakdown of bone tissue).
OPG counter-regulates RANK-L by blocking its ability to bind to
RANK.
Eventual therapeutic interventions may make use of OPG or other
RANK-L inhibitors to slow the process of bone destruction in
skeletal tumors in cats and dogs, Barger said. Although not a cure,
this could reduce the pain and other complications associated with
bone cancer. Such therapies have proven effective at reducing
pathologic bone loss in human bone cancer patients.
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 The researchers are the first to verify that the expression of
this protein, which worsens the effects of bone cancer in humans,
also occurs in cats and dogs with skeletal tumors. Their study
appears in the January-February issue of the Journal of Veterinary
Internal Medicine.
"Osteosarcoma is much more common in veterinary medicine than in
human medicine," Barger said. "And in dogs it is fairly common."
Other studies have reported a 10-fold greater incidence of bone
cancer in dogs than in humans.
"Owners often make decisions to euthanize based on pain," Barger
said. "If we can lessen the pain associated with the tumor, we can
improve the quality of life and the lifespan."
[Text from
news
release from the University of Illinois at Urbana-Champaign]
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