Dogs, humans, put heads together to find cure for br...(erinary neurologist Natasha Olby along w...)

Previous researchers had pinpointed a particular tumor-suppressing gene on human chromosome 22, known as NF2, as a possible contributor to meningioma. They believed that the deletion of NF2, with its tumor suppressing abilities, could trigger tumor growth.

In looking at genetic changes across the whole genome, Breen's team compared human chromosome 22 to its canine counterpart. In dogs, the region shared with 22 is "split up" across three separate dog chromosomes - numbers 10, 26 and 27- with the NF2 gene appearing on dog chromosome 26. The researchers discovered that in dogs with meningioma, chromosome 26, and hence NF2, was rarely affected, casting doubt on this gene as playing a significant role in the disease. Instead, dogs with meningioma frequently showed loss of parts of dog chromosome 27. This led the researchers to focus on the portion of human chromosome 22 that corresponds to canine chromosome 27.

"Now, instead of looking at 50 million base pairs that contain several hundred genes, we can focus on the portion of human chromosome 22 that is evolutionarily conserved with dog chromosome 27," Breen says. "By looking at dog and human meningiomas together we reduce the amount of searching we need to do 50-fold. It's the old needle/haystack dilemma, except that using information from dog and human tumors allows us to concentrate our search on the two percent of the haystack that actually contains the needle, and not spend time and resources on the other 98 percent."

Breen also noticed that the other chromosome involved for canines that suffer from meningioma is dog chromosome 17, which correlates with part of human chromosom
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