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U of M researchers develop model for better testing, targeting of MPNST
Date:5/20/2013

rs," said Eric Rahrmann, Ph.D., the paper's lead author and a postdoctoral fellow in the Largaespada lab. "When we turn off FOXR2, the growth ability of these MPNSTs drastically decreases."

Other findings showed interesting evidence of pathways that could be viable targets for therapeutics. The activation of the Wnt signaling pathway was shown to drive MPNSTs. This pathway has been highly implicated in colon cancer but not previously linked to MPNSTs.

Researchers also found many of the MPNSTs have dual loss of the genes called NF1 and PTEN. This pairing of lost genes causes MPNST formation. Both of these genes have previously been shown as pathways related to MPNSTs but it wasn't clear the extent to which they work together.

Now, researchers are applying these findings to the testing of therapeutics currently on the market for other drugs. This research is continuing both in the mouse model and within primary tumor settings of human cell lines.

"We want to know if these drugs, which are not currently directed at MPNSTs, could be repurposed to provide alternate therapies for patients," said Largaespada.

Researchers are also looking into more direct ways to target tumors through the Wnt pathway and paired NF1 and PTEN pathways, utilizing mouse models and human cell lines in the lab setting.


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Contact: Caroline Marin
crmarin@umn.edu
612-624-5680
University of Minnesota Academic Health Center
Source:Eurekalert

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