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How 'phenotype switching' can make melanoma become metastatic and resistant to drugs
Date:10/19/2013

BRAF cell lines to determine their Wnt5A and ROR2 status, as well as their sensitivity to BRAF inhibitors, the researchers found a significant correlation between BRAF inhibitor resistance and Wnt5A expression. Additionally, in a small cohort of patients, they found that seven out of nine patients who demonstrated less than a 33 percent clinical response to vemurafenib had a positive expression of Wnt5A, and only two of the remaining 15 patients who had a 38% or greater clinical response to vemurafenib exhibited any Wnt5A expression. When they silenced ROR2 in tumors xenografted in mice, the tumors responded far better to simultaneous treatment with the BRAF inhibitor vemurafenib. Conversely, when ROR1 was silenced, the tumors became more resistant to the drug.

Additionally, in eight patients who had undergone BRAF inhibitor therapy, the levels of Wnt5A were much lower in tumor cells prior to therapy compared to cells that were tested for Wnt5A after those same patients had relapsed.

"By using Wnt5A as a biomarker, we could determine which patients are likely to respond better to therapy with vemurafenib and help prolong that response," Weeraratna said. "There is also the potential to explore small molecule inhibitors of ROR2, since there is now a clear association between that and the ability of melanoma to become not only metastatic, but also therapy-resistant. This link between metastasis and therapy resistance is what we find the most exciting and intriguing, as therapies designed to target one process may have a significant impact on the other as well. "


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Contact: Ben Leach
bleach@wistar.org
215-495-6800
The Wistar Institute
Source:Eurekalert

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