Abstract
9005 Background: Resistance mechanisms acquired during BRAF inhibitor (BRAFi) treatment were shown to involve multiple signalling pathways including MAPK, PI3K pathways and tumor microenvironment. They may also be complicated by intra-tumor heterogeneity of BRAF mutational status which paradoxically enhances wild-type BRAF cells proliferation. We therefore wanted to evaluate using a quantitative pyrosequencing assay whether the level of BRAFV600 mutation in tumor tissue could predict clinical response and outcome of BRAFV600melanoma patients treated with the BRAFi, vemurafenib. Methods: melanoma specimen from 44 patients with advanced melanoma treated with vemurafenib were available at abseline. The BRAFV600 mutation level was defined as the ratio of the BRAFV600 allele quantification to the percentage of tumor cells in the sample. The main end point were response according to RECIST, progression free survival, overall survival and ratio of the mutated allele to percentage of tumor cells. Results: The BRA...
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