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Differential sensitivity of melanoma cell lines with BRAF .sup. V600E .sup.mutation to the specific Raf inhibitor PLX4032
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Differential sensitivity of melanoma cell lines with BRAF .sup. V600E .sup.mutation to the specific Raf inhibitor PLX4032
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Differential sensitivity of melanoma cell lines with BRAF .sup. V600E .sup.mutation to the specific Raf inhibitor PLX4032
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Journal Article
Differential sensitivity of melanoma cell lines with BRAF .sup. V600E .sup.mutation to the specific Raf inhibitor PLX4032
2010
Overview
Blocking oncogenic signaling induced by the BRAF.sup.V600E .sup.mutation is a promising approach for melanoma treatment. We tested the anti-tumor effects of a specific inhibitor of Raf protein kinases, PLX4032/RG7204, in melanoma cell lines. PLX4032 decreased signaling through the MAPK pathway only in cell lines with the BRAF.sup.V600E .sup.mutation. Seven out of 10 BRAF.sup.V600E .sup.mutant cell lines displayed sensitivity based on cell viability assays and three were resistant at concentrations up to 10 [mu]M. Among the sensitive cell lines, four were highly sensitive with IC.sub.50 values below 1 [mu]M, and three were moderately sensitive with IC.sub.50 values between 1 and 10 [mu]M. There was evidence of MAPK pathway inhibition and cell cycle arrest in both sensitive and resistant cell lines. Genomic analysis by sequencing, genotyping of close to 400 oncogeninc mutations by mass spectrometry, and SNP arrays demonstrated no major differences in BRAF locus amplification or in other oncogenic events between sensitive and resistant cell lines. However, metabolic tracer uptake studies demonstrated that sensitive cell lines had a more profound inhibition of FDG uptake upon exposure to PLX4032 than resistant cell lines. In conclusion, BRAF.sup.V600E .sup.mutant melanoma cell lines displayed a range of sensitivities to PLX4032 and metabolic imaging using PET probes can be used to assess sensitivity.
Publisher
BioMed Central Ltd
