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Genome-wide copy number variation in human metastatic melanoma cell lines

ABSTRACT: Illumina HumanExon510S-DUO bead arrays (Illumina Inc) were performed according to the manufacturer's protocol. Genome-wide copy number variation analysis was performed on the genomic DNA of two pairs of cell lines comprising of parental melanoma cell lines and corresponding resistant sub-lines.

ORGANISM(S): Homo sapiens

SUBMITTER: Mikyung Lee

PROVIDER: E-GEOD-24890 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation.

Nazarian Ramin R Shi Hubing H Wang Qi Q Kong Xiangju X Koya Richard C RC Lee Hane H Chen Zugen Z Lee Mi-Kyung MK Attar Narsis N Sazegar Hooman H Chodon Thinle T Nelson Stanley F SF McArthur Grant G Sosman Jeffrey A JA Ribas Antoni A Lo Roger S RS

Nature 20101124 7326

Activating B-RAF(V600E) (also known as BRAF) kinase mutations occur in ∼7% of human malignancies and ∼60% of melanomas. Early clinical experience with a novel class I RAF-selective inhibitor, PLX4032, demonstrated an unprecedented 80% anti-tumour response rate among patients with B-RAF(V600E)-positive melanomas, but acquired drug resistance frequently develops after initial responses. Hypotheses for mechanisms of acquired resistance to B-RAF inhibition include secondary mutations in B-RAF(V600E) ...[more]

PMID: 21107323

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