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Article

Pharmacodynamic Characterization of the Efficacy Signals Due to Selective BRAF Inhibition with PLX4032 in Malignant Melanoma

1 Aug 2010

Abstract excerpt

PURPOSE: About 65% to 70% of melanomas harbor a mutation in v-raf murine sarcoma viral oncogene homolog B1 (BRAF) that causes the steady-state activation of extracellular signal-regulated kinase (ERK). We sought to investigate the efficacy of PLX4032 (BRAF inhibitor) to identify patterns/predictors of response/resistance and to study the effects of BRAF in melanoma. EXPERIMENTAL DESIGN: Well-characterized...

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Identifiers

PMID: 20689758
DOI: 10.1593/neo.10414

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Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Pharmacodynamic Characterization of the Efficacy Signals Due to Selective BRAF Inhibition with PLX4032 in Malignant MelanomaPMID 20689758Read ↗

Differential sensitivity of melanoma cell lines with BRAFV600E mutation to the specific Raf inhibitor PLX4032.Semantic proximity Read ↗

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

Clinical efficacy of a RAF inhibitor needs broad target blockade in BRAF-mutant melanoma.Semantic proximity Read ↗

Identification of PLX4032-resistance mechanisms and implications for novel RAF inhibitors.Semantic proximity Read ↗

Targeting BRAF in advanced melanoma: a first step toward manageable disease.Semantic proximity Read ↗

Multiple murine BRaf<sup>V600E</sup> melanoma cell lines with sensitivity to PLX4032Semantic proximity Read ↗

Analysis of BRAF inhibitor resistance in melanoma cellsSemantic proximity Read ↗

RG7204 (PLX4032), a selective BRAFV600E inhibitor, displays potent antitumor activity in preclinical melanoma models.Semantic proximity Read ↗

The RAF inhibitor PLX4032 inhibits ERK signaling and tumor cell proliferation in a V600E BRAF-selective manner.Semantic proximity Read ↗

The CSPG4-specific monoclonal antibody enhances and prolongs the effects of the BRAF inhibitor in melanoma cells.Semantic proximity Read ↗

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