p53 Reactivation by PRIMA-1(Met) (APR-246) sensitises (V600E/K)BRAF melanoma to vemurafenib

Intrinsic and acquired resistance of metastatic melanoma to (V600E/K)BRAF and/or MEK inhibitors, which is often caused by activation of the PI3K/AKT survival pathway, represents a major clinical challenge. Given that p53 is capable of antagonising PI3K/AKT activation we hypothesised that pharmacolog...

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Veröffentlicht in:	European journal of cancer (1990) 2016-03, Vol.55, p.98
Hauptverfasser:	Krayem, Mohammad, Journe, Fabrice, Wiedig, Murielle, Morandini, Renato, Najem, Ahmad, Salès, François, van Kempen, Leon C, Sibille, Catherine, Awada, Ahmad, Marine, Jean-Christophe, Ghanem, Ghanem
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antineoplastic Combined Chemotherapy Protocols - pharmacology Apoptosis - drug effects Cell Line, Tumor Cell Proliferation - drug effects Dose-Response Relationship, Drug Drug Resistance, Neoplasm Drug Synergism Genetic Predisposition to Disease Humans Indoles - pharmacology Male Melanoma - drug therapy Melanoma - enzymology Melanoma - genetics Melanoma - pathology Mice, Nude Molecular Targeted Therapy Mutation Phosphatidylinositol 3-Kinase - metabolism Protein Kinase Inhibitors - pharmacology Proto-Oncogene Proteins B-raf - antagonists & inhibitors Proto-Oncogene Proteins B-raf - genetics Proto-Oncogene Proteins B-raf - metabolism Proto-Oncogene Proteins c-akt - metabolism Quinuclidines - pharmacology Signal Transduction - drug effects Skin Neoplasms - drug therapy Skin Neoplasms - enzymology Skin Neoplasms - genetics Skin Neoplasms - pathology Sulfonamides - pharmacology Time Factors Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Xenograft Model Antitumor Assays
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