Sandra Orlow Waterfall Nude3/17/2024 ![]() ![]() Methodology In this study, we assessed the individual kinase activity profiles in 26 tumor samples obtained from patients with metastatic malignant melanoma using peptide arrays with 144 kinase substrates. Better markers for targeted therapy are therefore urgently needed. However, drug resistance is a recurring problem, and prognoses are still very bad for patients harboring BRAF wild-type. Kristensen, Vessela Geisler, Jürgenīackground Treatment of metastatic malignant melanoma patients harboring BRAF(V600E) has improved drastically after the discovery of the BRAF inhibitor, vemurafenib. de Wijn, Rik Risberg, Karianne Busch, Christian Lønning, Per E. ![]() Tahiri, Andliena Røe, Kathrine Ree, Anne H. Our results provide the evidence that overexpression of wild-type B-Raf, in part but not always as a result of gene amplification, is one of the mechanisms underlying constitutive activation of the MAPK pathway that stimulates growth of MM cells.ĭifferential Inhibition of Ex-Vivo Tumor Kinase Activity by Vemurafenib in BRAF(V600E) and BRAF Wild-Type Metastatic Malignant Melanoma Not only downregulation of the endogenously overexpressed wild-type B-Raf by antisense oligonucleotide but also a treatment with an inhibitor of mitogen-activated protein kinase kinase (MAPKK, MEK) reduced phosphorylated ERK1/2 and cell growth, whereas the exogenously expressed wild-type B-Raf promoted cell growth in MM cells. MM cells that carried wild-type BRAF and NRAS showed constitutive overexpression of B-Raf protein and phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), even after serum starvation. Among 40 cell lines, the eight lines that revealed neither BRAF nor NRAS mutations showed even higher levels of BRAF mRNA expression than the 32 mutated lines, although DNA amplification at 7q33-q34 was not detected in every lines overexpressing BRAF. We found this gene to be amplified to a remarkable degree in the MM cell lines that exhibited high-level gains at 7q33-q34 in CGH. Tanami, Hideaki Imoto, Issei Hirasawa, Akira Yuki, Yasuhiro Sonoda, Itaru Inoue, Jun Yasui, Kohichiro Misawa-Furihata, Akiko Kawakami, Yutaka Inazawa, JohjiĬomparative genomic hybridization (CGH) using 40 cell lines derived from malignant melanomas (MMs) revealed frequent amplification at 7q33-q34 containing BRAF gene, which often is mutated in MM. Involvement of overexpressed wild-type BRAF in the growth of malignant melanoma cell lines. ![]()
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