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资源简介：
The goal of this study is to identify genomic mutations that drive melanoma resistance to BRAF or BRAF/MEK inhibitors.
应用场景：
创建时间：
2020-09-05
相关数据集
Gene expression profiling of oncogenic NRAS driven mouse melanomas that have developed resistance to NRAS withdrawal. Mus musculus
Targeted therapies have the potential to revolutionize cancer care by providing personalized treatment strategies that are less toxic and more effective but it is clear that for most solid tumors supp
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Acetylcytidine modification of DDX41 and ZNF746 by N-acetyltransferase 10 contributes to chemoresistance of melanoma
We performed RNA-seq to analyse the different expression genes of DTIC-resistant (DR) A375 cells and wild-type control. Examination of differentially expressed genes in DR A375 cells compared with wil
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Table ST6 from ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma
Table ST6: Differential expressed lipids and their FDRs in sensitive vs resistant cells (negative values are upregulated in sensitive cells).
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Proteomics identifies markers of MAPKi resistance offering new therapeutic strategies in melanoma- Cytoplasmic (cyt), nuclear (ne) and secreted (sn) proteins of MAPKi sensitive melanoma cells
MAPK inhibitors (MAPKi) show outstanding clinical response rates in melanoma patients harbouring BRAF mutations, but resistance is common. High-throughput, subcellular proteome analyses at two differe
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Honokiol Bis-Dichloroacetate (Honokiol DCA) Demonstrates Activity in Vemurafenib-Resistant Melanoma in Vivo.
The majority of human melanomas bears BRAF mutations and thus is treated with inhibitors of BRAF, such as vemurafenib. While patients with BRAF mutations often demonstrate an initial dramatic response
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