A5050215128- Melanoma and MAPK Pathways
- Cancer, Lipids, and Metabolism
- Click Chemistry and Applications
- Peroxisome Proliferator-Activated Receptors
- Nanoplatforms for cancer theranostics
- Inflammatory mediators and NSAID effects
- Cancer-related molecular mechanisms research
- Circular RNAs in diseases
- Cancer Research and Treatments
- Kruppel-like factors research
- Mesenchymal stem cell research
- Wound Healing and Treatments
- Forest Insect Ecology and Management
- Cancer, Hypoxia, and Metabolism
- Angiogenesis and VEGF in Cancer
- Plant Pathogens and Fungal Diseases
- PI3K/AKT/mTOR signaling in cancer
ETH Zurich
2018-2023
Board of the Swiss Federal Institutes of Technology
2021
Treatment of BRAFV600E -mutant melanomas with MAPK inhibitors (MAPKi) results in significant tumor regression, but acquired resistance is pervasive. To understand nonmutational mechanisms underlying the adaptation to MAPKi and identify novel vulnerabilities treated MAPKi, we focused on initial response phase during treatment MAPKi.By screening proteins expressed cell surface melanoma cells, identified fatty acid transporter CD36 as most consistently upregulated protein upon short-term MAPKi....
Abstract Recent studies have revealed the importance of long noncoding RNAs (lncRNAs) as tissue-specific regulators gene expression. There is ample evidence that distinct types vasculature undergo tight transcriptional control to preserve their structure, identity, and functions. We determine a comprehensive map lineage-specific lncRNAs in human dermal lymphatic blood vascular endothelial cells (LECs BECs), combining RNA-Seq CAGE-Seq. Subsequent antisense oligonucleotide-knockdown...
miRNAs are small noncoding RNAs that regulate mRNA targets in a cell-specific manner. miR-29 is expressed murine and human skin, where it may functions skin repair. Cutaneous wound healing model miR-29a/b1 gene knockout mice was used to identify the matrix, angiogenesis maturation of provisional granulation tissue enhanced response genetic deletion miR-29. Consistently, antisense-mediated inhibition promoted vitro by autocrine paracrine mechanisms. These processes likely mediated target...
ABSTRACT Introduction Malignant melanoma is an aggressive tumour characterised by poor prognosis and therapeutic resistance. It partly driven the MAPK signalling pathway, providing a rationale for development of inhibitors (MAPKi) targeting key components activated pathway. MAPKi induce regression improve progression-free overall survival metastatic patients. However, due to drug resistance, even in patients displaying complete response, eventually progress. Both genetic non-genetic...
Abstract Recent studies have revealed the importance of long noncoding RNAs (lncRNAs) as tissue-specific regulators gene expression. There is ample evidence that distinct types vasculature undergo tight transcriptional control to preserve their structure, identity, and functions. We determined, for first time, global lineage-specific lncRNAome human dermal blood lymphatic endothelial cells (BECs LECs), combining RNA-Seq CAGE-Seq. A subsequent genome-wide antisense oligonucleotide-knockdown...
<p>Table S5, related to Figure S5C</p>
<p>Table S3, related to Figure 1 and S1</p>
<p>Contains Supplementary materials and methods, Figures S1-S9, Table S2, S4, Supplemental References Figure S1, related to 1. Cell surface marker screening of A375P cells treated with vehicle (DMSO) or PLX. CD36 is a biomarker the early stage MAPK inhibition in melanoma. S3, induces maintains CD36+ population melanoma 2. MAPKi induce expression genes involved lipid catabolism BRAFV600E melanomas. S5, 3. decreased glycolytic flux BRAF-mutated cells. S6, 4. Phenotypic metabolic...
<p>Table S1 contains antibody details of the LEGENDScreen Human PE Kit from Biolegend</p>
<div>AbstractPurpose:<p>Treatment of <i>BRAF<sup>V600E</sup></i>-mutant melanomas with MAPK inhibitors (MAPKi) results in significant tumor regression, but acquired resistance is pervasive. To understand nonmutational mechanisms underlying the adaptation to MAPKi and identify novel vulnerabilities treated MAPKi, we focused on initial response phase during treatment MAPKi.</p>Experimental Design:<p>By screening proteins expressed cell surface...
<div>AbstractPurpose:<p>Treatment of <i>BRAF<sup>V600E</sup></i>-mutant melanomas with MAPK inhibitors (MAPKi) results in significant tumor regression, but acquired resistance is pervasive. To understand nonmutational mechanisms underlying the adaptation to MAPKi and identify novel vulnerabilities treated MAPKi, we focused on initial response phase during treatment MAPKi.</p>Experimental Design:<p>By screening proteins expressed cell surface...
<p>Table S1 contains antibody details of the LEGENDScreen Human PE Kit from Biolegend</p>
<p>Table S3, related to Figure 1 and S1</p>
<p>Contains Supplementary materials and methods, Figures S1-S9, Table S2, S4, Supplemental References Figure S1, related to 1. Cell surface marker screening of A375P cells treated with vehicle (DMSO) or PLX. CD36 is a biomarker the early stage MAPK inhibition in melanoma. S3, induces maintains CD36+ population melanoma 2. MAPKi induce expression genes involved lipid catabolism BRAFV600E melanomas. S5, 3. decreased glycolytic flux BRAF-mutated cells. S6, 4. Phenotypic metabolic...
<p>Table S5, related to Figure S5C</p>