about
Deregulation of the PI3K and KRAS signaling pathways in human cancer cells determines their response to everolimusReplacement of normal with mutant alleles in the genome of normal human cells unveils mutation-specific drug responsesGenetic targeting of the kinase activity of the Met receptor in cancer cellsWild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer.Association of KRAS p.G13D mutation with outcome in patients with chemotherapy-refractory metastatic colorectal cancer treated with cetuximab.The First-in-class Anti-EGFR Antibody Mixture Sym004 Overcomes Cetuximab Resistance Mediated by EGFR Extracellular Domain Mutations in Colorectal Cancer.Identification of cancer genes by mutational profiling of tumor genomesBRAF V600E is a determinant of sensitivity to proteasome inhibitorsActive PI3K pathway causes an invasive phenotype which can be reversed or promoted by blocking the pathway at divergent nodesThe stress phenotype makes cancer cells addicted to CDT2, a substrate receptor of the CRL4 ubiquitin ligase.Tivantinib (ARQ197) displays cytotoxic activity that is independent of its ability to bind MET.Knock-in of oncogenic Kras does not transform mouse somatic cells but triggers a transcriptional response that classifies human cancers.Mutation of a single allele of the cancer susceptibility gene BRCA1 leads to genomic instability in human breast epithelial cells.Integrated molecular dissection of the epidermal growth factor receptor (EGFR) [corrected] oncogenic pathway to predict response to EGFR-targeted monoclonal antibodies in metastatic colorectal cancer.Molecular Landscape of Acquired Resistance to Targeted Therapy Combinations in BRAF-Mutant Colorectal Cancer.Tivantinib (ARQ 197) affects the apoptotic and proliferative machinery downstream of c-MET: role of Mcl-1, Bcl-xl and Cyclin B1.Emergence of Multiple EGFR Extracellular Mutations during Cetuximab Treatment in Colorectal Cancer.Targeted knock-in of the polymorphism rs61764370 does not affect KRAS expression but reduces let-7 levels.Acquired RAS or EGFR mutations and duration of response to EGFR blockade in colorectal cancer.Modeling tumor progression by the sequential introduction of genetic alterations into the genome of human normal cells.Expression and functional regulation of myoglobin in epithelial cancers.Understanding how kinase-targeted therapies work.MM-151 overcomes acquired resistance to cetuximab and panitumumab in colorectal cancers harboring EGFR extracellular domain mutations.Codon bias imposes a targetable limitation on KRAS-driven therapeutic resistance.p21(WAF1/CIP1) mediates the growth response to TGF-beta in human epithelial cells.PIK3CA cancer mutations display gender and tissue specificity patterns.Blockade of EGFR and MEK intercepts heterogeneous mechanisms of acquired resistance to anti-EGFR therapies in colorectal cancer.Isogenic mutant human cells: a new tool for personalized cancer medicine.Reliance upon ancestral mutations is maintained in colorectal cancers that heterogeneously evolve during targeted therapies.Erratum to: Integrated molecular dissection of the epidermal growth factor receptor (EGFR) oncogenic pathway to predict response to EGFR-targeted monoclonal antibodies in metastatic colorectal cancerExposure to the Tobacco Smoke Constituent 4-Aminobiphenyl Induces Chromosomal Instability in Human Cancer CellsCharacterization of tumor-derived mesenchymal stem cells potentially differentiating into cancer-associated fibroblasts in lung cancerHigh-dose vitamin C enhances cancer immunotherapyVitamin C Restricts the Emergence of Acquired Resistance to EGFR-Targeted Therapies in Colorectal CancerAdaptive mutability of colorectal cancers in response to targeted therapiesA Subset of Colorectal Cancers with Cross-Sensitivity to Olaparib and OxaliplatinPatient-Derived Xenografts and Matched Cell Lines Identify Pharmacogenomic Vulnerabilities in Colorectal CancerEGFR blockade reverts resistance to KRAS G12C inhibition in colorectal cancer
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P50
description
hulumtuese
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onderzoeker
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researcher
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հետազոտող
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name
Sabrina Arena
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Sabrina Arena
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Sabrina Arena
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Sabrina Arena
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type
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Sabrina Arena
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Sabrina Arena
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Sabrina Arena
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Sabrina Arena
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Sabrina Arena
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Sabrina Arena
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Sabrina Arena
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Sabrina Arena
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P106
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8930746700
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P31
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0000-0002-1318-2494