Identification of genotype-correlated sensitivity to selective kinase inhibitors by using high-throughput tumor cell line profiling. - sprookjes - yvandenbroek - TriplyDB

Identification of genotype-correlated sensitivity to selective kinase inhibitors by using high-throughput tumor cell line profiling.

Identification of genotype-correlated sensitivity to selective kinase inhibitors by using high-throughput tumor cell line profiling.

http://www.wikidata.org/entity/Q36288956

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Development and Characterization of Bladder Cancer Patient-Derived Xenografts for Molecularly Guided Targeted Therapy High-throughput identification of genotype-specific cancer vulnerabilities in mixtures of barcoded tumor cell lines Perturbation of the mutated EGFR interactome identifies vulnerabilities and resistance mechanisms Dysregulation of the Met pathway in non-small cell lung cancer: implications for drug targeting and resistance Cancer Cell Line Panels Empower Genomics-Based Discovery of Precision Cancer Medicine Tumor-Derived Cell Lines as Molecular Models of Cancer Pharmacogenomics Will kinase inhibitors make it as glioblastoma drugs?Cortactin phosphorylated by ERK1/2 localizes to sites of dynamic actin regulation and is required for carcinoma lamellipodia persistence Using drug response data to identify molecular effectors, and molecular "omic" data to identify candidate drugs in cancer Small-molecule kinase inhibitors provide insight into Mps1 cell cycle function MEK1 mutations confer resistance to MEK and B-RAF inhibition.BRAF gene amplification can promote acquired resistance to MEK inhibitors in cancer cells harboring the BRAF V600E mutation.Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer.Vemurafenib synergizes with nutlin-3 to deplete survivin and suppresses melanoma viability and tumor growth.Organoid development in cancer genome discovery PTEN loss contributes to erlotinib resistance in EGFR-mutant lung cancer by activation of Akt and EGFR Novel small molecule Raf kinase inhibitors for targeted cancer therapeutics Induction of stable drug resistance in human breast cancer cells using a combinatorial zinc finger transcription factor library A novel SND1-BRAF fusion confers resistance to c-Met inhibitor PF-04217903 in GTL16 cells through [corrected] MAPK activation Oncolytic effects of a novel influenza A virus expressing interleukin-15 from the NS reading frame Systematic identification of combinatorial drivers and targets in cancer cell lines Comparison of the cancer gene targeting and biochemical selectivities of all targeted kinase inhibitors approved for clinical use Understanding the Interplay between Expression, Mutation and Activity of ALK Receptor in Rhabdomyosarcoma Cells for Clinical Application of Small-Molecule Inhibitors Predicting Anticancer Drug Responses Using a Dual-Layer Integrated Cell Line-Drug Network Model Anti-proliferative effect of cytohesin inhibition in gefitinib-resistant lung cancer cells The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity Systematic identification of genomic markers of drug sensitivity in cancer cells A chromatin-mediated reversible drug-tolerant state in cancer cell subpopulations COT drives resistance to RAF inhibition through MAP kinase pathway reactivation RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF Src inhibitors act through different mechanisms in Non-Small Cell Lung Cancer models depending on EGFR and RAS mutational status.Harnessing Connectivity in a Large-Scale Small-Molecule Sensitivity Dataset.Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.Loss of the tumor suppressor gene NF2, encoding merlin, constitutively activates integrin-dependent mTORC1 signaling.A mouse model for EML4-ALK-positive lung cancer Association of a cytarabine chemosensitivity related gene expression signature with survival in cytogenetically normal acute myeloid leukemia.Differential determinants of cancer cell insensitivity to antimitotic drugs discriminated by a one-step cell imaging assay Publisher’s Note:Abstraction for data integration:Fusing mammalian molecular, cellular and phenotype big datasets for better knowledge extraction.Integrating complex genomic datasets and tumour cell sensitivity profiles to address a 'simple' question: which patients should get this drug?Systematic analysis of genotype-specific drug responses in cancer.

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Identification of genotype-correlated sensitivity to selective kinase inhibitors by using high-throughput tumor cell line profiling.

http://www.wikidata.org/entity/Q36288956

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Identification of genotype-cor ...... put tumor cell line profiling.

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Identification of genotype-cor ...... put tumor cell line profiling.

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Identification of genotype-cor ...... put tumor cell line profiling.

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Identification of genotype-cor ...... put tumor cell line profiling.

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Identification of genotype-cor ...... put tumor cell line profiling.

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Identification of genotype-cor ...... put tumor cell line profiling.

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A John Iafrate

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Angela Tam

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Ching Ni Njauw

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Clara Montagut

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Daniel A Haber

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Diana Lee

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Heidi Archibald

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Hensin Tsao

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Jeff H Hanke

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Jeffrey G Supko

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P2860

KRAS mutations and primary resistance of lung adenocarcinomas to gefitinib or erlotinib

Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752

Cluster analysis and display of genome-wide expression patterns

A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

Mutations of the BRAF gene in human cancer

Guilty as charged: B-RAF is a human oncogene

Cancer. Addiction to oncogenes--the Achilles heal of cancer

BRAF mutation predicts sensitivity to MEK inhibition

Where next for gefitinib in patients with lung cancer?

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