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Title[redir]:
A RAS Renaissance: Emerging Targeted Therapies for KRAS-Mutated NonβSmall Cell Lung Cancer - PMC
Description:
Of the numerous oncogenes implicated in human cancer, the most common and perhaps the most elusive to target pharmacologically is RAS. Since the discovery of RAS in the 1960s, numerous studies have elucidated the mechanism of activity, regulation, ...
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Keywords {π}
doi, ras, kras, pubmed, google, scholar, cancer, cell, lung, signaling, pmc, mutations, inhibitors, patients, article, free, clinical, tumor, cancers, combination, inhibition, nsclc, trials, kinase, krasdriven, phase, therapy, targeting, figure, trial, inhibitor, selumetinib, krasmutated, small, proteins, cells, pathway, targeted, protein, increased, ftase, study, genes, oncogenic, membrane, clin, therapies, nonsmall, common, icmt,
Topics {βοΈ}
cross-species gene-expression analysis c-terminal c-a-a k-ras-induced myeloproliferative disease organ-specific kras-mutated cancer post-hoc biomarker analysis higher-stringency secondary screen rxrs/cyclin d1 expression kras-driven myeloproliferative disease kras-driven myeloprolifative disease real-time biomarker analysis kras-mutated nsclc derive cdk4/cdk6 dual antagonist pmc beta search c-rel proto-oncogene cumulative real-time results hras-driven murine tumors compartmentalized ras/mapk signaling small-cell lung cancer kras-mutated pancreatic cancer tgf-Ξ² activated kinase-1 small-molecule ligands bind gov/ct2/show/nct01833143 gov/ct2/show/nct01427946 ras-effector interactions lead water-soluble ras ligand regulates kras-driven oncogenesis inhibits rho/rock signaling mammalian pdeΞ΄-kras interaction kras-mutated lung cancers gov/ct2/show/nct01248247 gov/ct2/show/nct01229150 structure-based drug design kras-driven colon cancer hras-driven urothelial cancers decreased cdk4-mediated phosphorylation ras-inhibitor binding interface inhibit sos-mediated activation renal cell carcinoma kras-wildtype patient counterparts lung adenocarcinoma cells human cell lines egfr mutation/copy number mouse cell lines free bim forms synthetic lethal interactions ras gene amplification ras-pathway targeted therapies small gtpase downstream multiple targeted therapies downstream signaling pathways
Questions {β}
- Farnesyltransferase inhibitors: where are we now?
- Wilms tumor 1 (WT1) Transcription factor, tumor suppressor, oncogene (?
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