115 results on '"Yen, Ivana"'
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2. CRAF dimerization with ARAF regulates KRAS-driven tumor growth
3. ARAF mutations confer resistance to the RAF inhibitor belvarafenib in melanoma
4. Activation Mechanism of Oncogenic Deletion Mutations in BRAF, EGFR, and HER2
5. Data from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900
6. Supplemental Figure 5 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900
7. Supplemental Figure 8 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900
8. Supplemental Figure 6 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900
9. Supplemental Figure 3 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900
10. Supplemental Figure 7 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900
11. Supplemental Figure 4 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900
12. Supplemental Figure 2 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900
13. Supplemental Figure 1 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900
14. Structure of the BRAF-MEK Complex Reveals a Kinase Activity Independent Role for BRAF in MAPK Signaling
15. Structure-based optimization of hydroxylactam as potent, cell-active inhibitors of lactate dehydrogenase
16. RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth
17. Targeting KRAS Mutant Cancers via Combination Treatment: Discovery of a Pyridopyridazinone pan-RAF Kinase Inhibitor
18. Targeting KRAS Mutant Cancers via Combination Treatment: Discovery of a 5-Fluoro-4-(3H)-quinazolinone Aryl Urea pan-RAF Kinase Inhibitor
19. Conformational Dynamics and Binding Kinetics Drive Mutant Selective Degradation of EGFR
20. Pharmacological Induction of RAS-GTP Confers RAF Inhibitor Sensitivity in KRAS Mutant Tumors
21. Abstract 874: Pharmacologically induced RAS-GTP levels and CRAF-BRAF hetero-dimerization drive sensitization to Type II pan-RAF inhibitors in KRAS mutant cancer
22. 4-Aminoindazolyl-dihydrofuro[3,4-d]pyrimidines as non-covalent inhibitors of mutant epidermal growth factor receptor tyrosine kinase
23. ARAFmutations confer resistance to the RAF inhibitor belvarafenib in melanoma
24. Optimization of 5-(2,6-dichlorophenyl)-3-hydroxy-2-mercaptocyclohex-2-enones as potent inhibitors of human lactate dehydrogenase
25. Abstract 4967: RAF kinase inhibition synergizes with MEK inhibitors in KRAS mutant tumors
26. Identification of 3,6-disubstituted dihydropyrones as inhibitors of human lactate dehydrogenase
27. Discovery of the 1,7-diazacarbazole class of inhibitors of checkpoint kinase 1
28. Identification of substituted 3-hydroxy-2-mercaptocyclohex-2-enones as potent inhibitors of human lactate dehydrogenase
29. Identification of 2-amino-5-aryl-pyrazines as inhibitors of human lactate dehydrogenase
30. Identification of substituted 2-thio-6-oxo-1,6-dihydropyrimidines as inhibitors of human lactate dehydrogenase
31. Discovery of a Potent and Selective in Vivo Probe (GNE-272) for the Bromodomains of CBP/EP300
32. Discovery of a Noncovalent, Mutant-Selective Epidermal Growth Factor Receptor Inhibitor
33. Cell Active Hydroxylactam Inhibitors of Human Lactate Dehydrogenase with Oral Bioavailability in Mice
34. Metabolic plasticity underpins innate and acquired resistance to LDHA inhibition
35. Abstract 4374: Activation mechanism of oncogenic C-helix shifting mutations in BRAF, EGFR, and HER2
36. Kinases as Molecular Switches: Catalytic and Non‐catalytic Functions of BRAF Reveal Novel Insights into Oncogenic Activation
37. Correction to Noncovalent Mutant Selective Epidermal Growth Factor Receptor Inhibitors: A Lead Optimization Case Study
38. 4-Aminoindazolyl-dihydrofuro[3,4- d ]pyrimidines as non-covalent inhibitors of mutant epidermal growth factor receptor tyrosine kinase
39. Pyridones as Highly Selective, Noncovalent Inhibitors of T790M Double Mutants of EGFR
40. Noncovalent Mutant Selective Epidermal Growth Factor Receptor Inhibitors: A Lead Optimization Case Study
41. Mitigation of Acetylcholine Esterase Activity in the 1,7-Diazacarbazole Series of Inhibitors of Checkpoint Kinase 1
42. Discovery of Selective and Noncovalent Diaminopyrimidine-Based Inhibitors of Epidermal Growth Factor Receptor Containing the T790M Resistance Mutation
43. Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900
44. A BRAF‐MEK complex reveals the molecular basis of oncogenic mutations
45. Abstract 2346: A B-RAF-MEK complex reveals a kinase-independent role for BRAF in MAPK pathway suppression.
46. Abstract B14: Inherent resistance to BRAF inhibitors in BRAFV600E colorectal tumors is driven by ligand-dependent activation of the EGFR pathway
47. Abstract 258: The role of EGFR on RAF inhibitor resistance in B-RAFV600E melanoma and colon tumors
48. A Plate-Based Assay to Measure Cellular ERK Substrate Phosphorylation: Utility for Drug Discovery of the MAPK-Signaling Cascade
49. Abstract 5753: RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth
50. Abstract B90: Understanding the effects of RAF inhibitors on RAF signaling in B‐RAF V600E mutant versus wild type tumors
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