490 results on '"SOMWAR, ROMEL"'
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2. Vepafestinib is a pharmacologically advanced RET-selective inhibitor with high CNS penetration and inhibitory activity against RET solvent front mutations
3. Prevalence and Therapeutic Targeting of High-Level ERBB2 Amplification in NSCLC
4. HER4 and EGFR Activate Cell Signaling in NRG1 Fusion-Driven Cancers: Implications for HER2-HER3-specific Versus Pan-HER Targeting Strategies
5. Combination Therapy With MDM2 and MEK Inhibitors Is Effective in Patient-Derived Models of Lung Adenocarcinoma With Concurrent Oncogenic Drivers and MDM2 Amplification
6. Author Correction: Vepafestinib is a pharmacologically advanced RET-selective inhibitor with high CNS penetration and inhibitory activity against RET solvent front mutations
7. Targeting farnesylation as a novel therapeutic approach in HRAS-mutant rhabdomyosarcoma
8. Characterization of a small molecule inhibitor of disulfide reductases that induces oxidative stress and lethality in lung cancer cells
9. MEK inhibitor resistance in lung adenocarcinoma is associated with addiction to sustained ERK suppression
10. Salt-Inducible Kinase 1 is a potential therapeutic target in Desmoplastic Small Round Cell Tumor
11. Novel Preclinical Patient-Derived Lung Cancer Models Reveal Inhibition of HER3 and MTOR Signaling as Therapeutic Strategies for NRG1 Fusion-Positive Cancers
12. Allele-Specific Role of ERBB2 in the Oncogenic Function of EGFR L861Q in EGFR-Mutant Lung Cancers
13. Acquired BRAF Rearrangements Induce Secondary Resistance to EGFR therapy in EGFR-Mutated Lung Cancers
14. Integrative Genomic Analyses Identifies GGA2 as a Cooperative Driver of EGFR-Mediated Lung Tumorigenesis
15. Overcoming clinical resistance to EZH2 inhibition using rational epigenetic combination therapy
16. Prevalence and Therapeutic Targeting of High Level ERBB2 Amplification in Non-Small Cell Lung Cancer
17. Resistance to TRK inhibition mediated by convergent MAPK pathway activation
18. Correction: Targeting farnesylation as a novel therapeutic approach in HRAS-mutant rhabdomyosarcoma
19. HER4 and EGFR activate cell signaling in NRG1 fusion-driven cancers: implications for HER2/HER3-specific vs. pan-HER targeting strategies
20. NTRK kinase domain mutations in cancer variably impact sensitivity to type I and type II inhibitors
21. Cabozantinib in patients with advanced RET-rearranged non-small-cell lung cancer: an open-label, single-centre, phase 2, single-arm trial
22. Abstract 5012: Characterizing the functional significance of PDGFRAK385I and PDGFRAK385L extracellular domain mutations in the newly defined myxoid glioneuronal tumor
23. Abstract 6127: MDM2 inhibition in combination with MEK inhibition in pre-clinical models of lung adenocarcinomas with MDM2 amplification
24. Supplementary Table from Zenocutuzumab, a HER2xHER3 Bispecific Antibody, Is Effective Therapy for Tumors Driven by NRG1 Gene Rearrangements
25. Abstract 4007: Efficacy of vepafestinib in preclinical models of RET fusion-driven sarcoma models
26. Supplementary Figure from Zenocutuzumab, a HER2xHER3 Bispecific Antibody, Is Effective Therapy for Tumors Driven by NRG1 Gene Rearrangements
27. Data from Zenocutuzumab, a HER2xHER3 Bispecific Antibody, Is Effective Therapy for Tumors Driven by NRG1 Gene Rearrangements
28. Supplementary Data from MYC Promotes Tyrosine Kinase Inhibitor Resistance in ROS1-Fusion-Positive Lung Cancer
29. Supplementary Movie 6 from Resistance Profile and Structural Modeling of Next-Generation ROS1 Tyrosine Kinase Inhibitors
30. Data from Resistance Profile and Structural Modeling of Next-Generation ROS1 Tyrosine Kinase Inhibitors
31. Data from MYC Promotes Tyrosine Kinase Inhibitor Resistance in ROS1-Fusion-Positive Lung Cancer
32. Supplementary Movie 5 from Resistance Profile and Structural Modeling of Next-Generation ROS1 Tyrosine Kinase Inhibitors
33. Data from Response to ERBB3-Directed Targeted Therapy in NRG1-Rearranged Cancers
34. Supplementary Figures from Response to ERBB3-Directed Targeted Therapy in NRG1-Rearranged Cancers
35. Supplementary Table from Response to ERBB3-Directed Targeted Therapy in NRG1-Rearranged Cancers
36. Supplementary Methods from Response to ERBB3-Directed Targeted Therapy in NRG1-Rearranged Cancers
37. Supplementary Movie 2 from Resistance Profile and Structural Modeling of Next-Generation ROS1 Tyrosine Kinase Inhibitors
38. Supplementary Movie 7 from Resistance Profile and Structural Modeling of Next-Generation ROS1 Tyrosine Kinase Inhibitors
39. Supplementary Figure from MYC Promotes Tyrosine Kinase Inhibitor Resistance in ROS1-Fusion-Positive Lung Cancer
40. Supplementary Movie 4 from Resistance Profile and Structural Modeling of Next-Generation ROS1 Tyrosine Kinase Inhibitors
41. Supplementary Movie 3 from Resistance Profile and Structural Modeling of Next-Generation ROS1 Tyrosine Kinase Inhibitors
42. Supplementary Movie 1 from Resistance Profile and Structural Modeling of Next-Generation ROS1 Tyrosine Kinase Inhibitors
43. Supplementary Movie 8 from Resistance Profile and Structural Modeling of Next-Generation ROS1 Tyrosine Kinase Inhibitors
44. Supplementary Table and Figures from Resistance Profile and Structural Modeling of Next-Generation ROS1 Tyrosine Kinase Inhibitors
45. Supplementary Data from Resistance Profile and Structural Modeling of Next-Generation ROS1 Tyrosine Kinase Inhibitors
46. Figure S3 from RASA1 and NF1 are Preferentially Co-Mutated and Define A Distinct Genetic Subset of Smoking-Associated Non–Small Cell Lung Carcinomas Sensitive to MEK Inhibition
47. Table S1 from RASA1 and NF1 are Preferentially Co-Mutated and Define A Distinct Genetic Subset of Smoking-Associated Non–Small Cell Lung Carcinomas Sensitive to MEK Inhibition
48. Figure S1 from Therapeutic Potential of NTRK3 Inhibition in Desmoplastic Small Round Cell Tumor
49. Supplementary Table from CIC-Mediated Modulation of MAPK Signaling Opposes Receptor Tyrosine Kinase Inhibitor Response in Kinase-Addicted Sarcoma
50. Supplementary Figure S3 from The Anti-HER3 mAb Seribantumab Effectively Inhibits Growth of Patient-Derived and Isogenic Cell Line and Xenograft Models with Oncogenic NRG1 Fusions
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