343 results on '"Greulich, Heidi"'
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2. Velcrin-induced selective cleavage of tRNALeu(TAA) by SLFN12 causes cancer cell death
3. Discovery of BAY 2666605, a Molecular Glue for PDE3A and SLFN12.
4. Mechanistic insights into cancer cell killing through interaction of phosphodiesterase 3A and schlafen family member 12
5. Characterizing genomic alterations in cancer by complementary functional associations
6. Discovering the anticancer potential of non-oncology drugs by systematic viability profiling
7. Structure of PDE3A-SLFN12 complex reveals requirements for activation of SLFN12 RNase
8. Velcrin compounds activate the SLFN12 tRNase to induce tomoptosis.
9. EXTH-38. VELCRIN MOLECULAR GLUES INDUCE CELL DEATH IN GLIOBLASTOMAS WITH HIGH PDE3A AND SLFN12 EXPRESSION
10. Medulloblastoma exome sequencing uncovers subtype-specific somatic mutations.
11. Subtype-specific genomic alterations define new targets for soft-tissue sarcoma therapy
12. EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy
13. Epidermal Growth Factor Receptor Activation in Glioblastoma through Novel Missense Mutations in the Extracellular Domain.
14. Abstract 4035: Preclinical activity of BAY 2927088 in HER2 mutant non-small cell lung cancer
15. Data from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
16. Interview with Dr. Meyerson from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
17. Supplementary Figure Legends 1-7 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
18. Supplementary Figures 1-7 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
19. Supplementary Table 1 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
20. Data from Modeling Genomic Diversity and Tumor Dependency in Malignant Melanoma
21. Supplementary Figures 1-3 from Inhibition of Hsp90 Down-regulates Mutant Epidermal Growth Factor Receptor (EGFR) Expression and Sensitizes EGFR Mutant Tumors to Paclitaxel
22. Supplementary Table 1 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
23. Supplementary Figure 2 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
24. Supplementary Figures 1 - 10 from Cetuximab Response of Lung Cancer–Derived EGF Receptor Mutants Is Associated with Asymmetric Dimerization
25. Data from Signal Transducer and Activator of Transcription 3 Is Required for the Oncogenic Effects of Non–Small-Cell Lung Cancer–Associated Mutations of the Epidermal Growth Factor Receptor
26. Supplementary Figure 7 from Hsp90 Inhibition Suppresses Mutant EGFR-T790M Signaling and Overcomes Kinase Inhibitor Resistance
27. Data from Cetuximab Response of Lung Cancer–Derived EGF Receptor Mutants Is Associated with Asymmetric Dimerization
28. Supplementary Methods, Figure Legends 1-3 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
29. Supplementary Figure 6 from Hsp90 Inhibition Suppresses Mutant EGFR-T790M Signaling and Overcomes Kinase Inhibitor Resistance
30. Data from Inhibition of Hsp90 Down-regulates Mutant Epidermal Growth Factor Receptor (EGFR) Expression and Sensitizes EGFR Mutant Tumors to Paclitaxel
31. Supplementary Figure 3 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
32. Supplementary Table 2 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
33. Supplementary Figure 8 from Hsp90 Inhibition Suppresses Mutant EGFR-T790M Signaling and Overcomes Kinase Inhibitor Resistance
34. Supplementary Information from Modeling Genomic Diversity and Tumor Dependency in Malignant Melanoma
35. Supplementary Methods, Legends for Figures 1-8 and Tables 1-3 from Hsp90 Inhibition Suppresses Mutant EGFR-T790M Signaling and Overcomes Kinase Inhibitor Resistance
36. Supplementary Figure 1 from Hsp90 Inhibition Suppresses Mutant EGFR-T790M Signaling and Overcomes Kinase Inhibitor Resistance
37. Supplementary Figure 5 from Hsp90 Inhibition Suppresses Mutant EGFR-T790M Signaling and Overcomes Kinase Inhibitor Resistance
38. Supplementary Figure 4 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
39. Supplementary Figure 3 from Hsp90 Inhibition Suppresses Mutant EGFR-T790M Signaling and Overcomes Kinase Inhibitor Resistance
40. Supplementary Figure 1 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
41. Data from Hsp90 Inhibition Suppresses Mutant EGFR-T790M Signaling and Overcomes Kinase Inhibitor Resistance
42. Supplementary Figure Legends 1-3 from Inhibition of Hsp90 Down-regulates Mutant Epidermal Growth Factor Receptor (EGFR) Expression and Sensitizes EGFR Mutant Tumors to Paclitaxel
43. Supplementary Table 1 from Signal Transducer and Activator of Transcription 3 Is Required for the Oncogenic Effects of Non–Small-Cell Lung Cancer–Associated Mutations of the Epidermal Growth Factor Receptor
44. Supplementary Methods from Cetuximab Response of Lung Cancer–Derived EGF Receptor Mutants Is Associated with Asymmetric Dimerization
45. Supplementary Figure 4 from Hsp90 Inhibition Suppresses Mutant EGFR-T790M Signaling and Overcomes Kinase Inhibitor Resistance
46. Supplementary Figure 2 from Hsp90 Inhibition Suppresses Mutant EGFR-T790M Signaling and Overcomes Kinase Inhibitor Resistance
47. Supplementary Figure Legend from Cetuximab Response of Lung Cancer–Derived EGF Receptor Mutants Is Associated with Asymmetric Dimerization
48. Genetic clues can be used to predict whether early-stage cancer will form an invasive tumour
49. Velcrin-induced selective cleavage of tRNALeu(TAA) by SLFN12 causes cancer cell death
50. Functional analysis of receptor tyrosine kinase mutations in lung cancer identifies oncogenic extracellular domain mutations of ERBB2
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