501 results on '"Martin, Scott E."'
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2. ARAF mutations confer resistance to the RAF inhibitor belvarafenib in melanoma
3. Enhanced Functional Genomic Screening Identifies Novel Mediators of Dual Leucine Zipper Kinase-Dependent Injury Signaling in Neurons
4. Targeting the Hippo pathway in cancers via ubiquitination dependent TEAD degradation
5. Correlates of persistent smoking in bars subject to smokefree workplace policy.
6. Multiple-gene targeting and mismatch tolerance can confound analysis of genome-wide pooled CRISPR screens
7. Figure S5 from Scaffolding Protein Connector Enhancer of Kinase Suppressor of Ras 1 (CNKSR1) Regulates MAPK Inhibition Responsiveness in Pancreas Cancer via Crosstalk with AKT Signaling
8. Data from Scaffolding Protein Connector Enhancer of Kinase Suppressor of Ras 1 (CNKSR1) Regulates MAPK Inhibition Responsiveness in Pancreas Cancer via Crosstalk with AKT Signaling
9. Table S1 from Scaffolding Protein Connector Enhancer of Kinase Suppressor of Ras 1 (CNKSR1) Regulates MAPK Inhibition Responsiveness in Pancreas Cancer via Crosstalk with AKT Signaling
10. Table S7 from Machine-Learning and Chemicogenomics Approach Defines and Predicts Cross-Talk of Hippo and MAPK Pathways
11. Data from CDK9 Blockade Exploits Context-dependent Transcriptional Changes to Improve Activity and Limit Toxicity of Mithramycin for Ewing Sarcoma
12. Figure S1 from Machine-Learning and Chemicogenomics Approach Defines and Predicts Cross-Talk of Hippo and MAPK Pathways
13. Supplementary Data from The Identification of MicroRNAs in a Genomically Unstable Region of Human Chromosome 8q24
14. Data from Machine-Learning and Chemicogenomics Approach Defines and Predicts Cross-Talk of Hippo and MAPK Pathways
15. Data from The Identification of MicroRNAs in a Genomically Unstable Region of Human Chromosome 8q24
16. Supplementary Table S1 from CDK9 Blockade Exploits Context-dependent Transcriptional Changes to Improve Activity and Limit Toxicity of Mithramycin for Ewing Sarcoma
17. Supplementary Data from CDK9 Blockade Exploits Context-dependent Transcriptional Changes to Improve Activity and Limit Toxicity of Mithramycin for Ewing Sarcoma
18. Supplementary Files from A Single-Step, High-Dose Selection Scheme Reveals Distinct Mechanisms of Acquired Resistance to Oncogenic Kinase Inhibition in Cancer Cells
19. Supplementary Data from Integrated Genomic and Functional microRNA Analysis Identifies miR-30-5p as a Tumor Suppressor and Potential Therapeutic Nanomedicine in Head and Neck Cancer
20. Supplementary Table 3 from A Single-Step, High-Dose Selection Scheme Reveals Distinct Mechanisms of Acquired Resistance to Oncogenic Kinase Inhibition in Cancer Cells
21. Supplementary Figs S9-11 from ERBB3 and IGF1R Signaling Are Required for Nrf2-Dependent Growth in KEAP1-Mutant Lung Cancer
22. Supplementary Tables 1-6 from ERK Mutations and Amplification Confer Resistance to ERK-Inhibitor Therapy
23. Supplementary Figure S1-S6 from ERK Mutations and Amplification Confer Resistance to ERK-Inhibitor Therapy
24. Full Online Materials and Methods from A Single-Step, High-Dose Selection Scheme Reveals Distinct Mechanisms of Acquired Resistance to Oncogenic Kinase Inhibition in Cancer Cells
25. Supplementary File from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
26. Figure S1 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
27. Supplementary Figures and Legends from A Single-Step, High-Dose Selection Scheme Reveals Distinct Mechanisms of Acquired Resistance to Oncogenic Kinase Inhibition in Cancer Cells
28. Supplementary Tables S1-4 from ERBB3 and IGF1R Signaling Are Required for Nrf2-Dependent Growth in KEAP1-Mutant Lung Cancer
29. Supplementary Figs S7,8 from ERBB3 and IGF1R Signaling Are Required for Nrf2-Dependent Growth in KEAP1-Mutant Lung Cancer
30. Supplemental legend from ERK Mutations and Amplification Confer Resistance to ERK-Inhibitor Therapy
31. Supp Table S1, S3-8 from Integrated Genomic and Functional microRNA Analysis Identifies miR-30-5p as a Tumor Suppressor and Potential Therapeutic Nanomedicine in Head and Neck Cancer
32. Supplementary Figs S1-4 from ERBB3 and IGF1R Signaling Are Required for Nrf2-Dependent Growth in KEAP1-Mutant Lung Cancer
33. Data from ERBB3 and IGF1R Signaling Are Required for Nrf2-Dependent Growth in KEAP1-Mutant Lung Cancer
34. Supplementary Table 1 from A Single-Step, High-Dose Selection Scheme Reveals Distinct Mechanisms of Acquired Resistance to Oncogenic Kinase Inhibition in Cancer Cells
35. Supplementary References from A Single-Step, High-Dose Selection Scheme Reveals Distinct Mechanisms of Acquired Resistance to Oncogenic Kinase Inhibition in Cancer Cells
36. Supplementary Table 2 from A Single-Step, High-Dose Selection Scheme Reveals Distinct Mechanisms of Acquired Resistance to Oncogenic Kinase Inhibition in Cancer Cells
37. Data from A Single-Step, High-Dose Selection Scheme Reveals Distinct Mechanisms of Acquired Resistance to Oncogenic Kinase Inhibition in Cancer Cells
38. Data from ATR Inhibitors VE-821 and VX-970 Sensitize Cancer Cells to Topoisomerase I Inhibitors by Disabling DNA Replication Initiation and Fork Elongation Responses
39. Supplemental Table S1 from ATR Inhibitors VE-821 and VX-970 Sensitize Cancer Cells to Topoisomerase I Inhibitors by Disabling DNA Replication Initiation and Fork Elongation Responses
40. Data from Transcription Poisoning by Topoisomerase I Is Controlled by Gene Length, Splice Sites, and miR-142-3p
41. Supplementary Table 4 from Cisplatin Sensitivity Mediated by WEE1 and CHK1 Is Mediated by miR-155 and the miR-15 Family
42. Supplementary Figures 1 - 6, Tables 1 - 3 from Transcription Poisoning by Topoisomerase I Is Controlled by Gene Length, Splice Sites, and miR-142-3p
43. Supplemental Figure S3 from ATR Inhibitors VE-821 and VX-970 Sensitize Cancer Cells to Topoisomerase I Inhibitors by Disabling DNA Replication Initiation and Fork Elongation Responses
44. Supplementary Table 3 from Cisplatin Sensitivity Mediated by WEE1 and CHK1 Is Mediated by miR-155 and the miR-15 Family
45. Supplementary Figures 1-5, Tables 1-2, Table Legends 3-4 from Cisplatin Sensitivity Mediated by WEE1 and CHK1 Is Mediated by miR-155 and the miR-15 Family
46. Data from Cisplatin Sensitivity Mediated by WEE1 and CHK1 Is Mediated by miR-155 and the miR-15 Family
47. Scaffolding Protein Connector Enhancer of Kinase Suppressor of Ras 1 (CNKSR1) Regulates MAPK Inhibition Responsiveness in Pancreas Cancer via Crosstalk with AKT Signaling
48. USP7 small-molecule inhibitors interfere with ubiquitin binding
49. Whole-genome RNAi screen highlights components of the endoplasmic reticulum/Golgi as a source of resistance to immunotoxin-mediated cytotoxicity
50. Loss-of-function RNAi screens in breast cancer cells identify AURKB, PLK1, PIK3R1, MAPK12, PRKD2, and PTK6 as sensitizing targets of rapamycin activity
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