510 results on '"Lockwood, William W."'
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2. Uncovering molecular features driving lung adenocarcinoma heterogeneity in patients who formerly smoked
3. Methionine-producing tumor micro(be) environment fuels growth of solid tumors
4. Prevalence and Therapeutic Targeting of High-Level ERBB2 Amplification in NSCLC
5. New insights into the biology and development of lung cancer in never smokers—implications for early detection and treatment
6. Combination Therapy With MDM2 and MEK Inhibitors Is Effective in Patient-Derived Models of Lung Adenocarcinoma With Concurrent Oncogenic Drivers and MDM2 Amplification
7. MEK inhibitor resistance in lung adenocarcinoma is associated with addiction to sustained ERK suppression
8. Characterizing the secretome of EGFR mutant lung adenocarcinoma
9. An ErbB2 splice variant lacking exon 16 drives lung carcinoma
10. Prevalence and Therapeutic Targeting of High Level ERBB2 Amplification in Non-Small Cell Lung Cancer
11. Delineating spatial cell-cell interactions in the solid tumour microenvironment through the lens of highly multiplexed imaging
12. Cystine/glutamate antiporter xCT (SLC7A11) facilitates oncogenic RAS transformation by preserving intracellular redox balance
13. Integrative Genomic Analyses Identifies GGA2 as a Cooperative Driver of EGFR-Mediated Lung Tumorigenesis
14. ATG4B and ATG4A loss result in two-stage cell cycle defects in pancreatic ductal adenocarcinoma cells
15. Resistance to BET inhibitors in lung adenocarcinoma is mediated by casein kinase phosphorylation of BRD4
16. Brief Report: Real-World Treatment Patterns and Clinical Outcomes for Patients With Advanced ALK-Rearranged NSCLC in British Columbia
17. Abstract 6127: MDM2 inhibition in combination with MEK inhibition in pre-clinical models of lung adenocarcinomas with MDM2 amplification
18. Data from Response to ERBB3-Directed Targeted Therapy in NRG1-Rearranged Cancers
19. Supplementary Figures from Response to ERBB3-Directed Targeted Therapy in NRG1-Rearranged Cancers
20. Supplementary Table from Response to ERBB3-Directed Targeted Therapy in NRG1-Rearranged Cancers
21. Supplementary Methods from Response to ERBB3-Directed Targeted Therapy in NRG1-Rearranged Cancers
22. MIR155 Regulation of Ubiquilin1 and Ubiquilin2: Implications in Cellular Protection and Tumorigenesis
23. SMARCA4 loss is synthetic lethal with CDK4/6 inhibition in non-small cell lung cancer
24. Epithelial tumor suppressor ELF3 is a lineage-specific amplified oncogene in lung adenocarcinoma
25. Loss of ATG4B and ATG4A results in two-stage cell cycle defects in pancreatic ductal adenocarcinoma cells.
26. Supplementary Table 7 from Integrative Genomics Identified RFC3 As an Amplified Candidate Oncogene in Esophageal Adenocarcinoma
27. Figure S5 from In Vivo Validation of PAPSS1 (3′-phosphoadenosine 5′-phosphosulfate synthase 1) as a Cisplatin-sensitizing Therapeutic Target
28. Figure S4 from Activation of KRAS Mediates Resistance to Targeted Therapy in MET Exon 14–mutant Non–small Cell Lung Cancer
29. Supplemental Information from In Vivo Validation of PAPSS1 (3′-phosphoadenosine 5′-phosphosulfate synthase 1) as a Cisplatin-sensitizing Therapeutic Target
30. Supplementary Table 5 from Integrative Genomics Identified RFC3 As an Amplified Candidate Oncogene in Esophageal Adenocarcinoma
31. Supplementary Table 8 from Integrative Genomics Identified RFC3 As an Amplified Candidate Oncogene in Esophageal Adenocarcinoma
32. Supplementary Data from Drug Sensitivity and Allele Specificity of First-Line Osimertinib Resistance EGFR Mutations
33. Supplementary cfDNA Mutation Dataset from Drug Sensitivity and Allele Specificity of First-Line Osimertinib Resistance EGFR Mutations
34. Supplementary Figures 1-9 from Integrative Genomics Identified RFC3 As an Amplified Candidate Oncogene in Esophageal Adenocarcinoma
35. Data from Drug Sensitivity and Allele Specificity of First-Line Osimertinib Resistance EGFR Mutations
36. Supplementary Table 6 from Integrative Genomics Identified RFC3 As an Amplified Candidate Oncogene in Esophageal Adenocarcinoma
37. Supplementary Methods, Tables 1-4, Figure Legends 1-9 from Integrative Genomics Identified RFC3 As an Amplified Candidate Oncogene in Esophageal Adenocarcinoma
38. Supplementary Methods from Activation of KRAS Mediates Resistance to Targeted Therapy in MET Exon 14–mutant Non–small Cell Lung Cancer
39. Data from PIK3CA Mutations and Copy Number Gains in Human Lung Cancers
40. Supplementary Table 4 from YEATS4 Is a Novel Oncogene Amplified in Non–Small Cell Lung Cancer That Regulates the p53 Pathway
41. Supplementary Figure 1 from PIK3CA Mutations and Copy Number Gains in Human Lung Cancers
42. Supplementary Table 2 from YEATS4 Is a Novel Oncogene Amplified in Non–Small Cell Lung Cancer That Regulates the p53 Pathway
43. Supplementary Figure 1 from YEATS4 Is a Novel Oncogene Amplified in Non–Small Cell Lung Cancer That Regulates the p53 Pathway
44. Supplementary Figure Legend from YEATS4 Is a Novel Oncogene Amplified in Non–Small Cell Lung Cancer That Regulates the p53 Pathway
45. Data from YEATS4 Is a Novel Oncogene Amplified in Non–Small Cell Lung Cancer That Regulates the p53 Pathway
46. Supplementary Methods from PIK3CA Mutations and Copy Number Gains in Human Lung Cancers
47. Supplementary Table 3 from YEATS4 Is a Novel Oncogene Amplified in Non–Small Cell Lung Cancer That Regulates the p53 Pathway
48. Supplementary Table 1 from YEATS4 Is a Novel Oncogene Amplified in Non–Small Cell Lung Cancer That Regulates the p53 Pathway
49. Supplementary Figure 2 from YEATS4 Is a Novel Oncogene Amplified in Non–Small Cell Lung Cancer That Regulates the p53 Pathway
50. Supplementary Tables 1-6 from PIK3CA Mutations and Copy Number Gains in Human Lung Cancers
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