128 results on '"Park, Kwon-Sik"'
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2. Effect of chromatin modifiers on the plasticity and immunogenicity of small-cell lung cancer
3. CRACD loss induces neuroendocrine cell plasticity of lung adenocarcinoma
4. Regulation of UHRF1 acetylation by TIP60 is important for colon cancer cell proliferation
5. Opa1 and Drp1 reciprocally regulate cristae morphology, ETC function, and NAD+ regeneration in KRas-mutant lung adenocarcinoma
6. Phase I Study of Entinostat, Atezolizumab, Carboplatin, and Etoposide in Previously Untreated Extensive-Stage Small Cell Lung Cancer, ETCTN 10399
7. Robo1 loss has pleiotropic effects on postnatal development and survival
8. CRACD suppresses neuroendocrinal plasticity of lung adenocarcinoma
9. Data from Crebbp Loss Drives Small Cell Lung Cancer and Increases Sensitivity to HDAC Inhibition
10. Supplementary_table_S5 from Intertumoral Heterogeneity in SCLC Is Influenced by the Cell Type of Origin
11. Supplementary Figure S1-S17 from Intertumoral Heterogeneity in SCLC Is Influenced by the Cell Type of Origin
12. Data from Intertumoral Heterogeneity in SCLC Is Influenced by the Cell Type of Origin
13. Figures S1-S16 from Crebbp Loss Drives Small Cell Lung Cancer and Increases Sensitivity to HDAC Inhibition
14. Tables S1-S5 from Crebbp Loss Drives Small Cell Lung Cancer and Increases Sensitivity to HDAC Inhibition
15. Supplementary Data 2 from FGFR1 Is Critical for RBL2 Loss–Driven Tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell Lung Cancer
16. Figures S1-4 from A Novel, Fully Human Anti–fucosyl-GM1 Antibody Demonstrates Potent In Vitro and In Vivo Antitumor Activity in Preclinical Models of Small Cell Lung Cancer
17. Data from WNT5A–RHOA Signaling Is a Driver of Tumorigenesis and Represents a Therapeutically Actionable Vulnerability in Small Cell Lung Cancer
18. Supplementary Data from WNT5A–RHOA Signaling Is a Driver of Tumorigenesis and Represents a Therapeutically Actionable Vulnerability in Small Cell Lung Cancer
19. Supplementary Fig 4 from FGFR1 Is Critical for RBL2 Loss–Driven Tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell Lung Cancer
20. Supplementary Data 1 from FGFR1 Is Critical for RBL2 Loss–Driven Tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell Lung Cancer
21. Supplementary Figure from WNT5A–RHOA Signaling Is a Driver of Tumorigenesis and Represents a Therapeutically Actionable Vulnerability in Small Cell Lung Cancer
22. Supplementary Fig 2 from FGFR1 Is Critical for RBL2 Loss–Driven Tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell Lung Cancer
23. Supplementary Methods from FGFR1 Is Critical for RBL2 Loss–Driven Tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell Lung Cancer
24. Tables S1-4 from A Novel, Fully Human Anti–fucosyl-GM1 Antibody Demonstrates Potent In Vitro and In Vivo Antitumor Activity in Preclinical Models of Small Cell Lung Cancer
25. Supplementary Table from WNT5A–RHOA Signaling Is a Driver of Tumorigenesis and Represents a Therapeutically Actionable Vulnerability in Small Cell Lung Cancer
26. Supplementary File S1 from Fragmentation of Small-Cell Lung Cancer Regulatory States in Heterotypic Microenvironments
27. Supplementary Data 3 from FGFR1 Is Critical for RBL2 Loss–Driven Tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell Lung Cancer
28. Data from Fragmentation of Small-Cell Lung Cancer Regulatory States in Heterotypic Microenvironments
29. Supplementary Fig 3 from FGFR1 Is Critical for RBL2 Loss–Driven Tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell Lung Cancer
30. Supplementary Fig 1 from FGFR1 Is Critical for RBL2 Loss–Driven Tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell Lung Cancer
31. Supplementary Data from Fragmentation of Small-Cell Lung Cancer Regulatory States in Heterotypic Microenvironments
32. Data from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
33. Supplementary Figure 7 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
34. Supplementary Figure 6B from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
35. Supplementary Figure 5 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
36. Supplementary Figure Legends 1-8, Table 1, Methods from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
37. Supplementary Figure 1 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
38. Supplementary Figure 3 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
39. Supplementary Figure 4 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
40. Supplementary Figure 8 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
41. Supplementary Figure 2 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
42. BCAT1 inhibition affects CD8+T cell activation, exhaustion, and tumoral immunity by altering iron homeostasis
43. CRACD loss promotes small cell lung cancer tumorigenesis via EZH2-mediated immune evasion
44. CRACD, a gatekeeper restricting proliferation, heterogeneity, and immune evasion of small cell lung cancer
45. PCLAF-DREAM Drives Alveolar Cell Plasticity for Lung Regeneration
46. WNT5A–RHOA Signaling Is a Driver of Tumorigenesis and Represents a Therapeutically Actionable Vulnerability in Small Cell Lung Cancer
47. Opa1 and Drp1 reciprocally regulate cristae morphology, ETC function, and NAD+ regeneration in KRas-mutant lung adenocarcinoma
48. WNT5A-RHOA axis is a new vulnerability in small-cell lung cancer
49. KIX domain determines a selective tumor-promoting role for EP300 and its vulnerability in small cell lung cancer
50. Opa1 and Drp1 reciprocally regulate cristae morphology, ETC function, and NAD+regeneration in KRas-mutant lung adenocarcinoma
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