264 results on '"Park, Kwon-Sik"'
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2. Genetically-engineered mouse models of small cell lung cancer: the next generation
3. Effect of chromatin modifiers on the plasticity and immunogenicity of small-cell lung cancer
4. Regulation of UHRF1 acetylation by TIP60 is important for colon cancer cell proliferation
5. CRACD loss induces neuroendocrine cell plasticity of lung adenocarcinoma
6. Opa1 and Drp1 reciprocally regulate cristae morphology, ETC function, and NAD+ regeneration in KRas-mutant lung adenocarcinoma
7. New Approaches to SCLC Therapy: From the Laboratory to the Clinic
8. Nfib Promotes Metastasis through a Widespread Increase in Chromatin Accessibility
9. Reprogramming fatty acyl specificity of lipid kinases via C1 domain engineering
10. Comprehensive genomic profiles of small cell lung cancer
11. Recent progress in mapping the emerging landscape of the small-cell lung cancer genome
12. Phase I Study of Entinostat, Atezolizumab, Carboplatin, and Etoposide in Previously Untreated Extensive-Stage Small Cell Lung Cancer, ETCTN 10399
13. Robo1 loss has pleiotropic effects on postnatal development and survival
14. CRACD suppresses neuroendocrinal plasticity of lung adenocarcinoma
15. Data from Crebbp Loss Drives Small Cell Lung Cancer and Increases Sensitivity to HDAC Inhibition
16. Supplementary_table_S5 from Intertumoral Heterogeneity in SCLC Is Influenced by the Cell Type of Origin
17. Supplementary Figure S1-S17 from Intertumoral Heterogeneity in SCLC Is Influenced by the Cell Type of Origin
18. Data from Intertumoral Heterogeneity in SCLC Is Influenced by the Cell Type of Origin
19. Figures S1-S16 from Crebbp Loss Drives Small Cell Lung Cancer and Increases Sensitivity to HDAC Inhibition
20. Tables S1-S5 from Crebbp Loss Drives Small Cell Lung Cancer and Increases Sensitivity to HDAC Inhibition
21. 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
22. 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
23. Data from WNT5A–RHOA Signaling Is a Driver of Tumorigenesis and Represents a Therapeutically Actionable Vulnerability in Small Cell Lung Cancer
24. Supplementary Data from WNT5A–RHOA Signaling Is a Driver of Tumorigenesis and Represents a Therapeutically Actionable Vulnerability in Small Cell Lung Cancer
25. 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
26. 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
27. Supplementary Figure from WNT5A–RHOA Signaling Is a Driver of Tumorigenesis and Represents a Therapeutically Actionable Vulnerability in Small Cell Lung Cancer
28. 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
29. Supplementary Methods from FGFR1 Is Critical for RBL2 Loss–Driven Tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell Lung Cancer
30. 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
31. Supplementary Table from WNT5A–RHOA Signaling Is a Driver of Tumorigenesis and Represents a Therapeutically Actionable Vulnerability in Small Cell Lung Cancer
32. Supplementary File S1 from Fragmentation of Small-Cell Lung Cancer Regulatory States in Heterotypic Microenvironments
33. 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
34. Data from Fragmentation of Small-Cell Lung Cancer Regulatory States in Heterotypic Microenvironments
35. 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
36. 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
37. Supplementary Data from Fragmentation of Small-Cell Lung Cancer Regulatory States in Heterotypic Microenvironments
38. Data from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
39. Supplementary Figure 7 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
40. Supplementary Figure 6B from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
41. Supplementary Figure 5 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
42. 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
43. Supplementary Figure 1 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
44. Supplementary Figure 3 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
45. Supplementary Figure 4 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
46. Supplementary Figure 8 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
47. Supplementary Figure 2 from Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
48. In situ 10-cell RNA sequencing in tissue and tumor biopsy samples
49. BCAT1 inhibition affects CD8+T cell activation, exhaustion, and tumoral immunity by altering iron homeostasis
50. CRACD loss promotes small cell lung cancer tumorigenesis via EZH2-mediated immune evasion
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