189 results on '"Zhu, Ying‐Hui"'
Search Results
2. HN1L-mediated transcriptional axis AP-2γ/METTL13/TCF3-ZEB1 drives tumor growth and metastasis in hepatocellular carcinoma
3. Expansion of cancer stem cell pool initiates lung cancer recurrence before angiogenesis
4. Overexpression of MUC13, a Poor Prognostic Predictor, Promotes Cell Growth by Activating Wnt Signaling in Hepatocellular Carcinoma
5. Lymphoid enhancer-binding factor-1 promotes stemness and poor differentiation of hepatocellular carcinoma by directly activating the NOTCH pathway
6. TROAP switches DYRK1 activity to drive hepatocellular carcinoma progression
7. The impact of adopting IFRS on corporate ETR and book-tax income gap
8. Data from Downregulation of RBMS3 Is Associated with Poor Prognosis in Esophageal Squamous Cell Carcinoma
9. Supplemental Figure Legends from Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma
10. Supplementary Figure 4 from Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma
11. Supplemental Methods and Reference from Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma
12. Supplemental Tables S1-S2 from Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma
13. Supplementary Methods, Figure Legends, and Tables 1 - 5 from Downregulation of the Novel Tumor Suppressor DIRAS1 Predicts Poor Prognosis in Esophageal Squamous Cell Carcinoma
14. Data from Downregulation of the Novel Tumor Suppressor DIRAS1 Predicts Poor Prognosis in Esophageal Squamous Cell Carcinoma
15. Supplemental Figure S1 from Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma
16. Supplementary Figure 1 from Downregulation of the Novel Tumor Suppressor DIRAS1 Predicts Poor Prognosis in Esophageal Squamous Cell Carcinoma
17. Data from Characterization of a Candidate Tumor Suppressor Gene Uroplakin 1A in Esophageal Squamous Cell Carcinoma
18. Supplementary Figure 1 from Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma
19. Supplementary Figure 2 from Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma
20. Supplementary Figure 3 from Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma
21. Data from Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma
22. Supplementary Methods from Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma
23. Supplementary Table 1 from Characterization of a Candidate Tumor Suppressor Gene Uroplakin 1A in Esophageal Squamous Cell Carcinoma
24. Supplementary Table 1 from Downregulation of RBMS3 Is Associated with Poor Prognosis in Esophageal Squamous Cell Carcinoma
25. Supplementary Figure Legend from Characterization of a Candidate Tumor Suppressor Gene Uroplakin 1A in Esophageal Squamous Cell Carcinoma
26. SSupplementary Tables 1 - 2 from Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma
27. Supplementary Table 2 from Characterization of a Candidate Tumor Suppressor Gene Uroplakin 1A in Esophageal Squamous Cell Carcinoma
28. Supplementary Figure 1 from Characterization of a Candidate Tumor Suppressor Gene Uroplakin 1A in Esophageal Squamous Cell Carcinoma
29. Retraction: ANGPTL1 Interacts with Integrin α1β1 to Suppress HCC Angiogenesis and Metastasis by Inhibiting JAK2/STAT3 Signaling
30. Is Leg-Driven Treadmill-Based Exoskeleton Robot Training Beneficial to Poststroke Patients
31. Hypoxia restrains the expression of complement component 9 in tumor-associated macrophages promoting non-small cell lung cancer progression
32. Is Leg-Driven Treadmill-Based Exoskeleton Robot Training Beneficial to Poststroke Patients: A Systematic Review and Meta-analysis.
33. The promoter hypermethylation of SULT2B1 accelerates esophagus tumorigenesis via downregulated PER1
34. PSCA acts as a tumor suppressor by facilitating the nuclear translocation of RB1CC1 in esophageal squamous cell carcinoma
35. Proteomic analysis of a nasopharyngeal carcinoma cell line and a nasopharyngeal epithelial cell line
36. SERPINA11 Inhibits Metastasis in Hepatocellular Carcinoma by Suppressing MEK/ERK Signaling Pathway
37. Downregulation of LGI1 promotes tumor metastasis in esophageal squamous cell carcinoma
38. Maelstrom Promotes Hepatocellular Carcinoma Metastasis by Inducing Epithelial-Mesenchymal Transition by Way of Akt/GSK-3β/Snail Signaling
39. Laminin γ2–mediating T cell exclusion attenuates response to anti–PD-1 therapy
40. Adenovirus-mediated delivery of human IFNγ gene inhibits prostate cancer growth
41. Tumor Fibroblast–Derived FGF2 Regulates Expression of SPRY1 in Esophageal Tumor–Infiltrating T Cells and Plays a Role in T-cell Exhaustion
42. MicroRNA-144 promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma through repression of PTEN
43. Intensive expression of UNC-51-like kinase 1 is a novel biomarker of poor prognosis in patients with esophageal squamous cell carcinoma
44. Clinical significance and function of RDH16 as a tumor‐suppressing gene in hepatocellular carcinoma
45. Influence of Chinese medicine of Jiangzhi Zhuanggu on bone morphogenetic protein and estrogen receptor expression in bone tissue of hyperlipidemia-induced osteoporosis rats
46. Overexpression of ubiquitin specific peptidase 14 predicts unfavorable prognosis in esophageal squamous cell carcinoma
47. Adenovirus-mediated delivery of interferon-γ gene inhibits the growth of nasopharyngeal carcinoma
48. Role of SIRT1 in hematologic malignancies
49. LINC01554-Mediated Glucose Metabolism Reprogramming Suppresses Tumorigenicity in Hepatocellular Carcinoma via Downregulating PKM2 Expression and Inhibiting Akt/mTOR Signaling Pathway
50. Overexpression of GPR39 contributes to malignant development of human esophageal squamous cell carcinoma
Catalog
Books, media, physical & digital resources
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.