40 results on '"Fan Guixiong"'
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2. Nuclear receptor coactivator 6 (NCoA6) promotes cell proliferation, migration, and invasion in pancreatic cancer
3. Figure S2 from MEN1 Degradation Induced by Neddylation and the CUL4B–DCAF7 Axis Promotes Pancreatic Neuroendocrine Tumor Progression
4. Table S4 from MEN1 Degradation Induced by Neddylation and the CUL4B–DCAF7 Axis Promotes Pancreatic Neuroendocrine Tumor Progression
5. Figure S2 from MEN1 Degradation Induced by Neddylation and the CUL4B–DCAF7 Axis Promotes Pancreatic Neuroendocrine Tumor Progression
6. Figure S1 from MEN1 Degradation Induced by Neddylation and the CUL4B–DCAF7 Axis Promotes Pancreatic Neuroendocrine Tumor Progression
7. Figure S1 from MEN1 Degradation Induced by Neddylation and the CUL4B–DCAF7 Axis Promotes Pancreatic Neuroendocrine Tumor Progression
8. Data from MEN1 Degradation Induced by Neddylation and the CUL4B–DCAF7 Axis Promotes Pancreatic Neuroendocrine Tumor Progression
9. Figure S1 from MEN1 Degradation Induced by Neddylation and the CUL4B–DCAF7 Axis Promotes Pancreatic Neuroendocrine Tumor Progression
10. Figure S2 from MEN1 Degradation Induced by Neddylation and the CUL4B–DCAF7 Axis Promotes Pancreatic Neuroendocrine Tumor Progression
11. Figure S1 from MEN1 Degradation Induced by Neddylation and the CUL4B–DCAF7 Axis Promotes Pancreatic Neuroendocrine Tumor Progression
12. Figure S2 from MEN1 Degradation Induced by Neddylation and the CUL4B–DCAF7 Axis Promotes Pancreatic Neuroendocrine Tumor Progression
13. FigureS1 from MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
14. Supplementary Data from MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
15. FigureS2 from MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
16. FigureS5 from MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
17. Supplementary Data from MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
18. FigureS6 from MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
19. FigureS3 from MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
20. FigureS4 from MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
21. Data from MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
22. FigureS7 from MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
23. Supplementary Data from MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
24. MEN1 Degradation Induced by Neddylation and the CUL4B–DCAF7 Axis Promotes Pancreatic Neuroendocrine Tumor Progression
25. SETD8 inhibits ferroptosis in pancreatic cancer by inhibiting the expression of RRAD
26. MEN1 promotes ferroptosis by inhibiting mTOR-SCD1 axis in pancreatic neuroendocrine tumors
27. Value of lymphadenectomy in patients with surgically resected pancreatic neuroendocrine tumors
28. Value Of Lymphadenectomy In Patients With Surgically Resected Grade 1 Pancreatic Neuroendocrine Tumors
29. Pevonedistat Suppresses Pancreatic Cancer Growth via Inactivation of the Neddylation Pathway
30. SETD8 induces stemness and epithelial–mesenchymal transition of pancreatic cancer cells by regulating ROR1 expression
31. ALDOA inhibits cell cycle arrest induced by DNA damage via the ATM-PLK1 pathway in pancreatic cancer cells
32. MTAP Deficiency–Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer
33. Improved tumor control with antiangiogenic therapy after treatment with gemcitabine and nab‐paclitaxel in pancreatic cancer
34. FGFBP1-mediated crosstalk between fibroblasts and pancreatic cancer cells via FGF22/FGFR2 promotes invasion and metastasis of pancreatic cancer
35. SETD8 potentiates constitutive ERK1/2 activation via epigenetically silencing DUSP10 expression in pancreatic cancer
36. Oncogenic function of TRIM2 in pancreatic cancer by activating ROS-related NRF2/ITGB7/FAK axis
37. Function and regulation of F‑box/WD repeat‑containing protein 7 (Review)
38. Pin1 promotes pancreatic cancer progression and metastasis by activation of NF‐κB‐IL‐18 feedback loop
39. Prognostic Value and Clinical Predictors of Lymph Node Metastases in Pancreatic Neuroendocrine Tumors
40. Ferroptosis: Final destination for cancer?
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