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4. Contributors

6. Supplementary Tables from DNA Methylation in Peripheral Blood and Risk of Gastric Cancer: A Prospective Nested Case–control Study

7. Figure S5 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

8. Figure S7 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

9. Figure S2 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

10. Table S1 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

11. Table S2 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

12. Figure S4 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

13. Figure S3 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

14. Data from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

15. Figure S6 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

16. Figure S5 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

17. Table S1 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

18. Figure S4 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

19. Data from DNA Methylation in Peripheral Blood and Risk of Gastric Cancer: A Prospective Nested Case–control Study

20. Supplementary Tables from DNA Methylation in Peripheral Blood and Risk of Gastric Cancer: A Prospective Nested Case–control Study

21. Table S2 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

22. Data from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

23. Data from DNA Methylation in Peripheral Blood and Risk of Gastric Cancer: A Prospective Nested Case–control Study

24. Table S3 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

25. Figure S6 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

26. Figure S1 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

27. Figure S2 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

28. Figure S1 from Rapid Resistance of FGFR-driven Gastric Cancers to Regorafenib and Targeted FGFR Inhibitors can be Overcome by Parallel Inhibition of MEK

34. Supp Legends and Table S1 and S2 from Frizzled-7 Is Required for Wnt Signaling in Gastric Tumors with and Without Apc Mutations

35. Data from Frizzled-7 Is Required for Wnt Signaling in Gastric Tumors with and Without Apc Mutations

37. Fig S7 from Frizzled-7 Is Required for Wnt Signaling in Gastric Tumors with and Without Apc Mutations

38. Data from Frizzled-7 Is Required for Wnt Signaling in Gastric Tumors with and Without Apc Mutations

40. Fig S5 from Frizzled-7 Is Required for Wnt Signaling in Gastric Tumors with and Without Apc Mutations

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