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1. Thoraxtrauma

2. MIF/NR3C2 Axis Regulates Glucose Metabolism Reprogramming in Pancreatic Cancer through MAPK-ERK and AP-1 Pathways

3. Hard wiring of normal tissue-specific chromosome-wide gene expression levels is an additional factor driving cancer type-specific aneuploidies

7. Abstract 6225: SERPINB3 promotes the aggressive basal-like/squamous subtype and correlates with poor prognosis in pancreatic ductal adenocarcinoma through metabolic reprogramming

9. Figure S1 from Chemoradiotherapy Resistance in Colorectal Cancer Cells is Mediated by Wnt/β-catenin Signaling

10. Table S3 from Chemoradiotherapy Resistance in Colorectal Cancer Cells is Mediated by Wnt/β-catenin Signaling

11. Data from Chemoradiotherapy Resistance in Colorectal Cancer Cells is Mediated by Wnt/β-catenin Signaling

12. Supplementary Figure and Table Legends from Chemoradiotherapy Resistance in Colorectal Cancer Cells is Mediated by Wnt/β-catenin Signaling

13. Supplementary Table 3 from The Rectal Cancer microRNAome – microRNA Expression in Rectal Cancer and Matched Normal Mucosa

14. Supplementary Table 2 from The Rectal Cancer microRNAome – microRNA Expression in Rectal Cancer and Matched Normal Mucosa

15. Supplementary Table 4 from The Rectal Cancer microRNAome – microRNA Expression in Rectal Cancer and Matched Normal Mucosa

16. Supplementary Table S2 from Integration of Metabolomics and Transcriptomics Revealed a Fatty Acid Network Exerting Growth Inhibitory Effects in Human Pancreatic Cancer

17. Supplementary Materials and Methods from Endothelial Nitric Oxide Synthase Traffic Inducer (NOSTRIN) is a Negative Regulator of Disease Aggressiveness in Pancreatic Cancer

18. Supplementary Figure S2 from Integration of Metabolomics and Transcriptomics Revealed a Fatty Acid Network Exerting Growth Inhibitory Effects in Human Pancreatic Cancer

19. Supplementary Table S4-S7 from Endothelial Nitric Oxide Synthase Traffic Inducer (NOSTRIN) is a Negative Regulator of Disease Aggressiveness in Pancreatic Cancer

20. Supplementary Figure 1 from The Rectal Cancer microRNAome – microRNA Expression in Rectal Cancer and Matched Normal Mucosa

21. Supplementary Figure 2 from The Rectal Cancer microRNAome – microRNA Expression in Rectal Cancer and Matched Normal Mucosa

22. Supplementary Table 1 from The Rectal Cancer microRNAome – microRNA Expression in Rectal Cancer and Matched Normal Mucosa

23. Supplementary Table S3 from Endothelial Nitric Oxide Synthase Traffic Inducer (NOSTRIN) is a Negative Regulator of Disease Aggressiveness in Pancreatic Cancer

24. Supplementary Data from Failure of Downregulation of Survivin Following Neoadjuvant Radiochemotherapy in Rectal Cancer Is Associated with Distant Metastases and Shortened Survival

25. Supplementary Materials and Methods from Integration of Metabolomics and Transcriptomics Revealed a Fatty Acid Network Exerting Growth Inhibitory Effects in Human Pancreatic Cancer

26. Supplementary Figure 4 from The Rectal Cancer microRNAome – microRNA Expression in Rectal Cancer and Matched Normal Mucosa

27. Supplementary Figure 3 from The Rectal Cancer microRNAome – microRNA Expression in Rectal Cancer and Matched Normal Mucosa

28. Data from Gene Expression Profiling Reveals a Massive, Aneuploidy-Dependent Transcriptional Deregulation and Distinct Differences between Lymph Node–Negative and Lymph Node–Positive Colon Carcinomas

29. Data from Aneuploidy-Dependent Massive Deregulation of the Cellular Transcriptome and Apparent Divergence of the Wnt/β-catenin Signaling Pathway in Human Rectal Carcinomas

30. Supplementary Table S3 from Genetic Amplification of the NOTCH Modulator LNX2 Upregulates the WNT/β-Catenin Pathway in Colorectal Cancer

31. Supplementary Tables 1-9 from Aneuploidy-Dependent Massive Deregulation of the Cellular Transcriptome and Apparent Divergence of the Wnt/β-catenin Signaling Pathway in Human Rectal Carcinomas

32. Supplementary Figure 1 from Gene Expression Profiling Reveals a Massive, Aneuploidy-Dependent Transcriptional Deregulation and Distinct Differences between Lymph Node–Negative and Lymph Node–Positive Colon Carcinomas

33. Supplementary Figure Legends 1-2 from Chromosomal Breakpoints in Primary Colon Cancer Cluster at Sites of Structural Variants in the Genome

34. Supplementary Figure S2 from Genetic Amplification of the NOTCH Modulator LNX2 Upregulates the WNT/β-Catenin Pathway in Colorectal Cancer

35. Data from Genetic Amplification of the NOTCH Modulator LNX2 Upregulates the WNT/β-Catenin Pathway in Colorectal Cancer

36. Supplementary Tables S1-S9 from A Novel MIF Signaling Pathway Drives the Malignant Character of Pancreatic Cancer by Targeting NR3C2

37. Supplementary Figure 1-12 from A Novel MIF Signaling Pathway Drives the Malignant Character of Pancreatic Cancer by Targeting NR3C2

39. Data from A Novel MIF Signaling Pathway Drives the Malignant Character of Pancreatic Cancer by Targeting NR3C2

40. Data from Chromosomal Breakpoints in Primary Colon Cancer Cluster at Sites of Structural Variants in the Genome

41. Supplementary Table 1 from Chromosomal Breakpoints in Primary Colon Cancer Cluster at Sites of Structural Variants in the Genome

42. Supplementary Tables 1-5 from Gene Expression Profiling Reveals a Massive, Aneuploidy-Dependent Transcriptional Deregulation and Distinct Differences between Lymph Node–Negative and Lymph Node–Positive Colon Carcinomas

43. Supplementary Figure 2 from Chromosomal Breakpoints in Primary Colon Cancer Cluster at Sites of Structural Variants in the Genome

45. Supplementary Figure 1 from Chromosomal Breakpoints in Primary Colon Cancer Cluster at Sites of Structural Variants in the Genome

46. Supplementary Information from A Novel MIF Signaling Pathway Drives the Malignant Character of Pancreatic Cancer by Targeting NR3C2

47. Supplementary Table 2 from Chromosomal Breakpoints in Primary Colon Cancer Cluster at Sites of Structural Variants in the Genome

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