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1. Remodelling of the fibre-aggregate structure of collagen gels by cancer-associated fibroblasts: a time-resolved grey-tone image analysis based on stochastic modelling

4. Lipid droplet degradation by autophagy connects mitochondria metabolism to Prox1-driven expression of lymphatic genes and lymphangiogenesis

11. Catalytically Inactive Human Cathepsin D Triggers Fibroblast Invasive Growth

13. The Plasminogen Activator Inhibitor PAI-1 Controls in Vivo Tumor Vascularization by Interaction with Proteases, Not Vitronectin: Implications for Antiangiogenic Strategies

17. Supplementary Data from Expression of MT4-MMP, EGFR, and RB in Triple-Negative Breast Cancer Strongly Sensitizes Tumors to Erlotinib and Palbociclib Combination Therapy

18. Supplementary Figure 3 from Stromal Estrogen Receptor-α Promotes Tumor Growth by Normalizing an Increased Angiogenesis

19. Data from Stromal Estrogen Receptor-α Promotes Tumor Growth by Normalizing an Increased Angiogenesis

20. Supplementary Table 1 to 4 from Tissue Factor Induced by Epithelial–Mesenchymal Transition Triggers a Procoagulant State That Drives Metastasis of Circulating Tumor Cells

21. Supplementary Figure 5 from Stromal Estrogen Receptor-α Promotes Tumor Growth by Normalizing an Increased Angiogenesis

22. Supplementary Figure 6 from Stromal Estrogen Receptor-α Promotes Tumor Growth by Normalizing an Increased Angiogenesis

23. Supplementary Figure 2 from Stromal Estrogen Receptor-α Promotes Tumor Growth by Normalizing an Increased Angiogenesis

24. Supplementary Figure 4 from Stromal Estrogen Receptor-α Promotes Tumor Growth by Normalizing an Increased Angiogenesis

25. Supplementary Figure 1 from Stromal Estrogen Receptor-α Promotes Tumor Growth by Normalizing an Increased Angiogenesis

26. Supplementary Materials and Methods from Tissue Factor Induced by Epithelial–Mesenchymal Transition Triggers a Procoagulant State That Drives Metastasis of Circulating Tumor Cells

27. Supplementary Figure Legends from Tissue Factor Induced by Epithelial–Mesenchymal Transition Triggers a Procoagulant State That Drives Metastasis of Circulating Tumor Cells

28. Supplementary Methods, Table 1 from Stromal Estrogen Receptor-α Promotes Tumor Growth by Normalizing an Increased Angiogenesis

29. Supplementary Figures S1-S7 from Tissue Factor Induced by Epithelial–Mesenchymal Transition Triggers a Procoagulant State That Drives Metastasis of Circulating Tumor Cells

30. Data from Tissue Factor Induced by Epithelial–Mesenchymal Transition Triggers a Procoagulant State That Drives Metastasis of Circulating Tumor Cells

31. Supplementary Figure 7 from Stromal Estrogen Receptor-α Promotes Tumor Growth by Normalizing an Increased Angiogenesis

47. Inhibition of Tumor Angiogenesis and Growth by a Small-Molecule Multi-FGF Receptor Blocker with Allosteric Properties

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