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1. Tumor-intrinsic expression of the autophagy gene Atg16l1 suppresses anti-tumor immunity in colorectal cancer

3. Colon tumour cell death causes mTOR dependence by paracrine P2X4 stimulation

4. Antibody targeting of E3 ubiquitin ligases for receptor degradation

5. Lgr5+ telocytes are a signaling source at the intestinal villus tip.

6. Obligate role for Rock1 and Rock2 in adult stem cell viability and function

7. Disruption of stem cell niche–confined R-spondin 3 expression leads to impaired hematopoiesis

8. Atoh1+ secretory progenitors possess renewal capacity independent of Lgr5+ cells during colonic regeneration

9. Parasitic helminths induce fetal-like reversion in the intestinal stem cell niche

10. Gremlin 1+ fibroblastic niche maintains dendritic cell homeostasis in lymphoid tissues

12. Opposing Activities of Notch and Wnt Signaling Regulate Intestinal Stem Cells and Gut Homeostasis

14. Lgr5-Expressing Cells Are Sufficient and Necessary for Postnatal Mammary Gland Organogenesis

22. Data from Targeting Superficial or Nodular Basal Cell Carcinoma with Topically Formulated Small Molecule Inhibitor of Smoothened

23. Supplementary Figure from Frequency and Genomic Aspects of Intrinsic Resistance to Vismodegib in Locally Advanced Basal Cell Carcinoma

24. Supplementary Data from Frequency and Genomic Aspects of Intrinsic Resistance to Vismodegib in Locally Advanced Basal Cell Carcinoma

25. Supplementary Data Figures from A Clinically Applicable Gene-Expression Classifier Reveals Intrinsic and Extrinsic Contributions to Consensus Molecular Subtypes in Primary and Metastatic Colon Cancer

26. Supplementary Data Tables from A Clinically Applicable Gene-Expression Classifier Reveals Intrinsic and Extrinsic Contributions to Consensus Molecular Subtypes in Primary and Metastatic Colon Cancer

28. Supplementary Data from Targeting Superficial or Nodular Basal Cell Carcinoma with Topically Formulated Small Molecule Inhibitor of Smoothened

29. Supplementary Table 3 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

33. Data from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

34. Supplementary Table 7 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

35. Supplementary Table 2 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

36. Data from Antibody-Drug Conjugates for the Treatment of Non–Hodgkin's Lymphoma: Target and Linker-Drug Selection

37. Supplementary Table 4 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

38. Data from Maternal Embryonic Leucine Zipper Kinase/Murine Protein Serine-Threonine Kinase 38 Is a Promising Therapeutic Target for Multiple Cancers

40. Supplementary Methods, Figure Legends 1-6 from Small Molecule Inhibition of GDC-0449 Refractory Smoothened Mutants and Downstream Mechanisms of Drug Resistance

41. Supplementary Figure 1 from Antibody-Drug Conjugates for the Treatment of Non–Hodgkin's Lymphoma: Target and Linker-Drug Selection

42. Supplementary Table 5 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

43. Supplementary Table 1 from Small Molecule Inhibition of GDC-0449 Refractory Smoothened Mutants and Downstream Mechanisms of Drug Resistance

45. Supplementary Table 6 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

46. Supplementary Figures 1-6 from Small Molecule Inhibition of GDC-0449 Refractory Smoothened Mutants and Downstream Mechanisms of Drug Resistance

47. Supplementary Table 1 from Antibody-Drug Conjugates for the Treatment of Non–Hodgkin's Lymphoma: Target and Linker-Drug Selection

48. Data from Small Molecule Inhibition of GDC-0449 Refractory Smoothened Mutants and Downstream Mechanisms of Drug Resistance

49. Supplementary Legends from Maternal Embryonic Leucine Zipper Kinase/Murine Protein Serine-Threonine Kinase 38 Is a Promising Therapeutic Target for Multiple Cancers

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