138 results on '"Villeval, Jean-Luc"'
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2. Exacerbation of thromboinflammation by JAK2V617F mutation worsens the prognosis of cerebral venous sinus thrombosis
3. Lessons from mouse models of MPN
4. Supplementary Table from RETRACTED: In Vivo Monitoring of Polycythemia Vera Development Reveals Carbonic Anhydrase 1 as a Potent Therapeutic Target
5. Data from RETRACTED: In Vivo Monitoring of Polycythemia Vera Development Reveals Carbonic Anhydrase 1 as a Potent Therapeutic Target
6. Supplementary Data from RETRACTED: In Vivo Monitoring of Polycythemia Vera Development Reveals Carbonic Anhydrase 1 as a Potent Therapeutic Target
7. Erythrocyte-derived microvesicles induce arterial spasms in [JAK2.sup.V617F] myeloproliferative neoplasm
8. Comparison of endothelial promoter efficiency and specificity in mice reveals a subset of Pdgfb‐positive hematopoietic cells
9. Rare type 1-like and type 2-like calreticulin mutants induce similar myeloproliferative neoplasms as prevalent type 1 and 2 mutants in mice
10. Calreticulin del52 and ins5 knock-in mice recapitulate different myeloproliferative phenotypes observed in patients with MPN
11. PPAR[gamma] agonists promote the resolution of myelofibrosis in preclinical models
12. SRSF2-P95H decreases JAK/STAT signaling in hematopoietic cells and delays myelofibrosis development in mice
13. Data from In Vivo Monitoring of Polycythemia Vera Development Reveals Carbonic Anhydrase 1 as a Potent Therapeutic Target
14. Supplementary Data from In Vivo Monitoring of Polycythemia Vera Development Reveals Carbonic Anhydrase 1 as a Potent Therapeutic Target
15. Supplementary Table from In Vivo Monitoring of Polycythemia Vera Development Reveals Carbonic Anhydrase 1 as a Potent Therapeutic Target
16. Supplementary Tables 1 to 11 from Ontogenic Changes in Hematopoietic Hierarchy Determine Pediatric Specificity and Disease Phenotype in Fusion Oncogene–Driven Myeloid Leukemia
17. Data from Ontogenic Changes in Hematopoietic Hierarchy Determine Pediatric Specificity and Disease Phenotype in Fusion Oncogene–Driven Myeloid Leukemia
18. Supplementary Figures and Legends from Ontogenic Changes in Hematopoietic Hierarchy Determine Pediatric Specificity and Disease Phenotype in Fusion Oncogene–Driven Myeloid Leukemia
19. Calreticulin mutants in mice induce an MPL-dependent thrombocytosis with frequent progression to myelofibrosis
20. SRSF2-P95H decreases JAK/STAT signaling in hematopoietic cells and delays myelofibrosis development in mice
21. In Vivo Monitoring of Polycythemia Vera Development Reveals Carbonic Anhydrase 1 as a Potent Therapeutic Target
22. Inferring the dynamics of mutated hematopoietic stem and progenitor cells induced by IFNα in myeloproliferative neoplasms
23. SRSF2-P95Hdelays Myelofibrosis Development through Altered JAK/STAT Signaling in JAK2-V617F Megakaryocytes
24. JAK2V617F myeloproliferative neoplasm eradication by a novel interferon/arsenic therapy involves PML
25. Calreticulin del52 and ins5 knock-in mice recapitulate different myeloproliferative phenotypes observed in patients with MPN.
26. Palbociclib Prevents CDK4/6 Dependent-Myeloproliferation and Myelofibrosis
27. In VitroandIn VivoInteractions between Stromal and Leukemic Cells
28. 1017 – INVESTIGATING THE MECHANISMS OF IFNALPHA THERAPY IN JAK2V617F AND CALR MUTATED MYELOPROLIFERATIVE NEOPLASMS
29. Ontogenic Changes in Hematopoietic Hierarchy Determine Pediatric Specificity and Disease Phenotype in Fusion Oncogene–Driven Myeloid Leukemia
30. Vascular endothelial cell expression of JAK2V617F is sufficient to promote a pro-thrombotic state due to increased P-selectin expression
31. Disease Phenotype and Clonal Amplification in Calreticulin del52 and ins5 Knock-in Mice Are Dependent on the Type of Mutations and Gene Dosage
32. Predicting the Long-Term Efficacy of Ifnα in JAK2V617F and Calr-Mutated MPN Patients
33. Differential Impact of Interferon Alpha on JAK2V617F and Calr Mutated Hematopoietic Stem and Progenitor Cells in Classical MPN
34. Specific and Synergistic Targeting of JAK2V617F Cells By Interferon Alpha and Arsenic
35. Rare type 1-like and type 2-like calreticulin mutants induce similar myeloproliferative neoplasms as prevalent type 1 and 2 mutants in mice
36. Vascular endothelial cell expression of JAK2V617F is sufficient to promote a pro-thrombotic state due to increased P-selectin expression
37. Endothelial JAK2 does not enhance liver lesions in mice with Budd-Chiari syndrome
38. HSP27 is a partner of JAK2-STAT5 and a potential therapeutic target in myelofibrosis
39. Endothelial-to-Mesenchymal Transition in Bone Marrow and Spleen of Primary Myelofibrosis
40. Following the in vivo expansion of a myeloproliferative disease
41. Endothelial-to-Mesenchymal Transition in Bone Marrow and Spleen of Primary Myelofibrosis
42. Inhibitors of the PI3K/mTOR pathway prevent STAT5 phosphorylation in JAK2V617F mutated cells through PP2A/CIP2A axis
43. HSP27: A Therapeutic Target in Myelofibrosis
44. Exacerbation of thrombo-inflammation by JAK2V617Fmutation worsens the prognosis of cerebral venous sinus thrombosis
45. Calreticulin mutants in mice induce an MPL-dependent thrombocytosis with frequent progression to myelofibrosis.
46. Complete Inhibition of STAT5 Phosphorylation Is Achieved By Combination of JAK1/2 and PI3K/mTOR Inhibitors in in Vitro and In Vivo MPN Models
47. JAK2 inhibition has different therapeutic effects according to myeloproliferative neoplasm development in mice
48. Consequences of the Presence of the JAK2V617F Mutation in Endothelial Cells: Towards a Better Understanding of the Increased Angiogenesis in Myeloproliferative Neoplasms
49. Calr Mutants Retroviral Mouse Models Lead to a Myeloproliferative Neoplasm Mimicking an Essential Thrombocythemia Progressing to a Myelofibrosis
50. Thrombopoietin Activates STAT2 Inducing Type I Interferon Effects and Gene Expression: Implications for in Vivo Tpo Treatment and for Myeloproliferative Neoplasms
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