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1. Targeting a lineage-specific PI3Kɣ–Akt signaling module in acute myeloid leukemia using a heterobifunctional degrader molecule

2. Matched Targeted Therapy for Pediatric Patients with Relapsed, Refractory, or High-Risk Leukemias: A Report from the LEAP Consortium

3. P2RY2-AKT activation is a therapeutically actionable consequence of XPO1 inhibition in acute myeloid leukemia

4. Cystine uptake inhibition potentiates front-line therapies in acute myeloid leukemia

7. Hematopoietic differentiation at single-cell resolution in NPM1-mutated AML

8. A multiparametric niche-like drug screening platform in acute myeloid leukemia

9. Tumor Lysis Syndrome and AKI: Beyond Crystal Mechanisms

10. Using antagonistic pleiotropy to design a chemotherapy-induced evolutionary trap to target drug resistance in cancer

12. Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

13. RETRACTED ARTICLE: LAMP2 expression dictates azacytidine response and prognosis in MDS/AML

16. Granulomonocytic progenitors are key target cells of azacytidine in higher risk myelodysplastic syndromes and acute myeloid leukemia

17. Figure S1 from The Folate Cycle Enzyme MTHFR Is a Critical Regulator of Cell Response to MYC-Targeting Therapies

18. Table S6 from The Folate Cycle Enzyme MTHFR Is a Critical Regulator of Cell Response to MYC-Targeting Therapies

19. Supplementary Data from Matched Targeted Therapy for Pediatric Patients with Relapsed, Refractory, or High-Risk Leukemias: A Report from the LEAP Consortium

20. Data from Matched Targeted Therapy for Pediatric Patients with Relapsed, Refractory, or High-Risk Leukemias: A Report from the LEAP Consortium

21. Supplementary Data from The Folate Cycle Enzyme MTHFR Is a Critical Regulator of Cell Response to MYC-Targeting Therapies

22. Figure S5 from Matched Targeted Therapy for Pediatric Patients with Relapsed, Refractory, or High-Risk Leukemias: A Report from the LEAP Consortium

23. Table S1 from Matched Targeted Therapy for Pediatric Patients with Relapsed, Refractory, or High-Risk Leukemias: A Report from the LEAP Consortium

24. Supplementary Tables 1 - 9 from Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

25. Supplementary Methods from Matched Targeted Therapy for Pediatric Patients with Relapsed, Refractory, or High-Risk Leukemias: A Report from the LEAP Consortium

26. Data from The Folate Cycle Enzyme MTHFR Is a Critical Regulator of Cell Response to MYC-Targeting Therapies

27. Supplementary Figures 1 -11 from Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

28. Data from Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

29. Supplementary Figure Legend from Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

30. Exploiting an Asp-Glu “switch” in glycogen synthase kinase 3 to design paralog-selective inhibitors for use in acute myeloid leukemia

31. Supplemental Figure 1 from Gene expression profiling of imatinib and PD166326-resistant CML cell lines identifies Fyn as a gene associated with resistance to BCR-ABL inhibitors

32. Supplemental Table 1 from Gene expression profiling of imatinib and PD166326-resistant CML cell lines identifies Fyn as a gene associated with resistance to BCR-ABL inhibitors

34. Data from Persistent Activation of the Fyn/ERK Kinase Signaling Axis Mediates Imatinib Resistance in Chronic Myelogenous Leukemia Cells through Upregulation of Intracellular SPARC

36. Supplementary Figures 1-6 from Persistent Activation of the Fyn/ERK Kinase Signaling Axis Mediates Imatinib Resistance in Chronic Myelogenous Leukemia Cells through Upregulation of Intracellular SPARC

39. Supplementary Methods from Persistent Activation of the Fyn/ERK Kinase Signaling Axis Mediates Imatinib Resistance in Chronic Myelogenous Leukemia Cells through Upregulation of Intracellular SPARC

41. Supplementary Figure Legends 1-6 from Persistent Activation of the Fyn/ERK Kinase Signaling Axis Mediates Imatinib Resistance in Chronic Myelogenous Leukemia Cells through Upregulation of Intracellular SPARC

44. Favorable pharmacokinetics and pharmacodynamics properties of Gilteritinib in cerebrospinal fluid: a potential effective treatment in relapsing meningeal acute myeloid leukaemia FLT3-ITD patients

45. MCB-613 exploits a collateral sensitivity in drug resistantEGFR-mutant non-small cell lung cancer through covalent inhibition of KEAP1

46. The creatine kinase pathway is a metabolic vulnerability in EVI1-positive acute myeloid leukemia

47. Retraction Note: LAMP2 expression dictates azacytidine response and prognosis in MDS/AML

48. Relative Mitochondrial Priming Predicts Survival in Older AML Patients Treated Intensively

49. JAK Inhibition Mediates Clonal Selection of RAS Pathway Mutations in Myeloproliferative Neoplasms

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