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12. Effects of Erythropoiesis-Stimulating Agents on Overall Survival of IPSS Low/INT-1 Risk Transfusion Independent Myelodysplastic Syndrome Patients, a FISM Study

13. O que família de crianças com deficiência tem a nos dizer sobre a inclusão escolar de seus filhos?

26. universal markers of minimal residual disease

32. Myelodysplastic syndromes

37. O-020 Erythropoietin alpha therapy in 1110 lower-risk MDS patients: A real life survey from the network of regional Italian MDS Registries

38. Deferasirox is a powerful NF- B inhibitor in myelodysplastic cells and in leukemia cell lines acting independently from cell iron deprivation by chelation and reactive oxygen species scavenging

39. Correction: Proteinase 3 (PR3) gene is highly expressed in CBF leukemias and codes for a protein with abnormal nuclear localization that confers drug sensitivity

40. Proteinase 3 (PR3) gene is highly expressed in CBF leukemias and codes for a protein with abnormal nuclear localization that confers drug sensitivity

42. Early prediction of treatment outcome in acute myeloid leukemia by measurement of WT1 transcript levels in peripheral blood samples collected after chemotherapy

43. Imatinib mesylate in the treatment of newly diagnosed or refractory/resistant c-KIT positive acute myeloid leukemia. Results of an italian multicentric phase II study.

44. P002 Clinical and epidemiological considerations on myelodysplastic syndromes (MDS). The experience of the Piedmont MDS Register

45. P052 Detection of humoral immune responses against Wilms tumor gene (WT1) product in patients affected by myelodysplastic syndromes

46. P137 Response to erythropoietin (EPO) with or without differentiating treatment with 13-cis-retinoic-acid and dihydroxylated vitamin D3 in myelodysplastic syndromes (MDS)

47. P036 The oral iron chelator ICL670 is a potent inhibitor of NF-kB and this activity is independent from iron overload in MDS cells

48. The NF-κB pathway blockade by the IKK inhibitor PS1145 can overcome Imatinib resistance

49. Correction: Proteinase 3 (PR3) gene is highly expressed in CBF leukemias and codes for a protein with abnormal nuclear localization that confers drug sensitivity

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