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1. Mutations in JAK2 and Calreticulin genes are associated with specific alterations of the immune system in myelofibrosis

2. Epigenetically induced ectopic expression of UNCX impairs the proliferation and differentiation of myeloid cells

3. Circulating Calreticulin Is Increased in Myelofibrosis: Correlation with Interleukin-6 Plasma Levels, Bone Marrow Fibrosis, and Splenomegaly

4. Integrated genomic-metabolic classification of acute myeloid leukemia defines a subgroup with NPM1 and cohesin/DNA damage mutations

5. Distinct pattern of alterations in tp53 mutated and wild type acute myeloid leukemia (AML) patients

6. Risk factors for infections in myelofibrosis: role of disease status and treatment. A multicenter study of 507 patients

7. Comparison of JAK2V617F-positive essential thrombocythaemia and early primary myelofibrosis: The impact of mutation burden and histology

8. Mutations and long-term outcome of 217 young patients with essential thrombocythemia or early primary myelofibrosis

9. Chromothripsis in AML patients: A new mechanism of cancer initiation and progression

10. You have accessAlterations in Pathways Regulating Phosphatidil Inositol 3 Phosphate (PI3P) Produce Both Cell Proliferation and Therapy Resistance, and Define a Group of Patients with Poor Prognosis in Acute Myeloid Leukemia (AML)

11. Mutations in

12. Risk factors for infections in myelofibrosis: role of disease status and treatment. A multicenter study of 507 patients

13. Mutations in JAK2 and Calreticulin genes are associated with specific alterations of the immune system in myelofibrosis

14. The relevance of a low JAK2V617F allele burden in clinical practice: a monocentric study

15. Epigenetically induced ectopic expression of UNCX impairs the proliferation and differentiation of myeloid cells

16. Abstract 5279: Metabolic profiling defines a new characterization of acute myeloid leukemia and identifies NPM1-mutated cases as a distinct subgroup

17. PF197 A NEW CLASSIFICATION OF ACUTE MYELOID LEUKEMIA BASED ON INTEGRATED GENOMICS AND METABOLOMICS

18. You have accessA New Entity of Acute Myeloid Leukemia Driven By Epigenetic and Somatic Dis-Regulation of Uncx, a Novel Homeobox Transcription Factor Gene

19. Abstract 656: Distinct pattern of alterations in TP53 mutated/deleted and wild-type high risk acute myeloid leukemia (AML) patients: Identification of new "targetable" genes/pathways

20. Comparison of JAK2

21. Assessment of the interlaboratory variability and robustness of JAK2V617F mutation assays: A study involving a consortium of 19 Italian laboratories

22. Tp53 mutation screening in adult acute myeloid leukemia (AML) patients shows a strong association with complex karyotype and poor outcome

23. Efficacy and Safety of Ruxolitinib in Elderly Patients (> 75 years) with Myelofibrosis

24. Circulating Calreticulin Is Increased in Myelofibrosis: Correlation with Interleukin-6 Plasma Levels, Bone Marrow Fibrosis, and Splenomegaly

25. A New Entity of Acute Myeloid Leukemia Driven By Epigenetic and Somatic Dis-Regulation of Uncx, a Novel Homeobox Transcription Factor Gene

26. Abstract 1766: Distinct pattern of alterations in tp53 mutated and wild type acute myeloid leukemia (AML) patients

27. Leukemia Associated TP53 Mutations in AML Patients ARE Strongly Associated with Complex Karyotype and Poor Outcome

28. Signals of the Inflammatory Microenvironment Promote a Mutation-Associated Functional Dysregulation of the Circulating Megakaryocyte Progenitors of Myelofibrosis

29. Abstract 4077: Crucial factors of the inflammatory microenvironment (IL-1β/TNF-α/TIMP-1) promote the selection of highly malignant hemopoietic clone of myelofibrosis

30. Abstract 3582: Chromothripsis in AML patients: A new mechanism of cancer initiation and progression

31. JAK2V617F-Positive Patients with Essential Thrombocythemia or Early Primary Myelofibrosis: The Impact of Histological Diagnosis on Outcome

32. Genomic-Wide Analysis By High Resolution SNP Array Identifies Novel Genomic Alteration in Acute Myeloid Leukemia

33. Risk Factors for Infections in Myelofibrosis: Role of Disease Status and Treatment. A Study on 507 Patients

34. Crucial Factors of the Inflammatory Microenvironment (IL-1 beta/TNF-alpha/TIMP-1) Promote Maintenance of the Malignant Hemopoietic Clone of Myelofibrosis By Stimulating the in Vitro Survival/Proliferation/Migration of Circulating CD34+ stem/Progenitor Cells

35. Abstract B03: Very poor outcome and chemoresistance of acute myeloid leukemia patients with TP53 mutations: Correlation with complex karyotype and clinical outcome

36. Abstract 4906: TP53 mutations are mutually exclusive with FLT3 and NPM mutations in AML patients and are strongly associated with complex karyotype and poor outcome

37. Key Immune Cell Subsets Are Dysregulated in Patients with Myelofibrosis

38. Mutations and Long-Term Outcome of 217 Young Patients with Essential Thrombocythemia or Early Primary Myelofibrosis

39. Loss of Heterozygosity At the C Wild-Type Allele of rs1042522 in the TP53 Gene Frequently Occurs During Progression of Adult BCR-ABL1 Positive Acute Lymphoblastic Leukemia (ALL)

40. Abstract 570: Tp53 mutation screening in adult acute myeloid leukemia (AML) patients shows a strong association with complex karyotype and poor outcome

41. Adult B-Cell Precursor Acute Lymphoblastic Leukemia (BC-ALL) Negative For Recurrent Fusion Genes Are Characterized By a High Complex Genetic Heterogeneity Influencing Prognosis

42. Very Poor Outcome and Chemoresistance of Acute Myeloid Leukemia Patients with TP53 Mutations: Correlation with Complex Karyotype and Clinical Outcome

43. Alterations in Pathways Regulating Phosphatidil Inositol 3 Phosphate (PI3P) Produce Both Cell Proliferation and Therapy Resistance, and Define a Group of Patients with Poor Prognosis in Acute Myeloid Leukemia (AML)

44. A New Entity of Acute Myeloid Leukemia Driven By Epigenetic and Somatic Dis-Regulation of Uncx, a Novel Homeobox Transcription Factor Gene

45. Crucial Factors of the Inflammatory Microenvironment Promote Maintenance of the Malignant Hemopoietic Clone of Myelofibrosis By Stimulating Survival and Inhibiting Proliferation of CD34(+) stem/Progenitor Cells

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