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1. Correction to: Exploring the ATR-CHK1 pathway in the response of doxorubicin-induced DNA damages in acute lymphoblastic leukemia cells

2. Exploring the ATR-CHK1 pathway in the response of doxorubicin-induced DNA damages in acute lymphoblastic leukemia cells

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

4. Safety profile and impact on survival of tyrosine kinase inhibitors versus conventional therapy in relapse or refractory FLT3 positive acute myeloid leukemia patients

6. Chromothripsis in acute myeloid leukemia: biological features and impact on survival

7. Supplementary Data from Release of IFNγ by Acute Myeloid Leukemia Cells Remodels Bone Marrow Immune Microenvironment by Inducing Regulatory T Cells

8. Data from Release of IFNγ by Acute Myeloid Leukemia Cells Remodels Bone Marrow Immune Microenvironment by Inducing Regulatory T Cells

10. Targeting WEE1 to enhance conventional therapies for acute lymphoblastic leukemia

11. Release of IFNγ by Acute Myeloid Leukemia Cells Remodels Bone Marrow Immune Microenvironment by Inducing Regulatory T Cells

13. Impact of Comorbidities on Prognosis of Elderly Patients with Acute Myeloid Leukemia Who Receive Hypomethylating Agents

14. Exploring the ATR-CHK1 pathway in the response of doxorubicin-induced DNA damages in acute lymphoblastic leukemia cells

15. Exploring the ATR-CHK1 Pathway in the Response of Doxorubicin-induced DNA Damages in Acute Lymphoblastic Leukemia Cells

16. Pharmacological Inhibition of WIP1 Sensitizes Acute Myeloid Leukemia Cells to the MDM2 Inhibitor Nutlin-3a

17. MEC (mitoxantrone, etoposide, and cytarabine) induces complete remission and is an effective bridge to transplant in acute myeloid leukemia

18. Exploiting genomic instability in Acute Myeloid Leukemia: when TP53 fails

19. Novel and Rare Fusion Transcripts Involving Transcription Factors and Tumor Suppressor Genes in Acute Myeloid Leukemia

20. The Prolonged Inhibition of Chk1/Chk2 Kinases Enhances Genetic Instability and Compromises the Efficacy of Chemotherapy Against Acute Lymphoblastic Leukemia Cells

21. AML-CM Score Predicts Prognosis in Hemato-Geriatric Patients with New-Onset Acute Myeloid Leukemia (AML) Who Receive Hypomethylating Agents (HMA)

22. Aurora Kinase a/MDM2-Mediated SETD2 Loss of Function in Chronic Myeloid Leukemia Patients in Blast Crisis Can be Therapeutically Targeted Inducing Apoptotic Cell Death in a Caspase-Dependent Way

23. In Systemic Masocytosis, Midostaurin Targets Both Kit and Aurora Kinase a Reverting H3K36Me3 Deficiency and Synergizes with Second-Generation Tyrosine Kinase Inhibitors

24. Identification of Two DNMT3A Mutations Compromising Protein Stability and Methylation Capacity in Acute Myeloid Leukemia

25. Abstract 5279: Metabolic profiling defines a new characterization of acute myeloid leukemia and identifiesNPM1-mutated cases as a distinct subgroup

26. Abstract 3100: Blinatumomab is safe and effective in relapsed and MRD positive B-ALL CD19+ patients: The bologna compassionate program experience

27. Abstract 2964: Pharmacological inhibition of WIP1 by GSK2830371 sensitizes AML cells to MDM2 inhibitor Nutlin-3a

28. Acute Myeloid Leukemia Mutations: Therapeutic Implications

29. Blinatumomab is safe and effective in relapsed and MRD-positive B-ALL CD19+ patients: The Bologna Compassionate Program Experience.

30. Exploiting genomic instability in Acute Myeloid Leukemia: when TP53 fails.

31. A cell cycle-related genomic and transcriptomic signature distinguish aneuploid and euploid acute myeloid leukemia

32. Specific chromosomic alterations confer therapy resistance in a cohort of 49 patients with newly diagnosed acute myeloid leukemia treated with intensive chemotherapy

33. Integrated genomic-metabolic classification of acute myeloid leukemia defines a subgroup with NPM1and cohesin/DNA damage mutations

34. Higher Expression of PALB2 Predict Poor Prognosis in AML Patients and Identifies Potential Targets of Synthetic Lethal Therapies

35. Biology of Acute Myeloid Leukemia (AML) with Monosomy of Chromosome 7 or Loss of 7q. a Study on 487 Patients Analyzed By Gene Expression Profile (GEP), Single Nucleotide Polymorphism (SNP) Arrays and Metabolomics

36. MDM2 and Aurora Kinase a Contribute to SETD2 Loss of Function in Advanced Systemic Mastocytosis: Implications for Pathogenesis and Treatment

37. Mitoxantrone, Etoposide and Cytarabine (MEC) Can Induce Deep Complete Remission and Is an Effective Bridge Therapy to Allotransplantation (SCT) in Refractory/Relapsed Acute Myeloid Leukemia (AML) Patients

38. Aurora Kinase a/MDM2-Mediated SETD2 Loss of Function in Chronic Myeloid Leukemia Patients in Blast Crisis Induces Genetic Instability and Can be Therapeutically Targeted

39. A New Gene Expression Profile Signature CRLF2 Overexpression Based Identifies Novel Adult "Triple Negative" Acute Lymphoblastic Leukemia Subgroups

40. Aneuploid acute myeloid leukemia exhibits a signature of genomic alterations in the cell cycle and protein degradation machinery

41. Abstract 3613: Lab-on-a-chip-based in-vitro functional profiling proves to be effective in predicting therapy outcome in AML patients

42. 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

44. Abstract 2539: Antiapoptotic gene expression signature reveals a combined talk to prevent apoptosis: A model to choose the proper BH-3 mimetic drug

45. Abstract 1872: Pharmacological inhibition of WIP1 sensitizes AML cells to MDM2 inhibitors

46. TP53 mutations are mutually exclusive with FLT3 and NPM mutations in AML patients and are strongly associated with complex karyotype and poor outcome

47. A Three-Genes Signature of Anti-Apoptotic Genes Showed Different Mechanisms in Preventing Apoptosis in Acute Myeloid Leukemia Cells and Could Provide an Useful Model to Establish the Proper BH3-Mimetich Drug or Combination

48. Abstract 4671: Co-occurrence of alterations in the DNA damage repair genes synergize with uncontrolled proliferation and associate with very-poor prognosis in acute myeloid leukemia patients

49. Abstract 3472: Separase overexpression defines a new subset of acute myeloma leukemia patients characterized by high CD34 and MYC levels

50. Abstract 3311: The alteration in key regulator genes of autophagy is mainstream mechanism of therapy resistance and impact prognosis of acute myelogenous leukemia (AML): results from diagnosis genomic analysis on 148 consecutive patients treated with intensive chemotherapy and long-term survival follow-up

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