190 results on '"Long, Nicola"'
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2. An expanded universe of cancer targets
3. Comparison and validation of the 2022 European LeukemiaNet guidelines in acute myeloid leukemia
4. Associating drug sensitivity with differentiation status identifies effective combinations for acute myeloid leukemia
5. Identification and prioritization of myeloid malignancy germline variants in a large cohort of adult patients with AML
6. Leukemic mutation FLT3-ITD is retained in dendritic cells and disrupts their homeostasis leading to expanded Th17 frequency
7. Reversible suppression of T cell function in the bone marrow microenvironment of acute myeloid leukemia
8. Mapping the proteogenomic landscape enables prediction of drug response in acute myeloid leukemia
9. Table S4 from Clinical Correlates of Venetoclax-Based Combination Sensitivities to Augment Acute Myeloid Leukemia Therapy
10. Supplementary Figure S2 from Clinical Correlates of Venetoclax-Based Combination Sensitivities to Augment Acute Myeloid Leukemia Therapy
11. Data from Clinical Correlates of Venetoclax-Based Combination Sensitivities to Augment Acute Myeloid Leukemia Therapy
12. Simultaneous kinase inhibition with ibrutinib and BCL2 inhibition with venetoclax offers a therapeutic strategy for acute myeloid leukemia
13. Genomic landscape of neutrophilic leukemias of ambiguous diagnosis
14. CSF1R inhibitors exhibit antitumor activity in acute myeloid leukemia by blocking paracrine signals from support cells
15. Clinical Correlates of Venetoclax-Based Combination Sensitivities to Augment Acute Myeloid Leukemia Therapy
16. Immune cell proportions correlate with clinicogenomic features and ex vivo drug responses in acute myeloid leukemia
17. CDK12 /13 dual inhibitors are potential therapeutics for acute myeloid leukemia
18. Functional genomic landscape of acute myeloid leukaemia
19. Supplementary Table 5 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
20. Supplementary Table 4 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
21. Supplementary Table 9 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
22. Supplementary Table 2 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
23. Supplementary Fig. 11 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
24. Supplementary Table 7 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
25. Supplementary Table 11 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
26. Supplementary Fig. 3 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
27. Supplementary Fig. 6 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
28. Data from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
29. Supplementary Fig. 5 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
30. Supplementary Table 6 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
31. Supplementary Fig. 7 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
32. Supplementary Table 8 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
33. Supplementary Fig. 4 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
34. Supplementary Materials and Methods from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
35. Supplementary Table 3 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
36. Supplementary Fig. 2 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
37. Supplementary Fig. 9 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
38. Supplementary Fig. 8 from Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
39. Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
40. NGS-defined measurable residual disease (MRD) after initial chemotherapy as a prognostic biomarker for acute myeloid leukemia
41. Defining Clinical and Molecular Biomarkers for Venetoclax-Based Drug Combinations to Augment AML Therapy
42. Integrative analysis of drug response and clinical outcome in acute myeloid leukemia
43. CDK12/13 dual inhibitors are potential therapeutics for acute myeloid leukemia.
44. Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
45. Associating Ex Vivo Drug Sensitivity with Differentiation Status Identifies Effective Drug Combinations for Acute Myeloid Leukemia
46. Not your average birth: considering the possibility of denied or concealed pregnancy
47. Royal Tourism: Excursions around Monarchy
48. Acute Myeloid Leukemia Differentiation State and Genotype Influence Anti-Apoptotic Protein Expression, Venetoclax Sensitivity, and Survival in AML
49. Patterns of Venetoclax Sensitivity in Chronic Lymphocytic Leukemia
50. Simultaneous Kinase Inhibition with Ibrutinib and BCL2 Inhibition with Venetoclax As a Therapeutic Strategy for Acute Lymphoblastic Leukemia
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