61 results on '"ŠKODA, Radek"'
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2. Iron is a modifier of the phenotypes of JAK2-mutant myeloproliferative neoplasms
3. Genetic basis and molecular profiling in myeloproliferative neoplasms
4. JAK2-mutant hematopoietic cells display metabolic alterations that can be targeted to treat myeloproliferative neoplasms
5. Ruxolitinib-induced defects in DNA repair cause sensitivity to PARP inhibitors in myeloproliferative neoplasms
6. JAK2 exon 12 mutant mice display isolated erythrocytosis and changes in iron metabolism favoring increased erythropoiesis
7. Homozygous calreticulin mutations in patients with myelofibrosis lead to acquired myeloperoxidase deficiency
8. Deletion of Stat3 in hematopoietic cells enhances thrombocytosis and shortens survival in a JAK2-V617F mouse model of MPN
9. Clonal evolution and clinical correlates of somatic mutations in myeloproliferative neoplasms
10. Genomic profiling for clinical decision making in myeloid neoplasms and acute leukemia
11. The DEAH-box helicase RHAU is an essential gene and critical for mouse hematopoiesis
12. SCL-mediated regulation of the cell-cycle regulator p21 is critical for murine megakaryopoiesis
13. Platelets regulate lymphatic vascular development through CLEC-2–SLP-76 signaling
14. Clonal analysis of deletions on chromosome 20q and JAK2-V617F in MPD suggests that del20q acts independently and is not one of the predisposing mutations for JAK2-V617F
15. Pronounced thrombocytosis in transgenic mice expressing reduced levels of Mpl in platelets and terminally differentiated megakaryocytes
16. MPN patients with low mutant JAK2 allele burden show late expansion restricted to erythroid and megakaryocytic lineages
17. Normal erythropoiesis but severe polyposis and bleeding anemia in Smad4-deficient mice
18. Adaptive functional differentiation of dendritic cells: integrating the network of extra- and intracellular signals
19. The Second Generation Type II JAK2 Inhibitor, AJ1-10502, Demonstrates Enhanced Selectivity, Improved Therapeutic Efficacy and Reduced Mutant Cell Fraction Compared to Type I JAK2 Inhibitors in Models of Myeloproliferative Neoplasms (MPNs)
20. Combination of 5-Azacytidine and Pegifna Is Able to Overcome Resistance in JAK2-V617F Positive MPN with Loss of Dnmt3a
21. Disrupting the Socs2-Mediated Negative Feedback to JAK-STAT Signaling Boosts Molecular Responses Induced By Interferon-α in a Mouse Model of Myeloproliferative Neoplasms
22. Exploring the Functional Role of an Alternative mRNA Transcript of the EPO Gene
23. Tuning the volume of the immune response: strength and persistence of stimulation determine migration and cytokine secretion of dendritic cells
24. Transition to homozygosity does not appear to provide a clonal advantage to hematopoietic progenitors carrying mutations in TET2
25. Inhibiting Glutamine Metabolism with CB-839 Reduces Erythrocytosis in MPN Mice
26. Loss of Dnmt3a Confers Resistance to Pegifnα in JAK2-V617F Mouse Model
27. Complex subclone structure that responds differentially to therapy in a patient with essential thrombocythemia and chronic myeloid leukemia
28. Aging of Bone Marrow Microenvironment Promotes Myeloid Bias of Hematopoietic Progenitors and Is a Target in Age-Related Myeloproliferative Neoplasms
29. A Gain-of-Function Mutation in EPO Gene Causes Familial Erythrocytosis
30. Targeting Cell Non-Autonomous MAPK Activation As a Novel Therapeutic Strategy in Myeloproliferative Neoplasms
31. Molecular and clinical features of the myeloproliferative neoplasm associated with JAK2 exon 12 mutations
32. Clonal analysis of TET2 and JAK2 mutations suggests that TET2 can be a late event in the progression of myeloproliferative neoplasms
33. Effects of the Sympathicomimetic Agonist Mirabegron on Disease Course, Mutant Allele Burden, Marrow Fibrosis, and Nestin Positive Stem Cell Niche in Patients with JAK2-Mutated Myeloproliferative Neoplasms. a Prospective Multicenter Phase II Trial SAKK 33/14
34. Clonal heterogeneity in polycythemia vera patients with JAK2 exon12 and JAK2-V617F mutations
35. Somatic mutations of JAK2 exon 12 in patients with JAK2 (V617F)-negative myeloproliferative disorders
36. A Study of the Role of Antiplatelet Therapy in the Prevention of Thrombosis in Patients with Calr-Mutated Low Risk Essential Thrombocythemia
37. Predisposition to Myeloproliferative Neoplasms
38. Somatic mutations in calreticulin can be found in pedigrees with familial predisposition to myeloproliferative neoplasms
39. Altered gene expression in myeloproliferative disorders correlates with activation of signaling by the V617F mutation of Jak2
40. Phosphorylation Of The Cytoplasmic Tyrosine Residues Of c-Mpl Is Not Required To Preserve Intact Receptor Dependent Hematopoietic Stem Cell Survival Signaling
41. Engraftment Of Human Polycythemia Vera CD34+ Cells In hSIRPα-Transgenic-Human-TPO-Expressing RAG2-/-, IL2Rγ-/- Immunodeficient Mice
42. Accelerating myelofibrosis through loss of Dnmt3a
43. Comparison of molecular markers in a cohort of patients with chronic myeloproliferative disorders
44. First Achievements of MPN&MPNr-EuroNet (COST Action BM0902), a New European Network Dedicated to the Diagnosis of Myeloproliferative Neoplasms and Hereditary Erythrocytosis and Thrombocytosis
45. JAK2-V617F Expressing Stem Cells Display a Competitive Advantage At Low Limiting Dilution and Are Capable of Initiating MPN Phenotype
46. Hereditary thrombocytosis not as innocent as thought? Development into acute leukemia and myelofibrosis
47. A Single-Base Deletion in the Thrombopoietin (TPO) Gene Causes Familial Essential Thrombocythemia Through a Mechanism of More Efficient Translation of TPO mRNA
48. Concordance of Assays Designed for the Quantitation of JAK2 1849G>T (V617F): A Multi-Centre Study.
49. The JAK2-V617F Mutation Load Remains Stable over Several Years in Most Patients with Myeloproliferative Disorders Analyzed in a Retrospective Single Center Study.
50. Ratio of Mutant JAK2-V617F to Wild Type Jak2 Determines the MPD Phenotypes in Transgenic Mice.
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