822 results on '"Koschmieder, Steffen"'
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2. Calreticulin and JAK2V617F driver mutations induce distinct mitotic defects in myeloproliferative neoplasms
3. Evaluation of chiral organosulfur compounds on their activity against the malaria parasite 'Plasmodium falciparum'
4. Cellular aging is accelerated in the malignant clone of myeloproliferative neoplasms
5. Correction: Quantification of hematopoietic stem and progenitor cells by targeted DNA methylation analysis
6. Quantification of hematopoietic stem and progenitor cells by targeted DNA methylation analysis
7. Proinflammatory phenotype of iPS cell-derived JAK2 V617F megakaryocytes induces fibrosis in 3D in vitro bone marrow niche
8. Non-canonical Hedgehog signaling mediates profibrotic hematopoiesis-stroma crosstalk in myeloproliferative neoplasms
9. CXCR4 and CD74 together enhance cell survival in response to macrophage migration-inhibitory factor in chronic lymphocytic leukemia
10. Breakthrough infections in MPN-COVID vaccinated patients
11. Recent advances in the genomics and therapy of BCR/ABL1-positive and -negative chronic myeloproliferative neoplasms
12. Kindlin-3 loss curbs chronic myeloid leukemia in mice by mobilizing leukemic stem cells from protective bone marrow niches
13. Germline variants in DNA repair genes, including BRCA1/2, may cause familial myeloproliferative neoplasms
14. Safety and efficacy of the combination of sonidegib and ruxolitinib in myelofibrosis: a phase 1b/2 dose-finding study
15. Contemporary insights into the pathogenesis and treatment of chronic myeloproliferative neoplasms
16. Is Treatment for Cytopenic Myelofibrosis Still an Unmet Clinical Need?
17. The telomerase inhibitor imetelstat differentially targets JAK2V617F versus CALR mutant myeloproliferative neoplasm cells and inhibits JAK-STAT signaling
18. JAK2-mutant hematopoietic cells display metabolic alterations that can be targeted to treat myeloproliferative neoplasms
19. P1004: ACTIVATING MUTATIONS IN JAK2 AND CALR DIFFERENTIALLY AFFECT INTRACELLULAR CALCIUM LEVELS AND CALCIUM FLUX
20. P988: MUTANT CALRETICULIN AND JAK2V617F DRIVER MUTATIONS INDUCE DISTINCT MITOTIC DEFECTS IN MYELOPROLIFERATIVE NEOPLASMS
21. P1008: THE TELOMERASE INHIBITOR IMETELSTAT DIFFERENTIALLY TARGETS JAK2V617F- VERSUS CALR-MUTANT MYELOPROLIFERATIVE NEOPLASM CELLS AND INHIBITS JAK-STAT SIGNALING
22. PB2195: CHARACTERISTICS OF PATIENTS WITH POLYCYTHEMIA VERA: RESULTS FROM A US ELECTRONIC HEALTH RECORDS DATABASE.
23. Tyrosine kinase inhibitor–induced defects in DNA repair sensitize FLT3(ITD)-positive leukemia cells to PARP1 inhibitors
24. Among classic myeloproliferative neoplasms, essential thrombocythemia is associated with the greatest risk of venous thromboembolism during COVID-19
25. Stem cell persistence in CML is mediated by extrinsically activated JAK1-STAT3 signaling
26. JAK2V617F but not CALR mutations confer increased molecular responses to interferon-α via JAK1/STAT1 activation
27. Ruxolitinib-induced defects in DNA repair cause sensitivity to PARP inhibitors in myeloproliferative neoplasms
28. Efficacy and safety of ruxolitinib in patients with newly-diagnosed polycythemia vera: futility analysis of the RuxoBEAT clinical trial of the GSG-MPN study group
29. The Ph-positive and Ph-negative myeloproliferative neoplasms: some topical pre-clinical and clinical issues
30. Outcome of 129 Pregnancies in Polycythemia Vera Patients: A Report of the European LeukemiaNET
31. Identification of Adult Patients With Classical Dyskeratosis Congenita or Cryptic Telomere Biology Disorder by Telomere Length Screening Using Age-modified Criteria
32. Exploiting Synthetic Lethality between Germline BRCA1 Haploinsufficiency and PARP Inhibition in JAK2V617F-Positive Myeloproliferative Neoplasms.
33. Mutant NRAS Q61K is responsible for MAPK pathway activation in the MARIMO cell line and renders these cells independent of the CALR–MPL–JAK2–STAT5 pathway
34. Recurrent somatic mutations are rare in patients with cryptic dyskeratosis congenita
35. Philadelphia chromosome-negative classical myeloproliferative neoplasms: revised management recommendations from European LeukemiaNet
36. KIT D816V Mast Cells Derived from Induced Pluripotent Stem Cells Recapitulate Systemic Mastocytosis Transcriptional Profile
37. Additional file 1 of Quantification of hematopoietic stem and progenitor cells by targeted DNA methylation analysis
38. Infliximab therapy together with tyrosine kinase inhibition targets leukemic stem cells in chronic myeloid leukemia
39. Hematopoietic stem and progenitor cell proliferation and differentiation requires the trithorax protein Ash2l
40. Differential roles of STAT1 and STAT2 in the sensitivity of JAK2V617F- vs. BCR-ABL-positive cells to interferon alpha
41. BOREAS: a global, phase III study of the MDM2 inhibitor navtemadlin (KRT-232) in relapsed/refractory myelofibrosis
42. Ruxolitinib Versus Best Available Therapy in Patients with Essential Thrombocythemia: Pre-Specified Interim Analysis of the Randomized Phase 2b Ruxobeat Clinical Trial of the German Study Group for Myeloproliferative Neoplasms (GSG-MPN)
43. Non-Canonical Gli1 Activation Mediates Profibrotic Hematopoiesis-Stroma Crosstalk in MPN
44. Protection Against Breakthrough Delta/Omicron Variants in Vaccinated Patients with Myeloproliferative Neoplasms (MPN)
45. Clinicohematologic and Molecular Response of Essential Thrombocythemia Patients Treated with Pegylated Interferon-Alpha: A Multicenter Study on Behalf of the German Study Group-MPN (GSG-MPN)
46. Nanopore Sequencing-Based High-Resolution Karyotyping Compared to Conventional Karyotyping in Patients with Acute Myeloid Leukemia
47. A Phase 2 Study of the LSD1 Inhibitor Bomedemstat (IMG-7289) for the Treatment of Advanced Myelofibrosis (MF): Updated Results and Genomic Analyses
48. Verify: A Phase 3 Study of the Hepcidin Mimetic Rusfertide (PTG-300) in Patients with Polycythemia Vera
49. MYF3001: A Randomized Open Label, Phase 3 Study to Evaluate Imetelstat Versus Best Available Therapy in Patients with Intermediate-2 or High-Risk Myelofibrosis Relapsed/Refractory to Janus Kinase Inhibitor
50. Combined inhibition of BCR-ABL1 and the proteasome as a potential novel therapeutic approach in BCR-ABL positive acute lymphoblastic leukemia
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