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74 results for “essential thrombocythemia”
Structural variants of calreticulin mutants associated with essential thrombocythemia
<p>Video S1. CALRwt molecular simulation with Ca2+ ions binding to the structure. This movie shows the dynamics of Ca2+ ions over the 40 ns and how they rapidly bind to the CALRwt structure. Most of the ions bind to the C-terminal part of CALRwt, where the majority of the negative residues are located. The binding of Ca2+ ions creates an interaction between residues that can induce specific folding. In this example, residues E407 and E416 interact with a calcium ion and fold, as shown at the end of the movie.</p> <p>Video S2. CALRwt molecular simulation with calcium ions binding to the structure. This movie shows the dynamics of CALRwt and Ca2+ ions over 400 ns and how ions are rapidly bound to the CALRwt structure. Most of the ions bind to the C-terminal region of CALRwt, where the majority of the negative residues are located. The binding of calcium ions creates an interaction between residues that can induce specific folding (a specific example of fold is shown on Video S1). On this full movie, we are able to see the unfolding of the N-terminal region of the helix and the stabilization of the C- terminal region thanks to calcium binding.</p> <p>Video S3. CALRwt molecular simulation with Na+ ions. This movie shows the dynamics of CALRwt with Na+ ions. The absence of binding from calcium ions leaves the structure free of any external constraint, especially for the C-terminal region. The latter appears to be flexible but this region is in fact quite stable at the local level and has its own dynamics, unstructured slightly the C-terminal of the helix.</p> <p>Video S4. CALRm class A molecular simulation. This movie shows the dynamics of CALRm class A over 400ns. The C-terminal region of the structure is quite flexible at first and interacts with the N-terminal region after several ns. This interaction locally constrains the structure around residues 400-404, stabilizing an unstructured structure for this region.</p> <p>Video S5. CALRm class B molecular simulation. This movie shows the dynamics of CALRm class B over 400ns. The first and last helices move away from their initial position with great flexibility of the coiled regions between the helices. The first helix interacts closely with the second helix and forms a specific T-shaped fold which stabilize the whole structure.</p> <p>Video S6. CALRm class C molecular simulation. This movie shows the dynamics of CALRm class C over 400ns. Extremities are highly flexible but the helix remains stable. This high flexibility allow the C- terminal region to have some interaction with the helix at some frames</p> <p>Video S7. CALRm class D molecular simulation. This movie shows the dynamics of CALRm class D over 400ns. The C-terminal region appears to be flexible, but the helix remains stable the whole simulation.</p> <p>Video S8. CALRm class E molecular simulation. This movie shows the dynamics of CALRm class E over 400ns. This movie shows the dynamics of CALRm class E and calcium ions over 400 ns and how ions are rapidly bound to the CALRwt structure. Most of the ions bind to the C-terminal region of CALRm class E, where the majority of the negative residues are located. The N-terminal region of the helix is being unstructured and the C-terminal region is stabilized with calcium ions. This simulation of CALRm class E is very similar to the simulation of CALRwt.</p> <p>Video S9. Dimeric form of CALRm class A molecular simulation. This movie shows the dynamics of two CALRm class A monomers forming a dimer through disulphide bonds. Both chains seem to repulse each other due to electrostatic charges, but disulphide bonds maintain the dimeric form, otherwise both chains would have been separated.</p> <p>Video S10. Dimeric form of CALRm class A with broken disulphide bonds molecular simulation. This movie shows the dynamics of two CALRm class A monomers and their attempt to form a dimer with broken disulfide bonds. As each monomer repels each other, the dimeric form cannot be stable without any disulfide bonds. This is demonstrated by the separation of each chain from each other.</p> <p>Video S11. Dimeric form of CALRm class B molecular simulation. This movie shows the dynamics of two CALRm class B monomers forming a dimer through disulphide bonds. Both chains are interacting together to form a specific shape, similar to the simulation of the monomer of class B. This interaction implies that even without any disulphide bonds, the dimeric form of class B could be stable, contrary to class A.</p> <p>Video S12. Dimeric form of CALRm class B molecular simulation. It is an interesting replicate of the same system than Video S11. Helices are also well maintained.</p> <p>Video S13. Dimeric form of CALRm class C molecular simulation. This movie shows the dynamics of two CALRm class C monomers forming a dimer through disulphide bonds. Both chains seem to repulse each other due to electrostatic charges, but disulphide bonds maintain the dimeric form, otherwise both chains would have been separated.</p> <p>Video S14. Dimeric form of CALRm class E molecular simulation. This movie shows the dynamics of two CALRm class E monomers and their attempt to form a dimer without any disulphide bonds. Chains repel and are moving away from each other after several ns, indicating the inability for class E to form a dimer.</p> <p>Video S15. Dimeric form of CALRwt molecular simulation. This movie shows the dynamics of two CALRwt monomers and their attempt to form a dimer. Some interactions occur between the N- terminus of each chain, but this is not sufficient and the chains move away from each other. Subsequently, the dynamics of each chain resembles the dynamics of the CALRwt monomer simulated with sodium ions (Video S2). CALRwt is not able to be stable as dimer.</p> <p>Video S16. Dimeric form of CALRm class D molecular simulation. This movie shows the dynamics of two CALRm class D monomers and their attempt to form a dimer without any disulphide bonds. Both chains are separated very quickly which indicate that they can not be stable as dimer.</p>
Study group charasteristics and sequencing data of patients with essential thrombocythemia and polycythemia vera
<p><span>Polycythemia vera (PV) and essential thrombocythemia (ET) are diseases driven by canonical mutations in <em>JAK2, CALR</em>, or <em>MPL </em>gene. Previous studies revealed that in addition to driver mutations, patients with PV and ET can harbor other mutations in various genes, with no established impact on disease phenotype. We hypothesized that the molecular profile of patients with PV and ET is dynamic throughout the disease. In this study we performed 37-gene targeted next-generation sequencing panel on the DNA samples collected from 49 study participants in two time points, separated by 78-141 months. We identified 78 variants across 37 analyzed genes in the study population. By analyzing the change in variant allele frequencies (VAFs) and revealing the acquisition of new mutations during the disease, we confirmed the dynamic nature of molecular profile of patients with PV and ET. We found connections of specific variants with the development of secondary myelofibrosis, thrombotic events, and response to treatment. We confronted our results with existing conventional and mutation-enhanced prognostic systems, showing the limited utility of available prognostic tools. Results of this study underline the significance of repeated molecular testing in patients with PV and ET and indicate the need for further research within this field to better understand the disease and improve available prognostic tools.</span></p>
Efficacy of Momelotinib Versus Best Available Therapy in Anemic or Thrombocytopenic Subjects With Primary Myelofibrosis (MF), Post-polycythemia Vera MF, or Post-essential Thrombocythemia MF
ClinicalTrials.gov study NCT02101268. IPD Sharing: Not stated. Countries: 8. Publications: 5.
Momelotinib in Transfusion-Dependent Adults With Primary Myelofibrosis (PMF) or Post-polycythemia Vera or Post-essential Thrombocythemia Myelofibrosis (Post-PV/ET MF)
ClinicalTrials.gov study NCT02515630. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Study to Determine the Safety and Efficacy of INCB018424 in Patients With Polycythemia Vera or Essential Thrombocythemia
ClinicalTrials.gov study NCT00726232. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Ruxolitinib (INCB018424) in Participants With Primary Myelofibrosis (PMF), Post Essential Thrombocythemia-myelofibrosis and Post Polycythemia Vera-myelofibrosis (PPV-MF)
ClinicalTrials.gov study NCT01348490. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Safety and Tolerability Study of Oral NS-018 in Patients With Primary Myelofibrosis (MF), Post-polycythemia Vera MF or Post-essential Thrombocythemia MF
ClinicalTrials.gov study NCT01423851. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Trial of Fedratinib in Subjects With DIPSS, Intermediate or High-Risk Primary Myelofibrosis, Post-Polycythemia Vera Myelofibrosis, or Post-Essential Thrombocythemia Myelofibrosis and Previously Trea
ClinicalTrials.gov study NCT03755518. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Phase 2 Study: An Open-Label, Randomized, Phase 2 Dose-Finding Study of Pacritinib in Patients With Primary Myelofibrosis, Post-Polycythemia Vera Myelofibrosis, or Post- Essential Thrombocythemia Myel
ClinicalTrials.gov study NCT04884191. IPD Sharing: Not stated. Countries: 8. Publications: 1.
Study of the JAK Inhibitor Ruxolitinib Administered Orally to Patients With Primary Myelofibrosis (PMF), Post-Polycythemia Vera-Myelofibrosis (PPV-MF) or Post-Essential Thrombocythemia-Myelofibrosis (
ClinicalTrials.gov study NCT01317875. IPD Sharing: NO. Countries: 8. Publications: 1.
Randomized Trial of Pegylated Interferon Alfa-2a Versus Hydroxyurea in Polycythemia Vera (PV) and Essential Thrombocythemia (ET)
ClinicalTrials.gov study NCT01259856. IPD Sharing: Not stated. Countries: 4. Publications: 3.
Study of Bomedemstat in Participants With Essential Thrombocythemia (IMG-7289-CTP-201/MK-3543-003)
ClinicalTrials.gov study NCT04254978. IPD Sharing: NO. Countries: 7. Publications: 0.
A Study of Anagrelide and Hydroxyurea in High-Risk Essential Thrombocythemia Patients
ClinicalTrials.gov study NCT00202644. IPD Sharing: Not stated. Countries: 6. Publications: 2.
INC424 for Patients With Primary Myelofibrosis, Post Polycythemia Myelofibrosis or Post-essential Thrombocythemia Myelofibrosis.
ClinicalTrials.gov study NCT01493414. IPD Sharing: UNDECIDED. Countries: 25. Publications: 4.
French Observational Xagrid (FOX) Study In Adult Patients With Essential Thrombocythemia
ClinicalTrials.gov study NCT01192347. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Study group charasteristics and sequencing data of patients with essential thrombocythemia and polycythemia vera
Open the record for dataset details and reuse information.
Pegylated Interferon Alfa-2a Salvage Therapy in High Risk Polycythemia Vera (PV) or Essential Thrombocythemia (ET)
ClinicalTrials.gov study NCT01259817. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Safety Study Evaluating Twice-Daily Administration of Momelotinib in Primary Myelofibrosis or Post-Polycythemia Vera or Post-Essential Thrombocythemia Myelofibrosis
ClinicalTrials.gov study NCT01423058. IPD Sharing: Not stated. Countries: 2. Publications: 1.
The Ruxo-BEAT Trial in Patients With High-risk Polycythemia Vera or High-risk Essential Thrombocythemia
ClinicalTrials.gov study NCT02577926. IPD Sharing: NO. Countries: 1. Publications: 2.
Safety and Efficacy Study of CYT387 in Primary Myelofibrosis (PMF) or Post-polycythemia Vera (PV) or Post-essential Thrombocythemia (ET)
ClinicalTrials.gov study NCT00935987. IPD Sharing: Not stated. Countries: 3. Publications: 1.
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