|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Ruxolitinib, a selective JAK1/JAK2 inhibitor, is the current first line therapy for myelofibrosis (MF), which reduces symptomatology and splenomegaly, but does not clearly modify disease course.
|
31778911 |
2020 |
|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Moreover, 4 therapeutic JAK2 inhibitors (ruxolitinib, fedratinib, momelotinib, and pacritinib) have either been approved or are in advanced clinical development for myelofibrosis.
|
31560729 |
2019 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
The median age was 57years (range, 38 to 72); 75% had primary MF and 25% had secondary MF.JAK2 V617F was mutated in 61%.
|
30408564 |
2019 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Whether noncanonical and/or concomitant JAK2- and MPL-mutations exist in myelofibrosis (MF) regardless of phenotype-driver mutations is not yet elucidated.
|
31135094 |
2019 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Constitutive activation of JAK/STAT signaling through mutations in <i>JAK2, CALR</i>, or <i>MPL</i> is central to myelofibrosis pathogenesis.
|
30563936 |
2019 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
To identify key features that may help distinguish these 2 entities, we retrospectively studied 21 cases diagnosed as "CMML" with JAK2 V617F and bone marrow fibrosis that were identified from a cohort of 610 cases of CMML diagnosed in 2006 to 2016.
|
30447300 |
2019 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
ABSTRACT: Background The BCR-ABL-negative myeloproliferative neoplasms, i.e., polycythemia vera, essential thrombocythemia (ET), and myelofibrosis (MF), are characterized by mutations in JAK2, CALR, or MPL.
|
30889303 |
2019 |
|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Myelofibrosis in 2019: moving beyond JAK2 inhibition.
|
31511492 |
2019 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
The advances in molecular insights, especially the discovery of the Janus kinase 2 (JAK2) V617F mutation and its role in JAK-STAT pathway dysregulation, led to the development of the JAK inhibitor ruxolitinib, which currently represents the cornerstone of medical therapy in MF and hydroxyurea-resistant/intolerant PV.
|
31228096 |
2019 |
|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Fedratinib (INREBIC<sup>®</sup>) is a JAK2-selective inhibitor that has been developed as an oral treatment for myelofibrosis.
|
31571162 |
2019 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Effect of CALR and JAK2 mutations on the clinical and hematological phenotypes of the disease in patients with myelofibrosis - long-term experience from a single center.
|
29534592 |
2019 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
A JAK2 variant in addition to JAK2 V617F (n = 13) in myelofibrosis was associated with an increased cumulative risk of transformation into AML (P = .003).
|
30811597 |
2019 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
With the advent of targeted therapies, such as the Janus kinase inhibitors, many patients have experienced substantial clinical benefits, including reduction in splenomegaly and symptoms and, in some instances, improvement or stabilization of bone marrow fibrosis and reduction of JAK2 V617F allele burden.
|
30343328 |
2019 |
|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Treatment of patients with myelofibrosis with the type I JAK (Janus kinase) inhibitor ruxolitinib paradoxically induces JAK2 activation loop phosphorylation and is associated with a life-threatening cytokine-rebound syndrome if rapidly withdrawn.
|
30498775 |
2018 |
|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
To compare the efficacy and safety of JAK2 inhibitor pacritinib with that of best available therapy (BAT), including ruxolitinib, in patients with myelofibrosis and thrombocytopenia.
|
29522138 |
2018 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
One-hundred Mayo Clinic patients with high/intermediate-risk myelofibrosis (MF) received momelotinib (MMB; JAK1/2 inhibitor) between 2009 and 2010, as part of a phase 1/2 trial (NCT00935987); 73% harbored JAK2 mutations, 16% CALR, 7% MPL, 44% ASXL1, and 18% SRSF2.
|
29515114 |
2018 |
|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Ruxolitinib, a potent oral JAK1/JAK2 inhibitor remains the only Food and Drug Administration (FDA)-approved medicinal therapy for the treatment of MF.
|
29480036 |
2018 |
|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
We investigated the therapeutic potential of ruxolitinib, a JAK1/JAK2 inhibitor that has been FDA-approved for the treatment of myelofibrosis, to treat ovarian cancer either alone or in combination with conventional chemotherapy agents.
|
29849942 |
2018 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
JAK2 V617F mutation in plasma cell-free DNA preceding clinically overt myelofibrosis: Implications for early diagnosis.
|
29565699 |
2018 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Overall response rates (ORRs) in patients with JAK2 V617F-mutated PV, ET, and MF were 95%, 90.5%, and 9.1%, respectively, while patients with ET and MF without the JAK2 V617F mutations had ORRs of 43.7% and 0%, respectively.
|
30025280 |
2018 |
|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
In this report, we discuss the clinical history, pathological evaluation, and genomics findings in a patient with JAK2-positive myelofibrosis who developed a secondary myelodysplasia after hematopoietic stem cell transplantation and JAK1/2 inhibitor treatment.
|
30097215 |
2018 |
|
Myelofibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
JAK2 allele burdens were significantly lower among AYA JAK2V617F-mutated patients in both PV (p = 0.001) and MF (p = 0.005).
|
29143068 |
2018 |
|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Among JAK2 inhibitors, ruxolitinib (RUX) has been approved for (1) treatment of intermediate-2 and high-risk MF and (2) PV patients who are resistant to or intolerant to hydroxyurea.
|
30074114 |
2018 |
|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
We assessed the efficacy and safety of momelotinib, a JAK 1 and JAK 2 inhibitor, versus best available therapy (BAT) in patients with myelofibrosis who had suboptimal responses or haematological toxic effects with ruxolitinib.
|
29275119 |
2018 |
|
Myelofibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
JAK2-inhibitors and stem cell transplant are the two critical therapeutic approaches in myelofibrosis.
|
29713873 |
2018 |