Polycythemia Vera
|
0.490 |
GeneticVariation
|
disease |
BEFREE |
JAK1 and Tyk2 activation by the homologous polycythemia vera JAK2 V617F mutation: cross-talk with IGF1 receptor.
|
16239216 |
2005 |
Polycythemia Vera
|
0.490 |
Biomarker
|
disease |
BEFREE |
RESPONSE is an open-label phase 3 study evaluating the Janus kinase 1/Janus kinase 2 inhibitor ruxolitinib versus best available therapy for efficacy/safety in hydroxyurea-resistant or intolerant patients with polycythemia vera.
|
27102499 |
2016 |
Polycythemia Vera
|
0.490 |
AlteredExpression
|
disease |
BEFREE |
We found that JAK1/2 or JAK2 inhibition prevented the IL-6 activation of STAT3 and AKT pathways in polycythemia vera and HEL cells.
|
30571852 |
2019 |
Polycythemia Vera
|
0.490 |
Biomarker
|
disease |
BEFREE |
Ruxolitinib is a JAK1/2 inhibitor approved for the treatment of myelofibrosis (MF) and polycythemia vera (PV).
|
31711337 |
2020 |
Polycythemia Vera
|
0.490 |
GeneticVariation
|
disease |
CLINVAR |
JAK1 and Tyk2 activation by the homologous polycythemia vera JAK2 V617F mutation: cross-talk with IGF1 receptor.
|
16239216 |
2005 |
Polycythemia Vera
|
0.490 |
GeneticVariation
|
disease |
BEFREE |
The discovery of a JAK2 point mutation (JAK2 V617F) as the main cause of polycythemia vera lead to the development and FDA approval of a JAK1/2 inhibitor, ruxolitinib, in 2011.
|
28277287 |
2017 |
Polycythemia Vera
|
0.490 |
Biomarker
|
disease |
BEFREE |
MAJIC (ISRCTN61925716) is a randomized phase 2 trial of ruxolitinib (JAK1/2 inhibitor) vs best available therapy (BAT) in ET and polycythemia vera patients resistant or intolerant to HC.
|
29074595 |
2017 |
Polycythemia Vera
|
0.490 |
Biomarker
|
disease |
BEFREE |
Since its approval in 2011, the Janus kinase 1/2 (JAK1/2) inhibitor ruxolitinib has evolved to become the centerpiece of therapy for myelofibrosis (MF), and its use in patients with hydroxyurea resistant or intolerant polycythemia vera (PV) is steadily increasing.
|
28500170 |
2017 |
Polycythemia Vera
|
0.490 |
Biomarker
|
disease |
BEFREE |
Expert opinion: The JAK1/JAK2 inhibitor ruxolitinib has clearly enriched the therapeutic armamentarium of MPN and is now licenced for more than five years in MF and over three years as second line in PV.
|
29134817 |
2017 |
Polycythemia Vera
|
0.490 |
Biomarker
|
disease |
BEFREE |
The phase 3 RESPONSE trial evaluated the JAK1/JAK2 inhibitor ruxolitinib (n=110) versus best available therapy (BAT; n=112) in patients with PV who were hydroxyurea-resistant/intolerant.
|
28193568 |
2017 |
Polycythemia Vera
|
0.490 |
CausalMutation
|
disease |
CGI |
|
|
|
Leukemia, Myelocytic, Acute
|
0.430 |
CausalMutation
|
disease |
CGI |
|
|
|
Leukemia, Myelocytic, Acute
|
0.430 |
Biomarker
|
disease |
BEFREE |
Moreover, the JAK1/2 inhibitor ruxolitinib restored sensitivity to the BCL2 inhibitor venetoclax in AML patient cells ex vivo in different model systems and in vivo in an AML xenograft mouse model.
|
28619982 |
2017 |
Leukemia, Myelocytic, Acute
|
0.430 |
GeneticVariation
|
disease |
CLINVAR |
Sequencing a mouse acute promyelocytic leukemia genome reveals genetic events relevant for disease progression.
|
21436584 |
2011 |
Leukemia, Myelocytic, Acute
|
0.430 |
GeneticVariation
|
disease |
CLINVAR |
Key pathways are frequently mutated in high-risk childhood acute lymphoblastic leukemia: a report from the Children's Oncology Group.
|
21680795 |
2011 |
Leukemia, Myelocytic, Acute
|
0.430 |
GeneticVariation
|
disease |
BEFREE |
This is the first report to demonstrate somatic JAK1 mutations in AML and suggests that JAK1 mutations may function as disease-modifying mutations in AML pathogenesis.
|
18160671 |
2008 |
Leukemia, Myelocytic, Acute
|
0.430 |
Biomarker
|
disease |
BEFREE |
Therefore, our novel findings indicated that CUEDC2 interacted with SOCS1 to suppress SOCS1's ubiquitin-mediated degradation, JAK1-STAT3 pathway activation and leukaemogenesis of AML.
|
29991678 |
2018 |
Leukemia, Myelocytic, Acute
|
0.430 |
GeneticVariation
|
disease |
GWASCAT |
Genome-wide haplotype association study identify the FGFR2 gene as a risk gene for acute myeloid leukemia.
|
27903959 |
2017 |
Precursor Cell Lymphoblastic Leukemia Lymphoma
|
0.340 |
GeneticVariation
|
disease |
BEFREE |
Identification of a novel functional JAK1 S646P mutation in acute lymphoblastic leukemia.
|
28410228 |
2017 |
Precursor Cell Lymphoblastic Leukemia Lymphoma
|
0.340 |
AlteredExpression
|
disease |
LHGDN |
Somatically acquired JAK1 mutations in adult acute lymphoblastic leukemia.
|
18362173 |
2008 |
Precursor Cell Lymphoblastic Leukemia Lymphoma
|
0.340 |
GeneticVariation
|
disease |
BEFREE |
Acute lymphoblastic leukemia-associated JAK1 mutants activate the Janus kinase/STAT pathway via interleukin-9 receptor alpha homodimers.
|
19139102 |
2009 |
Precursor Cell Lymphoblastic Leukemia Lymphoma
|
0.340 |
GeneticVariation
|
disease |
BEFREE |
This mutation was identical to the JAK1 V658F mutation previously found in human APL and acute lymphoblastic leukemia samples.
|
21436584 |
2011 |
Precursor Cell Lymphoblastic Leukemia Lymphoma
|
0.340 |
CausalMutation
|
disease |
CGI |
|
|
|
Malignant neoplasm of prostate
|
0.320 |
Biomarker
|
disease |
CTD_human |
The long tail of oncogenic drivers in prostate cancer.
|
29610475 |
2018 |
Malignant neoplasm of prostate
|
0.320 |
Biomarker
|
disease |
BEFREE |
Because the activation of STAT3 is mediated by the action of an upstream Janus kinase (JAK) kinase, usually JAK1 or JAK2, the activation step for STAT3 might itself be a target for therapy in prostate cancer.
|
14749471 |
2004 |