|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
CTD_human |
Dynamics of clonal evolution in myelodysplastic syndromes.
|
27992414 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Enasidenib (formerly AG-221) is an oral small molecule selective targeted inhibitor of the mutant IDH2 enzyme, approved in August 2017 by the United States Food and Drug Administration for the treatment of patients with relapsed or refractory (R/R) <i>IDH2</i>-mutated AML.
|
30013764 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Enasidenib, a specific small-molecule inhibitor of IDH2, recently gained FDA approval for the treatment of patients with relapsed/refractory <i>IDH2</i>-mutated AML.
|
29769206 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
CausalMutation
|
disease |
CLINVAR |
Evaluation of mutations in the isocitrate dehydrogenase genes in therapy-related and secondary acute myeloid leukaemia identifies a patient with clonal evolution to IDH2 R172K homozygosity due to uniparental disomy.
|
21250968 |
2011 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
First-generation inhibitors of mutant IDH have entered clinical trials, and have shown encouraging results in patients with IDH-mutant AML.
|
26819452 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Firstly, by analyzing biomarkers associated with AML, to assist normal clinical tests, we confirmed that the patient was anormal karyo type, with NPM1 and IDH2 mutations and deregulation patterns of related genes, such as BAALC, ERG, MN1 and HOX family.
|
24867525 |
2014 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
FLT3 or IDH1/IDH2 inhibitors) for AML, timely and comprehensive molecular mutation screening has arrived in daily practice.
|
29728319 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
For example, in acute myeloid leukemia (AML) higher epigenetic age-predictions are associated with increased incidence of mutations in RUNX1, WT1, and IDH2, whereas mutations in TET2, TP53, and PML-PARA translocation are more frequent in younger age-predictions.
|
26110659 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Further studies addressing its biology and clinical significance may be especially relevant in the era of IDH inhibitors and recent work showing efficacy of ATRA therapy in NPM1 and IDH1-mutated AML.
|
29274134 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Furthermore, AML patients with IDH mutations display a significantly reduced number of other well characterized AML-associated mutations and/or associated chromosomal abnormalities, potentially implicating IDH mutation in a distinct mechanism of AML pathogenesis.
|
20171147 |
2010 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Here we describe two patients with IDH2-mutant AML who had a clinical response to enasidenib followed by clinical resistance, disease progression, and a recurrent increase in circulating levels of 2HG.
|
29950729 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Here we report that WT1, a sequence-specific transcription factor, is mutated in a mutually exclusive manner with TET2, IDH1, and IDH2 in acute myeloid leukemia (AML).
|
25601757 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
CausalMutation
|
disease |
CLINVAR |
Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity.
|
26619011 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
CLINVAR |
Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity.
|
26619011 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
IDH1 and IDH2 mutations occur frequently in some types of World Health Organization grades 2-4 gliomas and in acute myeloid leukemias with normal karyotype.
|
20513808 |
2010 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
IDH1 and IDH2 mutations occur frequently in gliomas and acute myeloid leukemia, leading to simultaneous loss and gain of activities in the production of α-ketoglutarate (α-KG) and 2-hydroxyglutarate (2-HG), respectively.
|
21251613 |
2011 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
IDH1 and IDH2 mutations were found in four (2.0%) and ten (5.0%) AML and in two (2.4%) and three (3.6%) MDS cases, but not in other patients.
|
21997850 |
2012 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
IDH1 and IDH2 mutations are negative prognostic markers in AML patients.
|
26189213 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
IDH1 and IDH2 mutations in patients with acute myeloid leukemia: Suitable targets for minimal residual disease monitoring?
|
30176240 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
CausalMutation
|
disease |
CLINVAR |
IDH1 and IDH2 mutations are frequent in Chinese patients with acute myeloid leukemia but rare in other types of hematological disorders.
|
20946881 |
2010 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
IDH1(R132) and IDH2(R140) mutations are frequently accompanied by normal cytogenetics and NPM1 mutation, whereas IDH2(R172) is frequently the only mutation detected in acute myeloid leukemia.
|
22917530 |
2012 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
IDH1- and IDH2-mutant primary human AML cells were more sensitive than IDH1/2 wild-type cells to ABT-199, a highly specific BCL-2 inhibitor that is currently in clinical trials for hematologic malignancies, both ex vivo and in xenotransplant models.
|
25599133 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
CausalMutation
|
disease |
CLINVAR |
Impact of genetic features on treatment decisions in AML.
|
22160010 |
2011 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
In addition to a brief summary of the factors that shape prognostication at diagnosis, this review attempts to expand on the current therapies under investigation that have shown promise in treating AML, including hypomethylating agents, gemtuzumab ozogamicin, FLT3 tyrosine kinase inhibitors, antisense oligonucleotides, and other novel therapies, including aurora kinases, mTOR and PI3 kinase inhibitors, PIM kinase inhibitors, HDAC inhibitors, and IDH targeted therapies.
|
23982740 |
2013 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
In addition to currently defined AML subgroups, three heterogeneous genomic categories emerged: AML with mutations in genes encoding chromatin, RNA-splicing regulators, or both (in 18% of patients); AML with TP53 mutations, chromosomal aneuploidies, or both (in 13%); and, provisionally, AML with IDH2(R172) mutations (in 1%).
|
27276561 |
2016 |