|
Nephroblastoma
|
0.310 |
Biomarker
|
disease |
CTD_human |
A Children's Oncology Group and TARGET initiative exploring the genetic landscape of Wilms tumor.
|
28825729 |
2017 |
|
Nephroblastoma
|
0.310 |
GeneticVariation
|
disease |
BEFREE |
These data support a model whereby activating MLLT1 mutations early in renal development result in the development of Wilms tumour.
|
26635203 |
2015 |
|
Bilateral Wilms Tumor
|
0.300 |
Biomarker
|
disease |
CTD_human |
A Children's Oncology Group and TARGET initiative exploring the genetic landscape of Wilms tumor.
|
28825729 |
2017 |
|
Body Height
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The efficiency of murine MLL-ENL-driven leukemia initiation changes with age and peaks during neonatal development.
|
31405949 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
MLL-ENL target genes were induced more efficiently in neonatal progenitors than in adult progenitors, consistent with the distinct AML initiation efficiencies.
|
31405949 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In summary, this is a pediatric case of AML presenting a novel complex t(11;16;19) variant with overexpression of ELL and MLLT1.
|
30974445 |
2019 |
|
Finding of Mean Corpuscular Hemoglobin
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The efficiency of murine MLL-ENL-driven leukemia initiation changes with age and peaks during neonatal development.
|
31405949 |
2019 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
We aimed at exploring the use of CSPG4-specific CAR T cells against mixed-lineage leukemia (MLL)-rearranged leukemic blasts, using the precursor B cell leukemia cell line KOPN8 (MLL-MLLT1 translocation) as a model.
|
31195686 |
2019 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Recently, we identified the YEATS domain of AF9 (ALL1 fused gene from chromosome 9) as a novel acetyl-lysine-binding module and showed that the ENL (eleven-nineteen leukemia) YEATS domain is an essential acetyl-histone reader in acute myeloid leukemias.
|
29437725 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our results indicate that MLLT1 and AFDN account for the majority (63%) of KMT2A gene partners in pediatric/young adult T-ALL/LBL, while no KMT2A/AFF1 or KMT2A/MLLT3 fusions were observed despite their common identification in B-ALL and acute myeloid leukemia, respectively.
|
30203571 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Recently, we identified the YEATS domain of AF9 (ALL1 fused gene from chromosome 9) as a novel acetyl-lysine-binding module and showed that the ENL (eleven-nineteen leukemia) YEATS domain is an essential acetyl-histone reader in acute myeloid leukemias.
|
29437725 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
This review will not only provide a fundamental understanding of the structure and function of ENL and update on the roles of ENL in AML, but also the development of new therapeutic strategies.
|
30066088 |
2018 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Recently, we identified the YEATS domain of AF9 (ALL1 fused gene from chromosome 9) as a novel acetyl-lysine-binding module and showed that the ENL (eleven-nineteen leukemia) YEATS domain is an essential acetyl-histone reader in acute myeloid leukemias.
|
29437725 |
2018 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Together, our data identify ENL as a histone acetylation reader that regulates oncogenic transcriptional programs in acute myeloid leukaemia, and suggest that displacement of ENL from chromatin may be a promising epigenetic therapy, alone or in combination with BET inhibitors, for aggressive leukaemia.
|
28241141 |
2017 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
To explain the mechanistic role of ENL in leukaemia pathogenesis and dynamic transcription control, a chemical genetic strategy was developed to achieve targeted protein degradation.
|
28241139 |
2017 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
CRISPR-Cas9-induced t(11;19)/MLL-ENL translocations initiate leukemia in human hematopoietic progenitor cells <i>in vivo</i>.
|
28572162 |
2017 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
MLL-ENL-mediated leukemia initiation at the interface of lymphoid commitment.
|
28068328 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Together, our data identify ENL as a histone acetylation reader that regulates oncogenic transcriptional programs in acute myeloid leukaemia, and suggest that displacement of ENL from chromatin may be a promising epigenetic therapy, alone or in combination with BET inhibitors, for aggressive leukaemia.
|
28241141 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
CRISPR-Cas9-induced t(11;19)/MLL-ENL translocations initiate leukemia in human hematopoietic progenitor cells <i>in vivo</i>.
|
28572162 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
MLL-ENL-mediated leukemia initiation at the interface of lymphoid commitment.
|
28068328 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here we found that the hematopoietically expressed homeobox gene Hhex is overexpressed in acute myeloid leukemia (AML) and is essential for the initiation and propagation of MLL-ENL-induced AML but dispensable for normal myelopoiesis, indicating a specific requirement for Hhex for leukemic growth.
|
26728554 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we found that inhibition of the kinase ATR, which is the primary sensor of DNA replication stress, induced chromosomal breakage and death of mouse AML(MLL) cells (with an MLL-ENL fusion and a constitutively active N-RAS independently of p53.
|
27625305 |
2016 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Global gene expression profiling revealed that CD9, CD32, and CD24 were over-represented in MLL-AF4, MLL-AF9, and MLL-ENL LICs compared with normal HSCs.
|
25538041 |
2015 |