|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
This study thus identified a novel small molecule that rapidly kills MLL-rearranged leukemia cells by targeting a metabolic vulnerability in a subset of low HIF1α/low MEIS1-expressing MLL-rearranged leukemia cells.
|
30670779 |
2019 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Aberrant fusion proteins involving the MLL histone methyltransferase (HMT) lead to recruitment of DOT1L, to a multi-protein complex resulting in aberrant methylation of histone H3 lysine 79 at MLL target genes, and ultimately enhanced expression of critical genes for hematopoietic differentiation, including HOXA9 and MEIS1, and as such defines the established mechanism for leukemogenesis in MLL-rearrangement (MLL-r) leukemias.
|
28229434 |
2017 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Herein, we identified a distinct expression pattern of Meis1 in patients with newly diagnosed AML without MLL abnormality.
|
28054140 |
2017 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Serving as an effective inhibitor, 28d demonstrates the mechanism of cell killing in both cell cycle arrest and apoptotic effect as well as downregulation of the pivotal mixed lineage leukemia (MLL) fusion target genes such as HOXA9 and MEIS1, which reflects the critical roles of type I PRMTs in MLL leukemia.
|
29019697 |
2017 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Moreover, PBX3/MEIS1 overexpression also caused AML in vivo, with a leukemic latency similar to that caused by forced expression of MLL-AF9, the most common form of MLL fusions.
|
26747896 |
2016 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
MLL-r leukemia cells that were resistant to the compound were characterised by significantly higher baseline gene expression levels of MEIS1 and BCL2 in comparison to CCI-007 sensitive MLL-r leukemia cells.In conclusion, we have identified CCI-007 as a novel small molecule that displays rapid toxicity towards a subset of MLL-r, CALM-AF10 and SET-NUP214 leukemia cell lines.
|
27317766 |
2016 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
A well-characterized member of this protein family is MEIS1, which orchestrates a transcriptional program required for the maintenance of MLL-rearranged acute myeloid leukemia (AML).
|
25349154 |
2015 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Mixed lineage leukemia (MLL) fusion proteins directly activate the expression of key downstream genes such as MEIS1, HOXA9 to drive an aggressive form of human leukemia.
|
24445817 |
2014 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Chromatin immunoprecipitation assays demonstrated that EZH2 was highly enriched around the transcription-start-site of p16, together with H3K27 methylation marks in MLL/ENL and Hoxa9/Meis1 transduced cells but not in E2A/HLF transduced cells.
|
24612037 |
2014 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Interestingly, forced expression of Plzf itself immortalized HSCs and myeloid progenitors in vitro without upregulation of Hoxa9/Meis1, which are well-known targets of MLL fusion proteins, whereas its mutant lacking the BTB/POZ domain did not.
|
23838347 |
2013 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Collectively, our data delineate an MLL-fusion/Tet1/Hoxa9/Meis1/Pbx3 signaling axis in MLL-rearranged leukemia and highlight TET1 as a potential therapeutic target in treating this presently therapy-resistant disease.
|
23818607 |
2013 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
Biomarker
|
disease |
BEFREE |
Chromatin immunoprecipitation followed by quantitative polymerase chain reaction was used to determine how binding of associating proteins compare across Hoxa9 and Meis1 in cell lines with and without MLL fusion proteins and how binding is altered during gene down-regulation and differentiation.
|
20854876 |
2011 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Silencing MYB in human leukemic cell lines and primary patient material evoked a global decrease in H3K4 methylation, an unexpected decrease in HOXA9 and MEIS1 gene expression, and decreased MLL and menin occupancy in the HOXA9 gene locus.
|
20093773 |
2010 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Suppression of MLL-AF4 is paralleled by a decreased expression of the homeotic genes HOXA7, HOXA9, and MEIS1.
|
16046533 |
2005 |
|
MIXED LINEAGE LEUKEMIA
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Co-expression of HoxA9 and Meis1 genes in the KP-L-RY cell line indicated possible functional similarity between MLL-AF4 and MLL-AF5q31.
|
12399976 |
2002 |