|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
In murine models of chronic (CML) and acute myeloid leukemia (AML) induced by BCR-ABL1 and MLL-AF9, respectively, knockdown of Fubp1 resulted in prolonged survival, decreased numbers of CML progenitor cells, decreased cell cycle activity and increased apoptosis.
|
30635626 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
With this approach, we assessed the effect of 114 murine cytokines on <i>MLL-AF9</i> AML mouse cells and identified the tumor necrosis factor ligand superfamily member 13 (TNFSF13) as a positive regulator of leukemia-initiating cells.
|
30819903 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
The 3-year DFS of KMT2A-rearranged AML was not significantly poorer than that of other AML (P = 0.09), and no significant difference was also seen in 3-year OS rate (P = 0.21).
|
31707119 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
We previously demonstrated that endogenous MLL1 is not required for the maintenance of MLL-FP-driven AML but is required for normal HSC homeostasis.
|
31161857 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Patients with acute myeloid leukemia frequently present translocations of MLL gene.
|
31727944 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Moreover, development of additional methods to detect specific translocation partners of KMT2A and leukemia-specific targeting drugs is important to improve further the outcomes of KMT2A-rearranged AML.
|
30869817 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Hif-1α Deletion May Lead to Adverse Treatment Effect in a Mouse Model of MLL-AF9-Driven AML.
|
30595549 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Transgenic <i>Stat3</i>β expression resulted in decelerated disease progression and extended survival in PTEN- and MLL-AF9-dependent AML mouse models.
|
31270081 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
KMT2A-MLLT10 is one of the common chimeric genes diagnosed in acute leukemia with KMT2A rearrangement (8%), especially in acute myeloid leukemia (AML; 18%).
|
30624859 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
This interaction is critical for the maintenance of <i>MLL</i> translocation driven AML by targeting MLL fusion proteins to the target genes <i>Meis1</i> and <i>Hoxa9</i>.
|
29774127 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Mixed lineage leukemia [MLL; now known as lysine methyltransferase 2A (KMT2A)] rearrangement-positive acute myeloid leukemia (AML) and juvenile myelomonocytic leukemia (JMML) are distinct diseases, although age of susceptibility (infancy or early childhood) and abnormal monocytosis are common clinical features.
|
30143999 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Stabilization of NF-κB-Inducing Kinase Suppresses MLL-AF9-Induced Acute Myeloid Leukemia.
|
29320732 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
However, the redox regulators that allow AML cell survival in this oxidized environment remain largely unknown.<b>Experimental Design:</b> Utilizing several chemical and genetically-encoded redox sensing probes across multiple human and mouse models of AML, we evaluated the role of the serine/threonine kinase PKC-epsilon (PKCε) in intracellular redox biology, cell survival and disease progression.<b>Results:</b> We show that RNA interference-mediated inhibition of PKCε significantly reduces patient-derived AML cell survival as well as disease onset in a genetically engineered mouse model (GEMM) of AML driven by MLL-AF9.
|
29127121 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Leukemia progenitors are selectively eliminated by the inhibitors, explaining their therapeutic efficacy with preserved hematopoiesis and leukemia cure potential; they eradicate leukemia in MLL-AF9 and Tet2<sup>-/-</sup>;Flt3<sup>ITD</sup> AML mouse models and in several patient-derived AML xenograft models, supporting their potential efficacy in curing human leukemia.
|
30146162 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Our study support the hypothesis that Piribedil could serve as a new drug for the treatment of MLL-r AML and provide new insight for further optimization of targeting MLL1 HMT activity.
|
29857126 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Here, we studied these characteristics of NK cells in MLL-AF9 induced mouse acute myeloid leukemia (AML) model.
|
29154208 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
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
|
0.600 |
Biomarker
|
disease |
BEFREE |
Here, we report the case of a 61-year-old woman who presented with an AML with MLL rearrangement and CD4+/CD56+ expression presenting as LC and that was misdiagnosed as BPDCN.
|
29660158 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Mouse AML cells that are defective in PirB signaling had decreased activation of CAMKs, and the forced expression of CAMK partially rescued the PirB-defective phenotype in the MLL-AF9 AML mouse model.
|
29482582 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Finally, in human NPM1-mutant and in MLL-translocated AML, high expression of PRDM16, which negatively impacts outcome, was associated with inflammatory gene expression, thus corroborating the mouse data.
|
29878897 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Chromosomal translocations involving the MLL1 gene characterize a poor prognosis subset of acute myeloid leukemia (AML), referred to as 11q23-AML.
|
29459712 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
The polymerase-associated factor complex (PAFc) is an epigenetic co-activator complex that makes direct contact with MLL fusion proteins and is involved in AML, however, its functions are not well understood.
|
28945229 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
PML-RARA, RUNX1-RUNX1T1, and KMT2A-rearrangement are common genetic rearrangements that drive the development of acute myeloid leukemia (AML).
|
29688850 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
Biomarker
|
disease |
BEFREE |
Twenty MLL-rearranged AML patients along with a control cohort of 138 AML patients are included in this work.
|
29384595 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
The initial level of MLL-partial tandem duplication affects the clinical outcomes in patients with acute myeloid leukemia.
|
28745571 |
2018 |