Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In addition, KMT2A depletion effectively suppressed cancer metastasis in vivo.
|
31090199 |
2019 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Chromosomal rearrangements involving the mixed-lineage leukemia (MLL1) gene are common in a unique group of acute leukemias, with more than 100 fusion partners in this malignancy alone.
|
30548174 |
2019 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Although this fusion is out of frame, as the antisense strand of BTN3A1 is fused to the sense strand of KMT2A, the loss of heterozygosity of the BTN3A1 gene might contribute to the malignancy of leukemic cells.
|
28785923 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Oxidative stress on Trx1/CD30 is a trigger of cancer disease, and the selected oxidation and immune products are a biomarker system for aging and cancer.
|
30788039 |
2019 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
T(4;11) MLL-AF4 acute leukemia is one of the most aggressive malignancies in infant and pediatric populations.
|
31381950 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We validated MLL1 and MLL2 as direct targets of TP53<sup>R249S</sup> and affirmed their association in the Cancer Genome Atlas dataset.
|
31560893 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The pathogenesis of t(4;11)/KMT2A-AFF1<sup>+</sup> (MLL-AF4<sup>+</sup>) infant B-cell acute lymphoblastic leukemia remains difficult to model, and the pathogenic contribution in cancer of the reciprocal fusions resulting from derivative translocated-chromosomes remains obscure.
|
30679323 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, 28 is a valuable menin-MLL1 inhibitor that can be used for potential therapeutic applications and in further studies regarding the role of menin in cancer.
|
29738674 |
2018 |
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
As a member of the human histone‑lysine N‑methyltransferase SETD1A (SET1)/histone‑lysine N‑methyltransferase 2A (MLL) complexes that are required for full SET1/MLL methyltransferase activity, protein dpy‑30 homolog (DPY30) catalyzes histone H3K4 methylation, and its dysfunction has been associated with the occurrence of cancer.
|
30221689 |
2018 |
Malignant Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
MLL/SET methyltransferases catalyze methylation of histone 3 lysine 4 and play critical roles in development and cancer.
|
29474905 |
2018 |
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Furthermore, compounds 1, 23 and 44 were chosen to evaluate for their antiproliferative activities on the MLL-AF4-expression acute leukemia cell line (MV4-11), other cancer cell lines (MDA-MB-231, A549, 22Rv1) and the non-cancer cell lines (HUV-EC-C, MRC5, RPTEC).
|
29730189 |
2018 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
KMT2/MLL proteins are commonly overexpressed or mutated in cancer and have been shown to support cancer maintenance.
|
29925347 |
2018 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We show that different cancer mutations in MLL1 lead to a loss or increase in activity, illustrating the complex and tumor-specific role of MLL1 in carcinogenesis.
|
28182322 |
2017 |
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Here, immunohistochemical examination of clinical colorectal cancer (CRC) specimens revealed that human thioredoxin1 (hTrx1), but not human glutaredoxin1 (hGrx1), was up-regulated along with human RR large subunit (RRM1) in cancer tissues, and the expression levels of both proteins were correlated with cancer malignancy stage.
|
28411237 |
2017 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Acute lymphoblastic leukemia (ALL) in infants is an aggressive malignancy with a poor clinical outcome, and is characterized by translocations of the Mixed Lineage Leukemia (MLL) gene.
|
27588400 |
2017 |
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Moreover, KMT2A knockdown suppressed tumorsphere formation and the expression of cancer stem cell markers, which was also reversed by hTERT overexpression.
|
28726783 |
2017 |
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Strikingly, however, these effects of MLL1 inhibition on SASP gene expression do not impair OIS and, furthermore, abolish the ability of the SASP to enhance cancer cell proliferation.
|
26833731 |
2016 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we determined that the RBP insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) is specifically overexpressed in mixed lineage leukemia-rearranged (MLL-rearranged) B-acute lymphoblastic leukemia (B-ALL), which constitutes a subtype of this malignancy associated with poor prognosis and high risk of relapse.
|
26974154 |
2016 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The cancer COMPASS: navigating the functions of MLL complexes in cancer.
|
25794446 |
2015 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Among the 1827 children enrolled in the Tokyo Children's Cancer Study Group ALL studies L95-14, L99-15, L99-1502, L04-16, and L07-1602 (1995-2009), 25 MLL-r ALL patients (1.3 %) were identified.
|
26410102 |
2015 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this review, we provide an overview of the roles of EZH2, SETD2, NSD family, SMYD family, MLL family and DOT1L PKMTs in cancer focusing on the effects of somatic cancer mutations in these enzymes.
|
25123655 |
2014 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
To prospectively address the role of MLL rearrangements in extramedullary B-lymphoblastic malignancies in infants, we suggest to assess both tumors and non-infiltrated bone marrow for the presence of this genetic abnormality.
|
24635731 |
2014 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We analyzed a series of seven ALK rearranged cancers, six KMT2A rearranged leukemias, and 77 ALK/KMT2A rearrangement-negative cancers, previously tested by fluorescence in situ hybridization (FISH).
|
24813172 |
2014 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Studying the MLL1 gene and its oncogenic variants has provided a paradigm for understanding cancer initiation and maintenance through aberrant epigenetic gene regulation.
|
25264566 |
2014 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Discovery of the enzymatic activity that catalyses oxidation of 5-methylcytosine (5mC) to generate 5-hydroxymethylcytosine (5hmC) mediated by the MLL (KMT2A) fusion partner TET1 has sparked intense research to understand the role this new DNA modification has in cancer.
|
25179374 |
2014 |