|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
These results reveal novel functions of MDM4 and TOP2A as well as their interactions in oncogenesis, suggesting that inhibition of the MDM4-TOP2A interaction may represent a novel strategy in specifically and simultaneously targeting TOP2A and MDM4 for cancer treatment.
|
30672125 |
2019 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
MDMX acidic domain inhibits p53 DNA binding in vivo and regulates tumorigenesis.
|
29581299 |
2018 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
In this short review, we discuss a recent set of data indicating that MDM4-S is more likely a passenger isoform during tumorigenesis and that targeting MDM4 splicing to prevent MDM4-FL protein expression appears as a promising strategy to reactivate p53 in cancer cells.
|
28230750 |
2017 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
MDM4 is a p53-interacting protein and plays an important role in carcinogenesis.
|
28099948 |
2017 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
However, in the absence of prospective studies, it is not clear whether expression of MDM4-S in itself is oncogenic or is simply an outcome of tumorigenesis.
|
28460439 |
2017 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Taken together, our results suggest that USP22 promotes NSCLC tumorigenesis in vitro and in vivo through MDMX upregulation and subsequent p53 inhibition.
|
25547493 |
2014 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The mouse double minute 4 (MDM4) oncoprotein may inhibit tumorigenesis by regulating the apoptotic mediator p53.
|
24445145 |
2014 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Our data indicate that the novel variant MDM4-B may play a role in glioma tumorigenesis or cancer progression.
|
23994448 |
2013 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
MDM2, MDMX and p53 in oncogenesis and cancer therapy.
|
23303139 |
2013 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Here we show that Mdm4 p53 binding protein homolog (MDM4), a negative regulator of p53, is upregulated in a substantial proportion (∼65%) of stage I-IV human melanomas and that melanocyte-specific Mdm4 overexpression enhanced tumorigenesis in a mouse model of melanoma induced by the oncogene Nras.
|
22820643 |
2012 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Mouse double minute 4 (MDM4), a homolog of MDM2, is one of the key negative regulators of p53, and its amplification or overexpression contributes to carcinogenesis by inhibiting the p53 tumor suppressor activity.
|
21540763 |
2011 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
We speculate that MDM4 might play a role in colorectal carcinogenesis that is not limited to negative regulation of p53 in combination with MDM2.
|
21503588 |
2011 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Mdm4 is thus a bona fide oncogene in vivo and cooperates with p53 heterozygosity to drive tumorigenesis.
|
20736370 |
2010 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Even modest decrease in Mdm4 levels affects tumorigenesis in mice, suggesting that genetic variants of MDM4 might have similar effects in humans.
|
21084273 |
2010 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
This report not only implicates MDM4 as a key regulator of tumorigenesis in the human breast and ovary, but also exploits for the first time evolutionary driven linkage disequilibrium as a means to select SNPs of p53 pathway genes that might be clinically relevant.
|
19497887 |
2009 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
It is worthy to note that the significant downregulation of full-length MDM4 in PTC reveals a novel status of this factor in human cancer that counsels careful evaluation of its role in human tumorigenesis and of its potential as therapeutic target.
|
18335186 |
2008 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
These results suggest that LRP expression observed in NSCLC, maintained through the carcinogenesis process of respiratory cells, is not altered by the increased number of copies of chromosome 16 and probably controlled by mechanisms different from those of MRP1 expression, whereas both proteins are associated with the MDR phenotype.
|
17438350 |
2007 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
These results suggest that deregulated expression of HDMX plays a role in carcinogenesis as an alternative way to inactivate p53.
|
11280734 |
2001 |