|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
However, the p73 gene is rarely mutated in tumors, so appropriate pharmacological manipulation of the p73 pathway is a very promising approach for cancer therapy.
|
21391908 |
2011 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The tumor repressor p53 plays a key role in DNA damage response, and has been found to be mutated in 50% of human cancer. p53, p63, and p73 are three members of the p53 gene family.
|
31090271 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Moreover, our results suggest that p73 compensates for loss of p53 and that targeting Mdm2 in p53-deficient cancers has therapeutic potential.<i>Cancer Res; 77(14); 3823-33.©2017 AACR</i>.
|
28576884 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
These findings implicate p73 in regulation of cancer metabolism and suggest that TAp73 influences glutamine and serine metabolism, affecting GSH synthesis and determining cancer pathogenesis.
|
24186203 |
2014 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
However, despite a remarkable structural and partly functional similarity among p53, p63, and p73, mouse knockout studies revealed an unexpected functional diversity among them. p63 and p73 knockouts exhibit severe developmental abnormalities but no increased cancer susceptibility, whereas this picture is reversed for p53 knockouts.
|
15280445 |
2004 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Interestingly, several studies have shown that p73, and more recently p63, are involved in cellular response to cancer therapy, while others have indicated that p63 and p73 are required for p53-induced apoptosis, delineating functional interplay between p53 family members.
|
19754415 |
2009 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In summary, according to the results of our meta-analysis, the TP73 polymorphism (G4C14-A4T14) probably associates with cancer risk.
|
21672615 |
2011 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Contribution of p53, p63, and p73 to the developmental diseases and cancer.
|
18348649 |
2008 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Finally, p73 participates in the control of angiogenesis in development and cancer.
|
31582429 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
Accordingly, although TP73 aberrant methylation was more frequent in meningiomas with 1p deletion (P<0.05), no association with the grade of malignancy could be established.
|
14734228 |
2004 |
|
Primary malignant neoplasm
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
The p73 gene was methylated in 94% of cases, a frequency that is the highest known for any human malignancy.
|
11786399 |
2002 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
This recently uncovered role of TAp73 in the regulation of cellular metabolism strongly affects oxidative balance, thus potentially influencing all the biological aspects associated with p73 function, including development, homeostasis and cancer.
|
29077094 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
A comprehensive understanding of p73 post-translational modifications will be extremely useful for the development of new strategies for treating and preventing cancer.
|
22419114 |
2012 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
One way to address this situation may be to activate the p53-related protein p73, which functions similarly, but unlike p53, is rarely lost or mutated in cancer.
|
18593889 |
2008 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
<i>TP73 G4C14-A4T14</i> polymorphism and cancer susceptibility: evidence from 36 case-control studies.
|
30420492 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
p63, p73 and p53 are transcription factors members of the p53 gene family involved in development, differentiation and cell response to stress. p53 gene is mutated in 50% of human cancer.
|
18289041 |
2007 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Here we discovered a novel synergistic mechanism leading to potent p73 activation and cancer cell death by oxidative stress and inhibition of 20S proteasomes.
|
25341038 |
2014 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
We also discuss the significance of p73 and p63 for cancer therapy and outline novel approaches in development of therapeutic drugs that specifically target the p53 family.
|
18801697 |
2009 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In addition p73 and p63 are, in contrast to p53, rarely mutated in human cancer.
|
10618710 |
1999 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Functional regulation of p73 and p63: development and cancer.
|
14659698 |
2003 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
This review is focused on recent findings leaving no doubt that N-terminally truncated p73 proteins are operative during oncogenesis, thus underscoring its significance as a marker for disease severity in patients and as target for cancer therapy.
|
18302944 |
2008 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The transcription factor p73 synthesizes a large number of isoforms and presents high structural and functional homology with p53, a well-known tumor suppressor and a famous "Holy Grail" of anticancer targeting. p73 has attracted increasing attention mainly because (a) unlike p53, p73 is rarely mutated in cancer, (b) some p73 isoforms can inhibit all hallmarks of cancer, and (c) it has the ability to mimic oncosuppressive functions of p53, even in p53-mutated cells.
|
30635889 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
p63, p73 and p53 compose a family of transcription factors involved in cell response to stress and development. p53 is the most frequently mutated gene in cancer (50%) and loss of p53 activity is considered to be ubiquitous to all cancers.
|
16601753 |
2006 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Our meta-analysis suggests that the p73 G4C14-to-A4T14 polymorphism genotypes (GC/AT+AT/AT) may be associated with an increased risk of cancer in most cancer types and ethnicities.
|
22011187 |
2012 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
These findings not only unveil a hitherto unexplained mechanism underlying the functional switchover from p53 to p73, but also validate p73 as a promising and potential target for cancer therapy in the absence of functional p53.
|
20675383 |
2010 |