|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Inhibitors of human p97 (also known as valosin-containing protein) have been actively pursued because of their potential therapeutic applications in cancer and other diseases.
|
30830772 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Changes in p97 expression or activity are associated with the development of cancer and several related neurodegenerative disorders.
|
31316150 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Alcohol-abuse drug disulfiram targets cancer via p97 segregase adaptor NPL4.
|
29211715 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Correspondingly, p97 has been linked to various pathophysiological states including cancer, neurodegeneration, and premature aging. p97 encompasses an N-terminal domain, two highly conserved ATPase domains and an unstructured C-terminal tail.
|
28451587 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
As p97 is a druggable target, p97 inhibition in the context of DDR has great potential for cancer therapy, as shown for other DDR components such as PARP, ATR and CHK1.This article is part of the themed issue 'Chromatin modifiers and remodellers in DNA repair and signalling'.
|
28847819 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this review, we will describe the cellular processes governed by p97, how the cofactors interact with both p97 and its ubiquitinated substrates, p97 enzymology and the current status in developing p97 inhibitors for cancer therapy.
|
28819009 |
2017 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We will also further examine the more recent findings concerning the role of p97 and how mutations in p97 cofactors, also known as adaptors, cause DNA replication stress induced genomic instability that leads to cancer and accelerated ageing.
|
27086594 |
2017 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
More than a decade ago, it was determined that up-regulation of p97 in many forms of cancer correlates with a poor clinical outcome.
|
25685910 |
2015 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Targeting the AAA ATPase p97 as an Approach to Treat Cancer through Disruption of Protein Homeostasis.
|
26555175 |
2015 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The p97 AAA (ATPase associated with diverse cellular activities), also called VCP (valosin-containing protein), is an important therapeutic target for cancer and neurodegenerative diseases. p97 forms a hexamer composed of two AAA domains (D1 and D2) that form two stacked rings and an N-terminal domain that binds numerous cofactor proteins.
|
24878061 |
2014 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our results provide a rationale for targeting p97 in cancer therapy.
|
21383145 |
2011 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
This suggests that HCAP1-M may be related to cancer susceptibility.
|
14603441 |
2004 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
A point mutation in YY1-recognition site 2, which was previously shown to stimulate P97 3.5-fold, could be detected in the HPV 16 LCRs from both primary tumor and metastasis, indicating that the mutation is a stable characteristic of HPV 16 DNA associated with the individual cancer.
|
7927871 |
1994 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In addition, the levels of the E7 oncoprotein were at least as high as in cancer derived cell lines, suggesting that E2 interruption, observed in cancer derived cell lines, is not causally related to the high level of E7 expression and, therefore, deregulation of the P97 promoter may not be a prerequisite for HPV-16 associated cancer development.
|
1651587 |
1991 |