Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Since pharmacological activation of ATF4 exerts potent anti-tumor effects, modulators of ATF4 activation may have potential in cancer therapy.
|
31461933 |
2019 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Our findings suggest that targeting the TGF-β<sub>1</sub>-mTORC1-ATF4 axis may represent a novel therapeutic strategy for interfering with myofibroblast function in fibrosis and potentially in other conditions, including cancer.
|
31113850 |
2019 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
This review highlights the recent literature on ferroptotic and apoptotic agent interactions through the ER stress-mediated PERK-eIF2α-ATF4-CHOP-PUMA pathway and implicates combined treatment to effectively enhance tumoricidal efficacy as a novel therapeutic strategy for cancer.<i></i>.
|
29592897 |
2018 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
We defined an eight-gene signature with prognostic potential, altered in 45% of 2,509 patients with breast cancer.<b>Conclusions:</b> ATF4 may represent a valuable prognostic biomarker and therapeutic target in patients with TNBC, and we identified a cell signaling pathway-based gene signature that may contribute to the development of combinatorial targeted therapies for breast cancer.<i>Clin Cancer Res; 24(22); 5697-709.©2018 AACR</i>.
|
30012564 |
2018 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Hence, ATF4 expression promotes cell migration and anchorage-independent cell growth, whereas siRNA-mediated knockdown of ATF4 attenuates these features of malignancy in human gliomas.
|
28553953 |
2017 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
In addition, an ATF4-dependent mechanism leading to cancer cell adaptation and resistance against taxol-induced cell death was evidenced.
|
25724736 |
2015 |
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These results indicate that increased expression of p-ATF4 (ser 245) may contribute to cancer development of non-small cell lung cancer and may be a potential cancer marker.
|
23975372 |
2014 |
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Accordingly, cancer cells treated with the ER stress-inducing agent nelfinavir showed reduced mTOR activity and associated increases in the expression levels of ATF4 and SESN2.
|
23916134 |
2013 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The AhR-VEGF pathway through ATF4 is a novel pathway in glucose-deprived liver cancer cells that is related to the microenvironment within a cancer tissue affecting liver cancer malignancy.
|
24330582 |
2013 |
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Our results reveal that the GCN2/ATF4 pathway promotes tumor growth and angiogenesis through AAD-mediated VEGF expression and, thus, is a potential target in cancer therapy.
|
23908598 |
2013 |
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Transcriptional up-regulation of ULK1 by ATF4 contributes to cancer cell survival.
|
23078367 |
2013 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Since ATF4 is induced by tumour microenvironmental factors, and regulates processes relevant to cancer progression, it might serve as a potential therapeutic target in cancer.
|
17466566 |
2008 |
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These results suggest that the Clock and ATF4 transcription system might play an important role in multidrug resistance through glutathione-dependent redox system, and also indicate that physiological potentials of Clock-controlled redox system might be important to better understand the oxidative stress-associated disorders including cancer and systemic chronotherapy.
|
17297441 |
2007 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Activating transcription factor 4 increases the cisplatin resistance of human cancer cell lines.
|
14695168 |
2003 |