Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The association between expression levels of ATG5 and tumor size was also significant (P = .02).
|
31837323 |
2020 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Real-time polymerase chain reaction and Western blot showed that PL treatment suppressed the expression of apoptosis and autophagy factors (LC3, Beclin1, Atg7, and Atg5), which are associated with tumor apoptosis and autophagy in SMMC-7721 cells.
|
30536473 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In mice that express oncogenic Kras in pancreatic cells, heterozygous disruption of Atg5 and reduced protein levels promotes tumor development, whereas homozygous disruption of Atg5 blocks tumorigenesis.
|
30296435 |
2019 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Most importantly, we find in multiple tumor types that ATG5 somatic mutations and alternative mRNA splicing specifically disrupt the ATG16L1-binding pocket in ATG5 and impair the essential ATG5-ATG16L1 interactions that are initially required for ATG12-ATG5 conjugation.
|
31636955 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Moreover, more than 50% of L-ATG5/mTOR DKO and L-ATG5/Raptor DKO mice already developed spontaneous tumors, but none of the L-ATG5 KO mice had developed any tumors at 6 months of age.
|
31095752 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we demonstrate that conditional impairment of the autophagy gene Atg5 (atg5-KO) extends the survival of KRAS<sup>G12V</sup>-driven tumor-bearing mice by 38%. atg5-KO tumors spread more slowly during late tumorigenesis, despite a faster onset. atg5-KO tumor cells displayed reduced mitochondrial function and increased mitochondrial fragmentation.
|
29956571 |
2018 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Finally, the blockade of autophagy enhances T<sub>H</sub>9 cell anticancer functions in vivo, and mice with T cell-specific deletion of Atg5 have reduced tumour outgrowth in an IL-9-dependent manner.
|
28916785 |
2017 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Furthermore, increased expression of ATG5 was observed in ESCC tumor tissue as compared to adjacent normal tissue.
|
29207660 |
2017 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
By examination of the specimens from 95 patients with glioblastoma, we found that ATG5 and p-KDR expression was strongly associated with the density of VM in tumors and poor clinical outcome.
|
28812437 |
2017 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05-0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21-0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34-0.87, P = 0.01).
|
27748080 |
2016 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Early treatment of Apc(Min/+)ATG5(+/-) mice with IFN-γ decreased tumor incidence rate to 16.7% and reduced the number of adenomas by 95.5% and late treatment led to regression of tumor.
|
25695667 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
On one hand, we observed that the depletion of essential autophagy-relevant gene products, such as ATG5 and Beclin 1, increased the sensitivity of human or mouse cancer cell lines to irradiation, both in vitro (where autophagy inhibition increased radiation-induced cell death and decreased clonogenic survival) and in vivo, after transplantation of the cell lines into immunodeficient mice (where autophagy inhibition potentiated the tumour growth-inhibitory effect of radiotherapy).
|
24037090 |
2014 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
ATG-5 expression was significantly associated with depth of wall invasion, TNM stages and distant metastasis of GC (P<0.05), whereas MRP-1 expression was significantly linked with tumor size, depth of wall invasion, lymph node metastasis, TNM stages and differentiation status (P<0.05).
|
25329677 |
2014 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Finally, upregulation of MIR34A, knockdown of HMGB1, or inhibition of autophagy (e.g., knockdown of ATG5 and BECN1) restores chemosensitivity and enhances tumor cell death in the retinoblastoma cell.
|
24418846 |
2014 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The AFP-Cre/LoxP-shRNA system target Atg5 gene could significantly sensitize MHCC97L/PLC cells to sorafenib-induced apoptosis in vitro and tumor growth suppression in vivo.
|
23468839 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Data suggest that ASP is involved in colorectal neoplasia and point to this enzyme as a potential useful diagnostic tool in clinical practice.
|
23948443 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In tumor-bearing Mastomys, ATG-5 and ATG-16 were negative in the tumors, whereas beclin-1 was positive in four of five animals.
|
23389729 |
2013 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
A follow-up of 158 primary melanoma patients showed that patients with low levels of ATG5 in their tumors had a reduced progression-free survival.
|
24027027 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we summarize the materials and methods used in our study as follows: establishment of neurosphere cultures from surgical samples of human glioblastoma multiformes; assessment of stem cell markers; examination of adenoviral receptors in BTSCs; evaluation of the cytotoxicity induced by oncolytic adenoviruses; and assessment of autophagy in oncolytic adenovirus-infected BTSCs in vitro, and finally we describe a method to detect upregulation of the autophagy-related protein Atg5 in tumors treated with Delta-24-RGD.
|
21948473 |
2012 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Targeted suppression of ATG5 or ATG7 expression by short hairpin (sh) RNA inhibited cell growth on soft agar and tumor formation in nude mice.
|
21300795 |
2011 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Finally, we determined that cells lacking the autophagy gene ATG5 were unable to activate the autophagic machinery in hypoxia, had decreased oxygen consumption and increased glucose uptake under hypoxia, had increased survival in hypoxic environments, and exhibited accelerated growth as xenografted tumors.
|
18551130 |
2008 |