|
Bladder Neoplasm
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
This is the first study to evaluate the role of germ line genetic variations in PI3K-AKT-mTOR pathway as cancer susceptibility factors that will help us identify high-risk individuals for bladder cancer.
|
19875696 |
2009 |
|
Bladder Neoplasm
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The AKT1 G49A (E17K) mutation was found in 2/44 (4.8%) bladder cancer cell lines and 5/184 (2.7%) bladder tumours.
|
19802009 |
2010 |
|
Bladder Neoplasm
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Energy balance, the PI3K-AKT-mTOR pathway genes, and the risk of bladder cancer.
|
20354165 |
2010 |
|
Bladder Neoplasm
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Methylation level of Akt1 has clinical relevance (P = 0.0043 by unpaired student's t test) with bladder cancer.
|
22189542 |
2012 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
The AKT and ERK pathways may reciprocally regulate, which are responsible for in vitro and in vivo epithelial to mesenchymal transition (EMT) process of bladder cancer.
|
22525723 |
2012 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, we concluded that UCA1 regulated cell cycle through CREB via PI3K-AKT dependent pathway in bladder cancer.
|
22285928 |
2012 |
|
Bladder Neoplasm
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Overall, mutated FGFR3 (FGFR3(mut)) and mutated FGFR3 (FGFR3(mut))-mutated PIK3CA (PIK3CA(mut)) genotypes were associated with low-grade bladder tumors and mutated PIK3CA (PIK3CA(mut))-mutated KRAS (KRAS(mut)) and mutated AKT1 (AKT1(mut)) were only present in high-grade tumors.
|
22417847 |
2012 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
We characterized the relationship between AKT pathway mutational status and sensitivity to the effects of the selective AKT kinase inhibitor AZ7328 using a panel of 12 well-characterized human bladder cancer cell lines.
|
22895070 |
2012 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
AIB1 predicts bladder cancer outcome and promotes bladder cancer cell proliferation through AKT and E2F1.
|
23511556 |
2013 |
|
Bladder Neoplasm
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Signaling activity in the PI3K and MAPK pathways was assessed by measuring intracellular levels of p-AKT and p-ERK at baseline and in response to pathway modulation; 66% (N = 19) of BC samples and 27% (N = 4) of NC samples met the "evaluable" criteria, i.e., at least 400,000 total cells available upon sample receipt with >2% of cells showing an epithelial phenotype.
|
23300058 |
2013 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Manipulating the expression of mutant or wild-type PIK3CA or DUSP1 confirmed that this mechanism is responsible for the induction of apoptosis and the inhibition of tumour proliferation in vitro and in vivo, to sensitise cells to AKT target therapy.Conclusion or interpretation:PIK3CA mutations confer sensitivity to AKT target therapy in BLCA by regulating DUSP1 expression and subsequent ERK1/2 dephosphorylation and can potentially serve as a stratifying biomarker for treatment.
|
25349966 |
2014 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
The PI3K/AKT pathway is considered to play a major role in bladder carcinogenesis, but its relationships with other molecular alterations observed in bladder cancer remain unknown.
|
24122582 |
2014 |
|
Bladder Neoplasm
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Mechanism studies suggest that ERα could control the expression of INPP4B to reduce AKT activity and consequently reduce BCa cell growth.
|
25277204 |
2014 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Moreover, CCDC34 silencing decreased the phosphorylation of MEK, ERK1/2, JNK, p38 and Akt, and the expressions of c-Raf and c-Jun, indicating MAPK and AKT pathways (ERK/MAPK, p38/MAPK, JNK/MAPK and PI3K/Akt) might be involved in CCDC34 regulation of bladder cancer cell proliferation and migration.
|
26312564 |
2015 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, these findings highlight for the first time that ANG could play a pivotal role in the development of bladder cancer through regulating AKT/mTOR signaling pathway.
|
25564356 |
2015 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data provide important clues on the therapeutic benefits of targeting Akt1 for bladder cancer therapy.
|
26148825 |
2015 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, GOLPH3 is likely to play important roles in bladder cancer progression via modulating AKT/mTOR signaling, and it is a novel prognostic biomarker and promising therapeutic target for bladder cancer.
|
26375441 |
2015 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
MicroRNA-608 inhibits proliferation of bladder cancer via AKT/FOXO3a signaling pathway.
|
28549468 |
2017 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Actein induces autophagy and apoptosis in human bladder cancer by potentiating ROS/JNK and inhibiting AKT pathways.
|
29348843 |
2017 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
RASAL2 inhibits tumor angiogenesis via p-AKT/ETS1 signaling in bladder cancer.
|
29702203 |
2018 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Further, transwell chambers assay showed that GA suppressed bladder cancer cell invasion and migration through p-AKT/MMP-2 signaling pathway.
|
29567231 |
2018 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
We discovered a positive feedback loop, in which the activation of p38 and AKT downstream from the altered FGFR3 upregulates <i>MYC</i> mRNA levels and stabilizes MYC protein, respectively, leading to the accumulation of MYC, which directly upregulates <i>FGFR3</i> expression by binding to active enhancers upstream from <i>FGFR3</i> Disruption of this FGFR3/MYC loop in bladder cancer cell lines by treatment with FGFR3, p38, AKT, or BET bromodomain inhibitors (JQ1) preventing <i>MYC</i> transcription decreased cell viability <i>in vitro</i> and tumor growth <i>in vivo</i> A relevance of this loop to human bladder tumors was supported by the positive correlation between <i>FGFR3</i> and <i>MYC</i> levels in tumors bearing <i>FGFR3</i> mutations, and the decrease in FGFR3 and MYC levels following anti-FGFR treatment in a PDX model bearing an <i>FGFR3</i> mutation.
|
29463565 |
2018 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Deregulation of the PI3K/AKT/mTOR pathway was observed in more than 40% of bladder tumors and suggested the use of mTOR as a target for the treatment of urothelial cancers.
|
29454321 |
2018 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, our study illustrated a novel signaling cascade of LINC00641/miR-197-3p/KLF10/PTEN/PI3K/AKT pathway regulating bladder cancer development.
|
30060954 |
2018 |
|
Bladder Neoplasm
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The <i>AKT1</i> rs2498801 variant is associated with a decreased risk of BC (OR=0.57, 95 % CI=0.39-0.82, p=0.003, AG vs AA; OR=0.74, 95 % CI=0.56-0.97, p=0.032, G vs A) while, AKT1 rs1130233 polymorphism considerably increased the risk of BC (OR=3.70, 95 % CI=2.52-5.43, p<0.0001, GA vs GG; OR=5.81, 95 % CI=1.53-21.97, p=0.010, AA vs GG; OR=2.71, 95 % CI=1.98-3.70, p<0.0001, A vs G).
|
29383014 |
2018 |