Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Aberrations of signal transducers in PI3K/Akt pathway have been found in many human cancers, and may play a critical role in carcinogenesis.
|
19628421 |
2009 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activated PI3K and its downstream target Akt are concernful signaling molecules and key survival factors involved in the control of cell proliferation, apoptosis and oncogenesis.
|
19276680 |
2009 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activated phosphoinositide 3-kinase (PI3K) and its downstream target Akt/PKB are important signaling molecules and key survival factors involved in the control of cell proliferation, apoptosis and oncogenesis.
|
17551921 |
2007 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Activated-PAK4 predicts worse prognosis in breast cancer and promotes tumorigenesis through activation of PI3K/AKT signaling.
|
28407679 |
2017 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activating mutations in RAS can lead to oncogenesis by enhancing downstream signaling, such as through the MAPK and PI3K pathways.
|
30735352 |
2019 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Activating mutations in the catalytic subunit of Phosphatidylinositol (3,4,5)-trisphosphate kinase (PI3K), encoded by the <i>Pik3ca</i> gene, are detected in approximately 20% of human anal cancers.<b>Experimental Design:</b> We asked if common activating mutations in <i>Pik3ca</i> contribute to anal carcinogenesis using an established mouse model for anal carcinogenesis in which mice are topically treated with the chemical carcinogen 7,12-Dimethylbenz(a)anthracene (DMBA).
|
30530704 |
2019 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activation of PI3K/Akt/mTOR signaling pathway correlates with oncogenesis, poor prognosis and chemotherapy resistance in NB.
|
29499203 |
2018 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activation of phosphatidylinositol 3-kinase (PI3K)/Akt signaling is associated with tumorigenesis and metastasis of colorectal cancer (CRC).
|
22696593 |
2012 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activation of phosphatidylinositol-3-kinase (PI3K) and downstream signalling by AKT/mammalian target of rapamycin (mTOR) modulates cellular processes such as increased cell growth, cell proliferation and increased cell migration as well as deregulated apoptosis and oncogenesis.
|
30649751 |
2019 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activation of the PI3k/Akt pathway controls key cellular processes and contributes to tumorigenesis in vivo, but investigation of the PI3k/Akt pathway has been limited by the lack of specific inhibitors directed against Akt.
|
15087394 |
2004 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activation of the PI3K and epidermal growth factor receptor (EGFR) pathway is able to drive oncogenesis in multiple human cancers, including head and neck squamous cell carcinoma.
|
22065749 |
2011 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activation of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway plays a critical role in carcinogenesis and resistance to anticancer drugs.
|
29181056 |
2017 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activation of the phosphatidylinositol-3 kinase (PI3K) pathway is a critical step in oncogenesis and plays a role in the development of treatment resistance for both estrogen receptor (ER) positive and human epidermal growth factor receptor 2 (HER2) positive breast cancers.
|
29252036 |
2018 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activation of β-catenin and PI3K pathways are crucial for the oncogenesis of colorectal cancer (CRC).
|
23583404 |
2013 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Although 3-phosphoinositide-dependent protein kinase-1 (PDK1) has been predominately linked to the phosphoinositide 3-kinase (PI3K)-AKT pathway, it may also evoke additional signaling outputs to promote tumorigenesis.
|
23887393 |
2013 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Although KRAS direct binding to and activation of PI3K is required for <i>KRAS</i>-driven lung tumorigenesis, the contribution of insulin receptor (IR) and insulin-like growth factor 1 receptor (IGF1R) in the context of mutant <i>KRAS</i> remains controversial.
|
29610318 |
2018 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Among them, three genes (PIK3CB, CAV2, and KANK1) are reportedly involved in tumorigenesis through the PI3K/Akt signaling pathway.
|
31642198 |
2019 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
An important oncogenic signaling pathway activated by E6 and E7 is the PI3K pathway, a key driver of carcinogenesis.
|
29440171 |
2018 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Astrocyte-elevated gene-1 (AEG-1) expression is increased in multiple cancers and plays a central role in Ha-ras-mediated oncogenesis through the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway.
|
19940250 |
2009 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Because activation of the PI3K pathway is critical for transformation of many human cells, we suggest that PI3K activation by K1 is involved in endothelial cell immortalization and contributes to KSHV-associated tumorigenesis.
|
16585191 |
2006 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis.
|
16453012 |
2006 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Both mechanisms are correlated to the Pi3K/Akt/mTOR pathway which is a major tumorigenesis pathway in nearly all phacomatoses.
|
28265819 |
2018 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Cadmium induces carcinogenesis in BEAS-2B cells through ROS-dependent activation of PI3K/AKT/GSK-3β/β-catenin signaling.
|
22884995 |
2012 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
CD133 promotes tumorigenesis partly through an interaction between its phosphorylated Y828 residue and the PI3K regulatory subunit p85, and the interaction with β-catenin.
|
26029999 |
2015 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Cellular pathways controlling chemotaxis, growth, survival, and oncogenesis are activated by receptor tyrosine kinases and small G-proteins of the Ras superfamily that stimulate specific isoforms of phosphatidylinositol-3-kinase (PI3K).
|
29211993 |
2017 |