|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, PI-3-K activation may be an early signalling event during CD95-induced apoptosis, and failure to stimulate PI-3-K may predict tumor cell resistance to CD95-triggered apoptosis.
|
9446703 |
1998 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Dysregulated signal transduction from receptor tyrosine kinases to phosphatidylinositol 3-kinase (PI3K), AKT (protein kinase B), and its effector FKBP-rapamycin-associated protein (FRAP) occurs via autocrine stimulation or inactivation of the tumor suppressor PTEN in many cancers.
|
10749120 |
2000 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Overexpression of wild-type or kinase-dead p110gamma in human colon cancer cells with mutations of the tumour suppressors APC and p53, or the oncogenes beta-catenin and Ki-ras, suppressed tumorigenesis.
|
10972292 |
2000 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This discrepancy prompted us to test the status of PTEN tumor suppressor gene, as it has been shown to be a negative regulator of PI 3'K activity.
|
11071655 |
2000 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PTEN is a tumor suppressor that antagonizes phosphatidylinositol-3 kinase (PI3K) by dephosphorylating the D3 position of phosphatidylinositol (3,4,5)-triphosphate (PtdIns-3,4,5-P3).
|
11359902 |
2001 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
To examine the possibility that PI3K is upregulated by amplification in this tumour set we assessed the phosphorylation status of Akt, a downstream target of PI3K.
|
11401316 |
2001 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Phosphatidylinositol 3'-kinase (PI3K)/Akt is a common signaling pathway for oncogenes and tumor suppressor genes and is involved in VEGF regulation.
|
11585776 |
2001 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Phosphatidylinositol 3-kinase (PI3K) and the PTEN tumor suppressor gene product phosphorylate and dephosphorylate the same 3' site in the inositol ring of membrane phosphatidylinositols.
|
11706404 |
2001 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, the PI3K-AKT pathway appears to be critical for the proliferation of ET cells both in vitro and in vivo and tumor cell growth in vivo may be better represented by the study of anchorage-independent multi-cellular spheroids.
|
11803474 |
2002 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Expression of PTEN tumor suppressor gene has been known to dephosphorylate the phosphatidylinositol 3' kinase (PI3K) products on the 3 prime inositol ring, resulting in reduced Akt activation.
|
12149650 |
2002 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Reportedly, cell survival signaling through Akt was constitutively active in U251MG cells and this effect may be dependent on autocrine signaling and dysfunction of PTEN, a tumor suppressor gene limiting phosphatidylinositol 3-kinase (PI3K) activity.
|
12430714 |
2002 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, PI3K blockade via Ad-PTEN may be a promising approach for the treatment of early- and late-stage melanoma, even in tumors that do not harbor PTEN mutations.
|
12435856 |
2002 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The purpose of this study was to examine whether activation of PPARgamma can increase the expression of the tumor suppressor PTEN and inhibit PI3K activity.
|
12535639 |
2003 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These data suggest that the oncogene R-Ras promotes tumor growth of cervical epithelial cells and increases their migration potential over collagen through a pathway that involves PI 3-K.
|
12548599 |
2003 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Although restoration of PTEN function to tumors is difficult to implement clinically, much of the effects of PTEN loss are attributable to overactive PI3K/Akt pathway signaling, and this overactivity can be modulated by pharmacologic approaches.
|
14555504 |
2003 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we show that 1) TGF-beta1 induced a rapid increase of the PI3K activity that was accompanied by increased expression (5-fold) of the uPA mRNA; 2) pharmacological inhibition of PI3K or AS-PI3K ODN transfection inhibited TGF-beta1-stimulated Akt phosphorylation; 3) both PI3K pharmacological inhibitors and forced expression of AS-PI3K ODN reduced TGF-beta1-stimulated uPA mRNA and protein expression by approximately 70% compared with controls; 4) concentrations of PI3K inhibitors, sufficient to inhibit uPA up-regulation, inhibited TGF-beta1-dependent HRA cell invasion; 5) the AS-PI3K ODN cells had a decreased ability to invade the extracellular matrix layer as compared with controls; and 6) when the AS-PI3K ODN cells were injected intraperitoneally into nude mice, the mice developed smaller intraperitoneal tumors and showed longer survival.
|
14597629 |
2004 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The balance of activities between the proto-oncogene phosphoinositide 3-kinase (PI3K) and the tumour suppressor gene PTEN has been shown to affect cellular growth and proliferation, as well as tumorigenesis.
|
14603260 |
2003 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The tumor suppressor phosphatase and tensin homologue deleted from chromosome 10 (PTEN) gene is a negative regulator of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt/PKB) signaling pathway.
|
14605666 |
2003 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Analysis of genes encoding proteins that may activate the pathway upstream of Pi3k revealed variable fractions of tumors with EGFR amplification (31%), PDGFRA amplification (8%), and IRS2 amplification (2%).
|
14655756 |
2003 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Therefore, PKN3 might represent a preferred target for therapeutic intervention in cancers that lack tumor suppressor PTEN function or depend on chronic activation of PI3K.
|
15282551 |
2004 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The relative roles of RAS-extracellular signal-regulated kinase 1/2 and phosphatidylinositol 3'-kinase (PI3K)-AKT pathways in the regulation of D-type cyclin expression in these tumors were then assessed.
|
15342383 |
2004 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Together, our data unveil a regulatory mechanism by which the Ras/MAPK and PI3K pathways converge on the tumor suppressor tuberin to inhibit its function.
|
15342917 |
2004 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Using primary human thyroid epithelial cells to model tumour initiation by Ras, we have shown previously that activation of both the MAP kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) effector pathways are necessary, but even when activated together are not sufficient, for Ras-induced proliferation.
|
15361839 |
2004 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Given the high percentage of CaP patients with mutations in the PTEN tumor suppressor gene, we sought to determine the involvement of the phosphatidylinositol 3'-kinase (PI3K) cascade in the development of CaP drug resistance.
|
15548710 |
2004 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Antiproliferative, proapoptotic, and anticancer effects were documented, showing that inhibition of the PI3K pathway in these cell lines suppresses tumour cell growth in vitro and reduces growth in nude mice.
|
15591514 |
2005 |