|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
BJ-1108, a 6-Amino-2,4,5-Trimethylpyridin-3-ol Analog, Inhibits Serotonin-Induced Angiogenesis and Tumor Growth through PI3K/NOX Pathway.
|
26824764 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Since PTEN has both PI3-lipid phosphatase-dependent and -independent tumor suppressor activities, we investigated the contribution of PI3K signaling to BRAFV600E-induced melanomagenesis using mouse models, cultured melanoma cells, and PI3K pathway-targeted inhibitors.
|
24200692 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Second, enhanced expression of PTEN (a known tumor suppressor) via negative regulation within a PI3K-AKT pathway, inhibits IDO expression.
|
27082119 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our data suggest that specifically targeting GPCR signaling to PI3Kβ could provide a therapeutic approach for tumors that depend on p110β for growth and metastasis.
|
23211529 |
2012 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
To address the role of PI3K/Akt/mTOR, we used a novel approach to study mesothelioma ex vivo as tumor fragment spheroids.
|
18511708 |
2008 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The tumor suppressor phosphatase and tensin homolog (PTEN) negatively regulates phosphatidylinositol 3-kinase (PI3K)-AKT signaling and is often inactivated by mutations (including deletions) in a variety of cancer types, including T-cell acute lymphoblastic leukemia.
|
27582570 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
ErbB3, a member of the ErbB family of receptor tyrosine kinases, is a potent activator of phosphatidyl inositol-3 kinase (PI3K) and mammalian target of rapamycin (mTOR) signaling, driving tumor cell survival and therapeutic resistance in breast cancers.
|
26148232 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
MicroRNA-195 targets VEGFR2 and has a tumor suppressive role in ACHN cells via PI3K/Akt and Raf/MEK/ERK signaling pathways.
|
27572273 |
2016 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Deregulation of the PI3K signaling pathway is observed in many human cancers and occurs most frequently through loss of PTEN phosphatase tumor suppressor function or through somatic activating mutations in the Class IA PI3K, PIK3CA.
|
18755892 |
2008 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this review we examine the role and interaction of three major cell signalling pathways, PI3K, MAPK and cAMP, in regulating tumour cell functions and discuss the prospects for exploiting this knowledge to better treat difficult to treat cancers, using glioblastoma, the most common and deadly malignant brain cancer, as the example disease.
|
30710631 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We hypothesized that the inhibition of the PI3K pathway in MTC may lead to a reduction in cell growth and NE tumor marker production.
|
17188151 |
2006 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The association between SR levels and response to PI3K inhibition might open new avenues for the treatment of tumors overexpressing this receptor.
|
22692904 |
2012 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
p55PIK, regulatory subunit of class IA phosphatidylinositol 3-kinase (PI3K), plays a crucial role in cell cycle progression by interaction with tumor repressor retinoblastoma (Rb) protein.
|
23509792 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here we review phosphatidylinositol-3-kinase (PI3K)/Akt/mTOR signaling as one of the primary mechanisms for sustaining tumor outgrowth and metastasis, recent advances in the development of mTOR inhibitors, and current studies addressing mTOR activation/inhibition in colorectal cancer (CRC).
|
24393708 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Inhibition of PI3K/Akt/mTOR signaling in PI3KR2-overexpressing colon cancer stem cells reduces tumor growth due to apoptosis.
|
28881576 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Activation of class I phosphatidylinositol 3' kinase (PI3K) regulates tumor proliferation, survival, etc.
|
24601221 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Finally, in nude mice bearing established HCT15 and H1975 subcutaneous tumor xenografts, the combined treatment with pimasertib and BEZ235 (a dual PI3K/mTOR inhibitor) or with sorafenib caused significant tumor growth delays and increase in mice survival as compared to single agent treatment.
|
23629727 |
2013 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In cellular assays, XL765 inhibits the formation of PIP(3) in the membrane, and inhibits phosphorylation of AKT, p70S6K, and S6 phosphorylation in multiple tumor cell lines with different genetic alterations affecting the PI3K pathway.
|
24634413 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our study highlights the genetic basis and the importance of PI3K/AKT/mTOR and Wnt pathway dysregulation in MBCs and provides a rationale for the metaplastic phenotype and the reported responses to PI3K/AKT/mTOR inhibitors in these tumors.<i></i>.
|
28153863 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PI3K pathway inhibitors are currently being evaluated in patients with tumors in which the PI3K pathway is deregulated.
|
21903247 |
2011 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Mutating sst2-Y71 disabled sst2 to interact with p85 and somatostatin to inhibit PI3K, consequently abrogating sst2's ability to suppress cell survival and tumor growth.
|
16917505 |
2006 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
To date, none of the inositol polyphosphate 5-phosphatases that inhibit PI3K/AKT signaling have been reported as tumor suppressors in breast cancer.
|
26267533 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
It has been suggested that PTEN, a negative regulator of PI3K/AKT signaling, is involved in tumor sensitivity to trastuzumab.
|
23650412 |
2013 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Predicting that survival signals would be delivered by phosphoinositide-3-kinase (PI3K), a major survival determinant in mature B cells, we indeed found that combining constitutive c-MYC expression and PI3K activity in germinal center B cells of the mouse led to BL-like tumors, which fully phenocopy human BL with regard to histology, surface and other markers, and gene expression profile.
|
22897848 |
2012 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway plays a critical role in the malignant transformation of human tumors and their subsequent growth, proliferation, and metastasis.
|
25677064 |
2015 |