|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The aims of this work were as follows: first, to use magnetic resonance spectroscopy (MRS) to identify and develop a robust pharmacodynamic (PD) biomarker for target inhibition and potentially tumor response following PI3K inhibition; second, to evaluate mechanisms underlying the MRS-detected changes.
|
20551061 |
2010 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Treatment with therapeutic doses of both BKM120 and antibody to PD-1 resulted in consistent inhibition of tumor growth compared with either agent alone.<b>Conclusions:</b> PI3K inhibition slows tumor growth, enhances antitumor immunity, and heightens susceptibility to immune checkpoint inhibitors.
|
28003307 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
However, it is not clear whether advanced UC tumors are PIK3CA-dependent and whether PI3K pathway inhibition is a good therapeutic option in such cases.
|
27465249 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Phosphatase and tensin homolog (PTEN) is a tumor suppressor that inhibits PI3K/Akt signaling.
|
20664988 |
2010 |
|
Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
Our study indicates that epigenetic silencing of tumor suppressor genes involved in the Ras/PI3K/AKT pathway plays an important role in OSCC radioresistance and this provides a rationale for exploring novel treatment strategies.
|
19509163 |
2009 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The results showed that downregulation of the tumor suppressor gene PTEN expression and the inhibition of PTEN/PI3K/AKT cell signaling pathway may be involved in the occurrence and development of RCC in children.
|
30655739 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The tumor suppressor PTEN, a major inhibitor of the phosphatidylinositol-3-OH kinase (PI3K)/Akt pathway, is frequently deleted in GBM tumors.
|
20736378 |
2010 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Phosphatase and tensin (PTEN), is a tumor suppressor gene and the loss of PTEN expression may activate the phosphoinositide-3-kinase (PI3K)/AKT signaling pathway which play a key role in tumors formation and progression.
|
29180042 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, combination therapy was more effective than monotherapy in: (i) inhibition of proliferation and angiogenesis, (ii) induction of apoptosis, and (iii) inhibition of the MAPK and PI3K pathways in xenograft tumors.
|
26299806 |
2015 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Overexpression of miRNA‑155 resulted in decreased brain‑derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) protein expression, increased caspase‑3 activity, tumor protein p53 (p53) and apoptosis regulator BAX (Bax) protein expression, and inhibited phosphoinositide 3‑kinase (PI3K), phosphorylated (p‑)protein kinase B (Akt) and p‑mechanistic target of rapamycin (mTOR) protein expression in epilepsy cells.
|
29901097 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We demonstrate that beta1 integrin interaction with polymerized collagen inhibits normal fibroblast proliferation by suppression of the phosphoinositide 3-kinase (PI3K)-Akt-S6K1 signal pathway due to maintenance of high phosphatase activity of the tumor suppressor phosphatase and tensin homologue (PTEN).
|
18541712 |
2008 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The tumor vessel stabilization effect of the PI3K inhibitor HS-173 also decreased the number of metastatic lung nodules in vivo metastasis model.
|
28688971 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Despite these challenges, we are optimistic that isoform-specific PI3K inhibitors, particularly in combination with other agents, may be valuable in treating appropriately selected patients with PI3K-dependent tumors.
|
30867161 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
FOXO transcription factors are negatively regulated by the PI3K-PKB/AKT signaling pathway and have been mainly considered to be tumor suppressors due to their inhibitory effect on cancer cell growth and survival.
|
29175105 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<i>PTEN</i> is a tumor suppressor gene that classically dampens the PI3K/AKT/mTOR growth-promoting signaling cascade.
|
31433956 |
2020 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Western-blot and cytokine detection results demonstrated that GLE suppressed growth and proliferation of tumors by the Jak-STAT signaling pathway, T cell receptor signaling pathway and PI3K-Akt signaling pathway, but also regulated the expression levels of serum immune cytokines and improved the anti-tumor immunostimulatory activity.
|
30139984 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Immunohistochemical analysis was performed on colorectal adenocarcinomas and adjacent normal mucosa for PI3K pathway components, including p85alpha, p110alpha, Akt1, Akt2, and the tumor suppressor PTEN, which inhibits PI3K.
|
16772787 |
2006 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
By RNA sequencing, we define tumor glycolysis as a specific PI3Kδ/γ-dependent pathway implicated in the metabolic reprogramming of cancer cells.
|
30352904 |
2019 |
|
Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
Mechanistic analysis revealed that the tumor growth‑inhibitory effect of ISL may depend on the action of ISL on the phosphorylation of PI3K and AKT.
|
30720124 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Utilizing a mouse model in which the loss of TET2 precedes the expression of oncogenic Kit, similar to the human disease, results in the development of a non-mast cell lineage neoplasm (AHNMD), which is responsive to PI3K inhibition.
|
29467326 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Genetic lesions in glioblastoma (GB) include constitutive activation of PI3K and EGFR pathways to drive cellular proliferation and tumor malignancy.
|
30506943 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The aim of this study was to test the hypothesis as to whether PI3K/AKT-pathway activation is a critical mechanism in ARID1A-mutated tumors and if consequently ARID1A-deficient tumors show increased sensitivity to treatment with PI3K- and AKT-inhibitors.
|
24979463 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Tumor cell killing correlates with regulation of proteins involved in the Wnt and PI3K pathways: beta-catenin, APC, GSK-3, JNK, and PTEN.
|
15851011 |
2005 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These data represent the rationale for AR-targeting treatment as a potentially new target therapy in breast cancer subset using androgen agonists in some AR-positive/ER-positive tumors, AR antagonists in triple-negative/AR-positive tumors and in combination with anti-HER2 agents or with other signaling pathways inhibitors (including PI3K/MYC/ERK) in HER2-positive/AR-positive tumors.
|
27528625 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The various genetic and epigenetic lesions resulting in pathway activation necessitate combined approaches using genetic, genomic, and protein biomarkers to accurately characterize "PI3K activated" tumors.
|
20803067 |
2010 |