|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The various expression levels within the tumor samples were independent of histological grade and tumor stage, due to different levels of activation of the PI3K/p-Akt pathway.
|
18587247 |
2008 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
ARID1A and PI3-Kinase (PI3K) pathway alterations are common in neoplasms originating from the uterine endometrium.
|
31391455 |
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 |
Biomarker
|
group |
BEFREE |
In this review, we highlight the known oncogenic and tumour suppressive effects of ubiquitin modifying enzymes in cancer relevant pathways with specific focus on PI3K, MAPK, TGFβ, WNT, and YAP pathways.
|
28923280 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PI3K activation occurred early in prostate intraepithelial neoplasia lesion formation in these animals, consistent with loss of PTEN function, and contributed to the etiology of tumors that developed in Pten(+/-) mice.
|
19395652 |
2009 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Cancer cells expressing constitutively active phosphatidylinositol-3 kinase (PI3K) are proliferative regardless of the absence of insulin, and they form dietary restriction (DR)-resistant tumors in vivo.
|
23986086 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, we also found that knockdown of hTERT was able to significantly suppress constitutive phosphorylation of Akt, PI3K, which might imply that reduction of hTERT inhibited tumor growth via the PI3K/Akt signaling pathway to some extent.
|
24920549 |
2014 |
|
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 |
Biomarker
|
group |
BEFREE |
The chemokine CXCL12 and its receptor CXCR4 promote glioma stem cell-mediated VEGF production and tumour angiogenesis via PI3K/AKT signalling.
|
21618540 |
2011 |
|
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 |
Biomarker
|
group |
BEFREE |
Knockdown of IQGAP1 or transfection of dominant-negative IQGAP1 impeded tumor cell proliferation and migration as well as PI3K/Akt signaling induced by MTA1.
|
29125886 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
It has been well documented that activation of the ErbB3-PI3K-Akt pathway is implicated in tumor survival and progression.
|
25451255 |
2014 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Additionally, we show that the selective inhibition of either the PI3K/AKT pathway prior to miR-28-5p stimulation prevents the expression of previously described tumor suppressor miRNAs that are family and cluster specific.
|
26160280 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Macropinocytosis of extracellular material by prostate cancer cells is a previously unappreciated tumor-microenvironment interaction that could be targeted therapeutically.<b>Significance:</b> As PTEN-deficient prostate cancer cells proliferate in low-nutrient environments by scavenging necrotic debris and extracellular protein via macropinocytosis, blocking macropinocytosis by inhibiting AMPK, RAC1, or PI3K may have therapeutic value, particularly in necrotic tumors and in combination with therapies that cause nutrient stress.<i>Cancer Discov; 8(7); 866-83.
|
29572236 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These results revealed a possible novel mechanism whereby ephrin-A1 is regulated in tumor microenvironment and promotes angiogenesis through a coordinated cross-talk with PI3K/Akt-dependent eNOS activation which may relate to normal vascular development and tumor neovascularization.
|
24040255 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These data suggest targeting SOX2 may provide therapeutic benefit in the subset of EGFR-mutant tumors with high constitutive levels of SOX2, and that until more direct means of inhibiting SOX2 are developed, PI3K/Akt inhibitors might be useful to inhibit SOX2 in EGFR TKI resistant tumors.
|
24746758 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Combined administration of U0126 (MEK inhibitor) and LY294002 (PI3K inhibitor) significantly enhanced ActD-induced apoptosis in vitro and suppressed xenograft tumor growth in vivo.
|
19205734 |
2009 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Importantly, the combination of PI3K and CDK 4/6 inhibitors overcomes intrinsic and adaptive resistance leading to tumor regressions in PIK3CA mutant xenografts.
|
25002028 |
2014 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
PIK3CA gene encoding a catalytic subunit of the phosphatidylinositol-3-kinase (PI3K) is mutated and/or amplified in various neoplasia, including lung cancer.
|
24533074 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Mutations activating the PI3K (phosphoinositide 3-kinase)/Akt signalling pathway and inactivating the TP53 tumour-suppressor gene are common mechanisms that cancer cells require to proliferate and escape pre-programmed cell death.
|
25109960 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In addition, fisetin inhibited melanoma cell proliferation and tumor growth by downregulating the PI3K pathway.
|
26517521 |
2016 |
|
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 |
Inactivation of the Pten tumor suppressor negatively regulates the PI3K-mTOR pathway.
|
24582960 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Consistently, p34(SEI-1) expression was found to be increased as the tumor invasiveness progressed in human breast tissues. p34(SEI-1) may promote cancer metastasis by activating the PI3K/AKT signaling pathway.
|
24789658 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We have for the first time revealed that MT1G appears to be functional tumor suppressor involved in thyroid carcinogenesis mainly through modulating the phosphatidylinositol-3-kinase (PI3K)/Akt pathway and partially through regulating the activity of Rb/E2F pathway in this study.
|
24098937 |
2013 |