|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
UNBS5162 induces growth inhibition and apoptosis via inhibiting PI3K/AKT/mTOR pathway in triple negative breast cancer MDA-MB-231 cells.
|
30344670 |
2018 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
We also review the aberrant activated signals found in different subgroups of TNBC, including androgen receptor (AR) and PI3K/AKT/mTOR, Notch, Wnt/β-catenin, Hedge-hog, and TGF-β signaling pathways, which play essential roles in multiple development stages of TNBC.
|
29069872 |
2017 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Consequently, targeted therapies based on the interaction of PI3K inhibition with BRCA1 mutations or HR deficiency in TNBC may be a promising strategy for the treatment of patients with TNBC.
|
31804921 |
2019 |
|
Triple Negative Breast Neoplasms
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The mutational profile of TNBC during treatment as inferred from patterns of mutant allele frequencies in matched pre-and post-NAC samples showed that RD harbored alterations of cell cycle progression, PI3K/Akt/mTOR, and EGFR tyrosine kinase inhibitor-resistance pathways.
|
31717320 |
2019 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Poly(ADP‑ribose) polymerase (PARP) inhibitors, phosphatidylinositol 3‑kinase (PI3K) inhibitors and carboplatin (CBP) have demonstrated sufficient efficacy and safety for their use as individual drugs for the treatment of TNBC; however, their effects on TNBC when used as a combination have not been investigated.
|
30272286 |
2018 |
|
Triple Negative Breast Neoplasms
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In this study, we analyzed PI3K pathway activation in 67 patient-derived xenografts (PDX) of breast cancer and investigated the anti-tumor activity of the mTOR inhibitor everolimus in 15 TNBC PDX with different expression and mutational status of PI3K pathway markers.
|
27374081 |
2016 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
In vivo in a mouse model of BRCA1-linked triple-negative breast cancer (K14-Cre BRCA1(f/f)p53(f/f)), the PI3K inhibitor BKM120 led to a precipitous drop in DNA synthesis within 8 h of drug treatment, whereas DNA synthesis in normal tissues was less affected.
|
27402769 |
2016 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Mass Spectrometry-Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers.
|
29472518 |
2018 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Triple-negative breast cancer (TNBC) classified by transcriptional profiling as the mesenchymal subtype frequently harbors aberrations in the phosphoinositide 3-kinase (PI3K) pathway, raising the possibility of targeting this pathway to enhance chemotherapy response.
|
27893038 |
2017 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
<b>Conclusion:</b> We demonstrated that DFO could upregulate expression of TfR1 and DMT1 , which enhanced iron uptake via activating IL-6/PI3K/AKT signaling pathway in aggressive TNBCs.
|
31213851 |
2019 |
|
Triple Negative Breast Neoplasms
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
As the phosphatidylinositol 3' kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) cascade is activated in TNBCs, mTOR is a potential molecular target for anticancer therapy.
|
22703543 |
2012 |
|
Triple Negative Breast Neoplasms
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Approximately 30% of triple-negative breast cancers (TNBC) harbor molecular alterations in PI3K/mTOR signaling, but therapeutic inhibition of this pathway has not been effective.
|
26676751 |
2016 |
|
Triple Negative Breast Neoplasms
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Expression analysis of the panel of TNBC cell lines indicates that the expression levels of IGF2BP3 can be used as a potential predictor for sensitivity to the PI3K/IGF1R inhibitor combination.
|
27196766 |
2016 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the present study, we aimed to investigate, the effect of phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway dual inhibitor, NVP-BEZ235 and Caffeic acid phenyl ester (CAPE) on TNBC cell line (MDA-MB-231), stimulated with TGF-β1 for 14days in vitro.
|
28528184 |
2017 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings suggest that the catalytic activities of MEK and PI3K might predict the response of TNBC to trametinib and wortmannin.
|
28576487 |
2017 |
|
Triple Negative Breast Neoplasms
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
CF33 was effective <i>in vitro</i> with potent cytotoxicity and efficient intracellular replication observed in TNBC lines with phosphatidylinositol 3-kinase (PI3K)/Akt pathway mutations that resulted in endogenous phospho-Akt (p-Akt) activity (BT549, Hs578T, and MDA-MB-468).
|
29988465 |
2018 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
We show in TNBC cells that PI3K inhibition leads to DNA damage, downregulation of BRCA1/2, gain in poly-ADP-ribosylation, and subsequent sensitization to PARP inhibition.
|
22915752 |
2012 |
|
Triple Negative Breast Neoplasms
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Mice bearing intracranial TNBC tumors (SUM149, MDA-MB-231Br, MDA-MB-468, or MDA-MB-436) were treated with MEK, PI3K, or platelet derived growth factor receptor (PDGFR; pazopanib) inhibitors alone or in combination.
|
28486691 |
2017 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our study suggests that the combination of WES and RNA-seq on human TNBC will lead to the identification of actionable therapeutic targets for precision medicine-guided TNBC treatment.<b>Significance:</b> Using combined WES and RNA-seq analyses, we identified sporadic oncogenic events in TNBC mouse models that share the capacity to activate the MAPK and/or PI3K pathways.
|
29203461 |
2018 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Further study of underlying mechanisms demonstrated that DANCR bound with RXRA and increased its serine 49/78 phosphorylation via GSK3β, resulting in activating PIK3CA transcription, and subsequently enhanced PI3K/AKT signaling and TNBC tumorigenesis.
|
30518934 |
2018 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, our findings show that triple negative breast cancers with apocrine differentiation constitute a distinct subset, characterized by a high frequency of PI3K pathway alterations similar to luminal subtypes of breast cancer.
|
26939876 |
2016 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Metalloprotease-processed CD95L (cl-CD95L) is a soluble cytokine that implements a PI3K/Ca(2+) signaling pathway in triple-negative breast cancer (TNBC) cells.
|
27367565 |
2016 |
|
Triple Negative Breast Neoplasms
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our data shows that PIK3CA mutations and PI3K/AKT pathway activation are common events in TNBC.
|
26540293 |
2015 |
|
Triple Negative Breast Neoplasms
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The AKT inhibitor capivasertib has shown preclinical activity in TNBC models, and drug sensitivity has been associated with activation of PI3K or AKT and/or deletions of PTEN.
|
31841354 |
2020 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
PI3K/mTOR inhibitors had an additive growth inhibitory effect when combined with genetic or pharmacological AR targeting in AR + TNBC cells.
|
25103565 |
2014 |