|
Solid Neoplasm
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
We report results for pictilisib (GDC-0941, a class I pan-PI3K inhibitor) plus erlotinib (an EGFR tyrosine kinase inhibitor) in patients with advanced solid tumors.
|
28798270 |
2017 |
|
Solid Neoplasm
|
0.400 |
AlteredExpression
|
phenotype |
BEFREE |
GDC-0941 is a highly specific PI3K inhibitor with promising anti-tumor activity in human solid tumors.
|
28147244 |
2017 |
|
Solid Neoplasm
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
<b>Purpose:</b> To evaluate the safety, MTD, pharmacokinetics, pharmacodynamics, and preliminary antitumor activity of TAK-117 (MLN1117/INK1117), an investigational PI3Kα-selective inhibitor, in patients with advanced solid tumors.<b>Experimental Design:</b> Seventy-one patients received oral TAK-117 once daily [100-300 mg (<i>n</i> = 24)] or 3 days per week [Monday-Wednesday-Friday (MWF), 200-1,200 mg (<i>n</i> = 27); Monday-Tuesday-Wednesday (MTuW), 200-900 mg (<i>n</i> = 20)], in 21-day cycles.
|
28490463 |
2017 |
|
Solid Neoplasm
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
The study did not meet its primary objective of demonstrating the anti-tumor activity of everolimus in PIK3CA amplification/mutation and/or PTEN loss patients with advanced solid tumors refractory to standard therapy.
|
28330462 |
2017 |
|
Solid Neoplasm
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
A Phase I study of intravenous PI3K inhibitor copanlisib in Japanese patients with advanced or refractory solid tumors.
|
27915408 |
2017 |
|
Solid Neoplasm
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Phase Ib Study of Safety and Pharmacokinetics of the PI3K Inhibitor SAR245408 with the HER3-Neutralizing Human Antibody SAR256212 in Patients with Solid Tumors.
|
28031425 |
2017 |
|
Solid Neoplasm
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
The primary endpoints were progression-free survival by local investigator assessment per Response Evaluation Criteria In Solid Tumors (version 1.1) in the total population, in patients with known (activated or non-activated) PI3K pathway status, and in PI3K pathway-activated patients.
|
28576675 |
2017 |
|
Solid Neoplasm
|
0.400 |
AlteredExpression
|
phenotype |
BEFREE |
Several clinical studies are being conducted to test the tolerability and clinical activity of dual MEK and PI3K pathway blockade in solid tumors.
|
26272063 |
2015 |
|
Solid Neoplasm
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
BYL719, which selectively inhibits the alpha isoform of the phosphatidylinositol 3-kinase (PI3K) catalytic subunit (p110a), is currently in clinical trials for the treatment of solid tumors, especially luminal breast cancers with PIK3CA mutations and/or HER2 amplification.
|
25544637 |
2015 |
|
Solid Neoplasm
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
First-in-human phase I study of pictilisib (GDC-0941), a potent pan-class I phosphatidylinositol-3-kinase (PI3K) inhibitor, in patients with advanced solid tumors.
|
25370471 |
2015 |
|
Solid Neoplasm
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
DS-7423, a novel, small-molecule dual inhibitor of phosphatidylinositol-3-kinase (PI3K) and mammalian target of rapamycin (mTOR), is currently in phase I clinical trials for solid tumors.
|
24504419 |
2014 |
|
Solid Neoplasm
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
Res treatment reduced the tumor size(s) and expression of anti-apoptotic proteins (e.g.PI3K, AKT, NFκB) in solid tumor.
|
24467951 |
2014 |
|
Solid Neoplasm
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
Escalating doses of PF-04691502 were administered to 23 patients with advanced solid tumors in sequential cohorts across the following dose levels: 2 mg, 4 mg, 8 mg, and 11 mg. 14 additional patients were enrolled in an expansion cohort at the MTD to ensure at least five matched pre- and post-treatment biopsies for biomarkers of PI3K activity.
|
24395457 |
2014 |
|
Solid Neoplasm
|
0.400 |
AlteredExpression
|
phenotype |
BEFREE |
Thus, the interaction between cancer cells and the stroma modulated the ability of PI3K inhibitors to induce the activation of apoptosis in solid tumors.
|
24648465 |
2014 |
|
Solid Neoplasm
|
0.400 |
AlteredExpression
|
phenotype |
BEFREE |
Mutational activation of PIK3CA is associated with poor prognosis in patients with solid tumors, and may predict favorable response to PI3K/AKT/mTOR pathway inhibitors.
|
23266353 |
2013 |
|
Solid Neoplasm
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
PTEN also modulates angiogenesis mediated by vascular endothelial growth factor (VEGF) via down-regulating PI3K/Akt pathway in many solid tumors.
|
21360018 |
2012 |
|
Solid Neoplasm
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Ultimately, an improved understanding of the clinical impact of PIK3CA mutations is critical for the development of optimally personalized therapeutics against breast cancer and other solid tumors.
|
22640628 |
2012 |
|
Solid Neoplasm
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
In conclusion, PIK3CA mutations were detected in 11.5% of patients with diverse solid tumors.
|
21216929 |
2011 |
|
Solid Neoplasm
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Because PI3Kalpha harbors recurrent somatic mutations resulting in gains of function in human cancers, it has emerged as an important drug target for many types of solid tumors.
|
19962457 |
2010 |
|
Solid Neoplasm
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
PIK3CA mutations in human solid tumors: role in sensitivity to various therapeutic approaches.
|
19305151 |
2009 |
|
Solid Neoplasm
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Recent studies have reported high frequencies of somatic mutations in the phosphoinositide-3-kinase catalytic-alpha (PIK3CA) gene in various human solid tumors.
|
16778113 |
2006 |
|
Solid Neoplasm
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
The catalytic subunit p110alpha of PI3K shows hot spot mutations in nearly 30% of several types of solid tumors.
|
15876869 |
2005 |
|
Solid Neoplasm
|
0.400 |
CausalMutation
|
phenotype |
CGI |
|
|
|