|
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Univariate analyses demonstrated that SCCRO overexpression correlated with nodal metastases (P = 0.05) and advanced stage (P = 0.02), whereas PIK3CA overexpression was associated with vascular invasion (P = 0.04).
|
12796399 |
2003 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Interestingly, the three metastases with mutations in PIK3CA all exhibited a strong expression of phosphorylated Akt.
|
16567976 |
2006 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Analysis at exons 1, 7, 9 and 20 of the PIK3CA gene revealed somatic mutations in 21% (8 of 39) of FAP invasive carcinomas, 21% (7 of 34) of HNPCC invasive carcinomas, 15% (8 of 52) of sporadic invasive carcinomas, and 14% (7 of 50) of sporadic colorectal metastases in the liver.
|
17546593 |
2007 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Heterogeneity between primary tumors and distant metastases was present in two patients (10%) for KRAS and one patient for PIK3CA (5%), but not for BRAF.
|
20103678 |
2010 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
PIK3CA mutations in primary breast cancer are detected in matched regional LNs (91.7%) and distant metastases (100%).
|
21617917 |
2011 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Overall, there was a net gain in mutation in metastatic disease, to 53%; nonetheless, there were instances where metastases were wild type in patients with PIK3CA mutant primary tumors.
|
20940279 |
2011 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
There is a high level of discordance in PTEN level, PIK3CA mutations, and receptor status between primary tumors and metastases that may influence patient selection and response to PI3K-targeted therapies.
|
21490305 |
2011 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Targeted therapy including PI3K pathway inhibitors might be a potential treatment for rare cases of adnexal carcinomas with metastases.
|
21423156 |
2011 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
PI3K expression and PIK3CA mutations are related to colorectal cancer metastases.
|
22851869 |
2012 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Our data support a functional cooperation between KRAS and PIK3CA in colorectal tumorigenesis and link somatic profiles to the sites of metastases.
|
23741067 |
2013 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
PIK3CA exon 9 mutations in primary tumors and loss of PTEN nuclear expression in metastases correlated with KRAS mutations.
|
22936063 |
2013 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In one case, a PIK3CA exon 9 mutation in the primary tumor could not be detected in the matched distant metastases (κ = 0.9).
|
23934607 |
2013 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Novel PI3K/mTOR inhibitors may oppose tumor metastasis independent of their growth inhibitory effects, providing a rationale for clinical investigation of PI3K/mTOR inhibitors in settings to prevent micrometastasis.
|
23430223 |
2013 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Tumors in which BCSCs have defects in PI3K/Akt signaling are significantly more likely to manifest nodal metastases.
|
23884447 |
2013 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Mutations of KRAS and PIK3CA as independent predictors of distant metastases in colorectal cancer.
|
24861917 |
2014 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Activation of the ERBB PI3K/Akt pathway was positively correlated with a higher stage (p=0.001), higher grade (p=0.001), histological type II disease (p=0.0003) and metastases (p=0.02).
|
24337234 |
2014 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Molecular profiling of patient-matched brain and extracranial melanoma metastases implicates the PI3K pathway as a therapeutic target.
|
24803579 |
2014 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Levels of concordance between primary tumors and metastases were 65.7%, 87.7%, 100% and 95.2% for c-MET, KRAS, BRAF and PIK3CA, respectively.
|
24863535 |
2014 |
|
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Expression levels of PI3K, Akt and survivin proteins were significantly correlated with TNM stage, differentiation grade, lymph node metastasis and metastases to other organs (P<0.05).
|
24726064 |
2014 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Neuroendocrine differentiation was significantly less concordant than KRAS/NRAS/BRAF/PIK3CA/TP53 mutational status in primary tumor/lymph node metastases pairs (65% versus 88%-99%; P < 0.0001) and primary tumor/distant metastases pairs (64% versus 83%-100%; P = 0.027 and P < 0.0001, respectively).
|
25337237 |
2014 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Single cell mutational analysis of PIK3CA in circulating tumor cells and metastases in breast cancer reveals heterogeneity, discordance, and mutation persistence in cultured disseminated tumor cells from bone marrow.
|
24947048 |
2014 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
KRAS, BRAF and PIK3CA mutations are highly concordant between primary tumors and corresponding metastases in CRC, but PTEN loss is not.
|
25639985 |
2015 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
PIK3CA mutations were significantly associated with less distant metastases (mutant-type: 8/105, wild-type: 98/666, p = 0.048).
|
26358014 |
2015 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The primary rectal cancer and the matched metastases (hepatic, pulmonary and lymph nodal) demonstrated no KRAS, NRAS, BRAF and PIK3CA mutations, a microsatellite stable phenotype, and no tumor protein p53 alterations or recurrent copy number alterations on chromosome 8.
|
26231173 |
2015 |
|
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Together, these results demonstrate that HGF/c-met can activate PI3K/Akt and downstream NF-κB signaling to promote HPA expression and subsequent tumor metastasis.
|
25727320 |
2015 |