|
Malignant neoplasm of breast
|
0.400 |
CausalMutation
|
disease |
CGI |
|
|
|
|
Malignant Head and Neck Neoplasm
|
0.400 |
CausalMutation
|
disease |
CGI |
|
|
|
|
Breast Carcinoma
|
0.400 |
CausalMutation
|
disease |
CGI |
|
|
|
|
Head and Neck Carcinoma
|
0.400 |
CausalMutation
|
disease |
CGI |
|
|
|
|
Head and Neck Neoplasms
|
0.300 |
CausalMutation
|
group |
CGI |
|
|
|
|
Neoplasm of uncertain or unknown behavior of breast
|
0.300 |
CausalMutation
|
disease |
CGI |
|
|
|
|
Breast adenocarcinoma
|
0.300 |
CausalMutation
|
disease |
CGI |
|
|
|
|
Rous Sarcoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
However, a drastically different binding specificity was observed with use of extracts of Rous sarcoma virus v-src-transformed cells, in which the majority of PI3K activity bound to the SH2 domain of p56lck in a phosphotyrosine-dependent manner.
|
7504174 |
1993 |
|
Leukemia, Mast-Cell
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In a human mast cell leukemia cell line HMC-1, c-kitR was found to be constitutively phosphorylated on tyrosine, activated, and associated with PI3K without the addition of SCF.
|
7691885 |
1993 |
|
HER2 gene amplification
|
0.100 |
Biomarker
|
disease |
BEFREE |
These data indicate that PI3K may be an especially important mediator of HRG-induced proliferation in mammary epithelial cells and is involved in the autonomous proliferation of growth factor-independent breast carcinoma cells with c-erbB-2 gene amplification.
|
8732665 |
1996 |
|
Invasive Ductal Breast Carcinoma
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
HRG was found to potently induce the recruitment of the M(r) 85,000 regulatory subunit of PI3K by phosphotyrosine proteins in both nonneoplastic H16N-2 mammary epithelial cells (which express normal c-erbB-2 levels) and in the 21MT-2 and 21MT-1 cell lines, which were all isolated from a single patient with intraductal and invasive ductal carcinoma of the breast and express c-erbB-3 but not c-erbB-4 in culture.
|
8732665 |
1996 |
|
Ataxia
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
The aim of this minireview is to report, discuss, and interpret some recent observations on this topic: (I) The relationship with the Ataxia-Telangectasia gene and with the signaling enzyme phosphatidylinositol 3-kinase (PI3K).
|
9367792 |
1997 |
|
Cerebellar Ataxia
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
The aim of this minireview is to report, discuss, and interpret some recent observations on this topic: (I) The relationship with the Ataxia-Telangectasia gene and with the signaling enzyme phosphatidylinositol 3-kinase (PI3K).
|
9367792 |
1997 |
|
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
PI-3-K stimulation seems to be critical for CD95 receptor signalling since, first, inhibition of PI-3-K prevents CD95-mediated apoptosis and, second, CD95 receptor ligation fails to induce tyrosine phosphorylation or activation of PI-3-K in CD95-resistant glioma cells.
|
9446703 |
1998 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, PI-3-K activation may be an early signalling event during CD95-induced apoptosis, and failure to stimulate PI-3-K may predict tumor cell resistance to CD95-triggered apoptosis.
|
9446703 |
1998 |
|
Mood Disorders
|
0.020 |
GeneticVariation
|
group |
BEFREE |
For this reason, messenger RNA expression of three G protein alpha-subunits and of phosphatidylinositol-3 kinase (PI-3 K) regulatory subunit p85 was examined in granulocytes from patients with bipolar or unipolar affective disorder and compared to healthy controls.
|
9857977 |
1998 |
|
Ewing Sarcoma/Peripheral Primitive Neuroectodermal Tumor
|
0.010 |
Biomarker
|
disease |
BEFREE |
Akt, a serine/threonine kinase activated downstream of PI 3-K, was investigated to determine whether its constitutive activation would render ESFT cells more resistant to doxorubicin.
|
10582694 |
1999 |
|
Malignant tumor of colon
|
0.100 |
Biomarker
|
disease |
BEFREE |
The aim of this study was to identify PI3Ks involved in the control of macroautophagic sequestration in human colon cancer HT-29 cells.
|
10625637 |
2000 |
|
Colon Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The aim of this study was to identify PI3Ks involved in the control of macroautophagic sequestration in human colon cancer HT-29 cells.
|
10625637 |
2000 |
|
Hyperactive behavior
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
We postulate that negative regulation of the PI 3-K/Akt pathway by PTEN may modulate the effects of the hyperactive epidermal growth factor receptor/mitogen-activated protein kinase pathway, contributing to the low proliferation and dysfunctional differentiation of laryngeal papillomas.
|
10728713 |
2000 |
|
Papilloma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
We have now found that phosphoinositol 3-kinase (PI 3-K) activity is significantly increased in papilloma tissue.
|
10728713 |
2000 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Finally, we observed strong activation of PI3K with beta(4) wild type and with those beta(4) deletion mutants that were able to stimulate invasion upon the expression in NIH3T3/ErbB-2 cells.
|
10744756 |
2000 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Dysregulated signal transduction from receptor tyrosine kinases to phosphatidylinositol 3-kinase (PI3K), AKT (protein kinase B), and its effector FKBP-rapamycin-associated protein (FRAP) occurs via autocrine stimulation or inactivation of the tumor suppressor PTEN in many cancers.
|
10749120 |
2000 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Because we have shown in an earlier study that there is also a defective regulation of p85 alpha PI3K gene expression in response to insulin, these data support the hypothesis that alterations in the regulation of gene expression could be involved in the pathogenesis of Type II diabetes.
|
10768097 |
2000 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We have examined the relative roles of the two major phospholipid products of PI3K activity, phosphatidylinositol 3,4-biphosphate [PtdIns(3,4)P2] and phosphatidylinositol 3,4,5-triphosphate [PtdIns(3,4,5)P3], in the regulation of PKB activity in glioblastoma cells containing high levels of both of these lipids due to defective PTEN expression.
|
10958682 |
2000 |