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 |
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 |
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 |
Adenocarcinoma
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In humans, p110gamma protein expression is lost in primary colorectal adenocarcinomas from patients and in colon cancer cell lines.
|
10972292 |
2000 |
Malignant tumor of colon
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In humans, p110gamma protein expression is lost in primary colorectal adenocarcinomas from patients and in colon cancer cell lines.
|
10972292 |
2000 |
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 |
Colorectal Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Colorectal carcinomas in mice lacking the catalytic subunit of PI(3)Kgamma.
|
10972292 |
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 |
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 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This discrepancy prompted us to test the status of PTEN tumor suppressor gene, as it has been shown to be a negative regulator of PI 3'K activity.
|
11071655 |
2000 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Overexpression of wild-type or kinase-dead p110gamma in human colon cancer cells with mutations of the tumour suppressors APC and p53, or the oncogenes beta-catenin and Ki-ras, suppressed tumorigenesis.
|
10972292 |
2000 |
Rhabdomyosarcoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
This is the first time that a defect in the IGF/PI3K/Akt pathway has been revealed in RD cells which provides another clue to future therapeutic treatment of Rhabdomyosarcoma.
|
10973962 |
2000 |
Childhood Rhabdomyosarcoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
This is the first time that a defect in the IGF/PI3K/Akt pathway has been revealed in RD cells which provides another clue to future therapeutic treatment of Rhabdomyosarcoma.
|
10973962 |
2000 |
Adult 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 |
Adult Rhabdomyosarcoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
This is the first time that a defect in the IGF/PI3K/Akt pathway has been revealed in RD cells which provides another clue to future therapeutic treatment of Rhabdomyosarcoma.
|
10973962 |
2000 |
Childhood 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 |
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 |