Sarcoma
|
0.310 |
GenomicAlterations
|
group |
CGI |
|
|
|
Other emphysema
|
0.200 |
Biomarker
|
phenotype |
MGD |
|
|
|
Neuroblastoma
|
0.050 |
Biomarker
|
disease |
BEFREE |
Finally, this study identified a breakpoint at 1p32 that was localized between the genes JUN and MYCL for one neuroblastoma thus establishing the order of these genes as centromere, JUN, MYCL, telomere.
|
2776489 |
1989 |
Central neuroblastoma
|
0.050 |
Biomarker
|
disease |
BEFREE |
Finally, this study identified a breakpoint at 1p32 that was localized between the genes JUN and MYCL for one neuroblastoma thus establishing the order of these genes as centromere, JUN, MYCL, telomere.
|
2776489 |
1989 |
Childhood Neuroblastoma
|
0.050 |
Biomarker
|
disease |
BEFREE |
Finally, this study identified a breakpoint at 1p32 that was localized between the genes JUN and MYCL for one neuroblastoma thus establishing the order of these genes as centromere, JUN, MYCL, telomere.
|
2776489 |
1989 |
Chronic Lymphocytic Leukemia
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Expression of proto-oncogene c-jun during differentiation of B-chronic lymphocytic leukemia.
|
2113601 |
1990 |
Lyme Disease
|
0.020 |
Biomarker
|
disease |
BEFREE |
Ninety-four serum specimens from patients having Lyme borreliosis were tested for reactivity with P39.
|
2380361 |
1990 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
It recently has been reported that certain nuclear receptors can antagonize the tumor promoter 12-O-tetradeconylphorbol-13-acetate (TPA) by direct interaction with the transcription factor AP-1, and that the AP-1 constituents cJun and cFos can inhibit receptor activity.
|
1791843 |
1991 |
Malignant transformation
|
0.050 |
AlteredExpression
|
phenotype |
BEFREE |
The proto-oncogene C-jun acts as a transcriptional activator or repressor for numerous cellular genes, and the overexpression of these genes may cause malignant transformation.
|
1404666 |
1992 |
Myeloid Leukemia
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
The present work demonstrates that treatment of human myeloid leukemia cells (HL-60, U-937, and KG-1) with CDDP is associated with increased expression of the c-jun gene and that this effect is related to activation by a transcriptional mechanism.
|
1737349 |
1992 |
Renal Cell Carcinoma
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
We investigated the expression of jun genes in renal cell cancer (RCC) and their regulation by cytokines and transforming growth factor beta 1 (TGF-b1).
|
1404666 |
1992 |
Malignant neoplasm of breast
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Estradiol increases and anti-estrogens antagonize the growth factor-induced activator protein-1 activity in MCF7 breast cancer cells without affecting c-fos and c-jun synthesis.
|
8314777 |
1993 |
Breast Carcinoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Estradiol increases and anti-estrogens antagonize the growth factor-induced activator protein-1 activity in MCF7 breast cancer cells without affecting c-fos and c-jun synthesis.
|
8314777 |
1993 |
Liver carcinoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The possibility that the hbx protein may activate certain protooncogenes was investigated and we found that hbx can activate the protooncogene c-jun promoter. c-Jun was found to be expressed at a very low level in normal liver tissue but at high levels in HCCs of HBV-infected patients.
|
8390762 |
1993 |
Osteosarcoma
|
0.350 |
Biomarker
|
disease |
BEFREE |
The binding of transcription factor AP-1 and vitamin D receptor (VDR) to the composite AP-1 plus vitamin-D-responsive promoter region (AP-1 + VDRE) of the human osteocalcin gene was characterized in osteocalcin-producing (MG-63) and non-producing (U2-Os, SaOs-2) human osteosarcoma cell lines.
|
8076631 |
1994 |
Reperfusion Injury
|
0.300 |
Biomarker
|
disease |
CTD_human |
Differential expression of c-jun, c-fos and hsp 70 mRNAs after folic acid and ischemia-reperfusion injury: effect of antioxidant treatment.
|
7922267 |
1994 |
Status Epilepticus
|
0.300 |
Biomarker
|
disease |
CTD_human |
Distinctive rat brain immediate early gene responses to seizures induced by lithium plus pilocarpine.
|
7984056 |
1994 |
Petit mal status
|
0.300 |
Biomarker
|
disease |
CTD_human |
Distinctive rat brain immediate early gene responses to seizures induced by lithium plus pilocarpine.
|
7984056 |
1994 |
Grand Mal Status Epilepticus
|
0.300 |
Biomarker
|
disease |
CTD_human |
Distinctive rat brain immediate early gene responses to seizures induced by lithium plus pilocarpine.
|
7984056 |
1994 |
Complex Partial Status Epilepticus
|
0.300 |
Biomarker
|
disease |
CTD_human |
Distinctive rat brain immediate early gene responses to seizures induced by lithium plus pilocarpine.
|
7984056 |
1994 |
Status Epilepticus, Subclinical
|
0.300 |
Biomarker
|
disease |
CTD_human |
Distinctive rat brain immediate early gene responses to seizures induced by lithium plus pilocarpine.
|
7984056 |
1994 |
Non-Convulsive Status Epilepticus
|
0.300 |
Biomarker
|
disease |
CTD_human |
Distinctive rat brain immediate early gene responses to seizures induced by lithium plus pilocarpine.
|
7984056 |
1994 |
Simple Partial Status Epilepticus
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Distinctive rat brain immediate early gene responses to seizures induced by lithium plus pilocarpine.
|
7984056 |
1994 |
Osteosarcoma of bone
|
0.030 |
Biomarker
|
disease |
BEFREE |
The binding of transcription factor AP-1 and vitamin D receptor (VDR) to the composite AP-1 plus vitamin-D-responsive promoter region (AP-1 + VDRE) of the human osteocalcin gene was characterized in osteocalcin-producing (MG-63) and non-producing (U2-Os, SaOs-2) human osteosarcoma cell lines.
|
8076631 |
1994 |
Childhood Osteosarcoma
|
0.030 |
Biomarker
|
disease |
BEFREE |
The binding of transcription factor AP-1 and vitamin D receptor (VDR) to the composite AP-1 plus vitamin-D-responsive promoter region (AP-1 + VDRE) of the human osteocalcin gene was characterized in osteocalcin-producing (MG-63) and non-producing (U2-Os, SaOs-2) human osteosarcoma cell lines.
|
8076631 |
1994 |