Malignant neoplasm of lung
|
0.340 |
AlteredExpression
|
disease |
BEFREE |
HES-1 protein is detected at abundant levels in most non-NE human lung cancer cell lines which lack hASH1 but is virtually absent in hASH1-expressing lung cancer cells.
|
9144241 |
1997 |
Carcinoma of lung
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
HES-1 protein is detected at abundant levels in most non-NE human lung cancer cell lines which lack hASH1 but is virtually absent in hASH1-expressing lung cancer cells.
|
9144241 |
1997 |
Primary malignant neoplasm of lung
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
HES-1 protein is detected at abundant levels in most non-NE human lung cancer cell lines which lack hASH1 but is virtually absent in hASH1-expressing lung cancer cells.
|
9144241 |
1997 |
Optic Atrophy 1
|
0.010 |
Biomarker
|
disease |
BEFREE |
PCR amplification of this part of exon 2 in four of the pedigrees affected by autosomal dominant optic atrophy mapping to chromosome 3q, followed by haplotype analysis, showed recombination between HRY and OPA1 in one pedigree.
|
9745030 |
1998 |
leukemia
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
Transforming polypeptides also demonstrated moderate to strong activation of the Su(H)/CBF1-sensitive HES-1 promoter, while polypeptides with weak or absent activity on this promoter failed to cause leukemia.
|
11003647 |
2000 |
Childhood Leukemia
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
Transforming polypeptides also demonstrated moderate to strong activation of the Su(H)/CBF1-sensitive HES-1 promoter, while polypeptides with weak or absent activity on this promoter failed to cause leukemia.
|
11003647 |
2000 |
Neuroblastoma
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
Our data show that functional sympathetic neuronal differentiation of neuroblastoma cells is associated with transient activation of HES-1 and down-regulation of HASH-1 expression.
|
11054669 |
2000 |
Central neuroblastoma
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
Our data show that functional sympathetic neuronal differentiation of neuroblastoma cells is associated with transient activation of HES-1 and down-regulation of HASH-1 expression.
|
11054669 |
2000 |
Childhood Neuroblastoma
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
Our data show that functional sympathetic neuronal differentiation of neuroblastoma cells is associated with transient activation of HES-1 and down-regulation of HASH-1 expression.
|
11054669 |
2000 |
Differentiating Neuroblastoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In gel mobility shift assays, using extracts from neuroblastoma cells, HES-1 bound to an oligonucleotide corresponding to a sequence in the HASH-1 promoter including the so-called N-box, suggesting that the transiently increased HES-1 activity in differentiating neuroblastoma cells is involved in down-regulation of HASH-1.
|
11054669 |
2000 |
Carcinoid Tumor
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
Generally, expression of the human homologue of Mash1 (HASH1) is detected in small cell carcinoma and carcinoids, while Hes1 seems to be expressed mainly in non-small cell carcinoma.
|
11193209 |
2001 |
Liver carcinoma
|
0.040 |
Biomarker
|
disease |
BEFREE |
Previous studies have established that there are transcriptional control elements in the first intron; in particular a silencer responsive to Hes-1 and YY1 has been identified in the human hepatoma line, HepG2.
|
11511924 |
2001 |
Liver neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
Previous studies have established that there are transcriptional control elements in the first intron; in particular a silencer responsive to Hes-1 and YY1 has been identified in the human hepatoma line, HepG2.
|
11511924 |
2001 |
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.070 |
AlteredExpression
|
disease |
BEFREE |
Parallel observations were made in humans, in that all T cell acute lymphoblastic leukemias examined showed expression of Notch3 and of the Notch target gene HES-1, as well as of pTalpha a and b transcripts, whereas the expression of all these genes was dramatically reduced or absent in remission.
|
11891328 |
2002 |
Medulloblastoma
|
0.050 |
AlteredExpression
|
disease |
BEFREE |
Notch pathway overactivity was demonstrated in the TE671 MB cell line expressing high levels of MSH1 through HES1-Luciferase transfections.
|
15064731 |
2004 |
Childhood Medulloblastoma
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
Notch pathway overactivity was demonstrated in the TE671 MB cell line expressing high levels of MSH1 through HES1-Luciferase transfections.
|
15064731 |
2004 |
Adult Medulloblastoma
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
Notch pathway overactivity was demonstrated in the TE671 MB cell line expressing high levels of MSH1 through HES1-Luciferase transfections.
|
15064731 |
2004 |
Anaplasia
|
0.010 |
Biomarker
|
disease |
BEFREE |
In hypoxic neuroblastoma cells, proneuronal lineage specifying transcription factors, and their dimerization partner E2-2, were downregulated, whereas their inhibitors Id2 and HES-1 were induced, providing a molecular mechanism for the hypoxia-provoked dedifferentiation of neuroblastoma cells.
|
15093745 |
2004 |
Medulloblastoma
|
0.050 |
Biomarker
|
disease |
BEFREE |
In addition, expression of the Notch pathway target gene Hes1 in medulloblastomas was associated with significantly shorter patient survival (P = 0.01).
|
15520184 |
2004 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Tumor development was associated with activation of Notch pathway, as evidenced by upregulation of Hes-1.
|
15531924 |
2004 |
Meningioma
|
0.320 |
AlteredExpression
|
disease |
BEFREE |
We have shown that the transcript and protein levels of HES1, the Notch2 and Notch1 receptors and the Jagged1 ligand are induced in meningiomas of all grades, whereas induction of TLE2 and TLE3 occurs specifically in higher-grade meningiomas.
|
15958550 |
2005 |
Astrocytoma
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
ASCL1 upregulation in progressive astrocytoma is accompanied by inhibition of Notch signaling as seen by uninduced levels of HES1, a transcriptional target of Notch1, increased levels of HES6, a dominant-negative inhibitor of HES1-mediated repression of ASCL1, and increased levels of Notch ligand Delta1, which is capable of inhibiting Notch signaling by forming intracellular Notch ligand autonomous complexes.
|
16103883 |
2005 |
Childhood Astrocytoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
ASCL1 upregulation in progressive astrocytoma is accompanied by inhibition of Notch signaling as seen by uninduced levels of HES1, a transcriptional target of Notch1, increased levels of HES6, a dominant-negative inhibitor of HES1-mediated repression of ASCL1, and increased levels of Notch ligand Delta1, which is capable of inhibiting Notch signaling by forming intracellular Notch ligand autonomous complexes.
|
16103883 |
2005 |
Neuroblastoma
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
Here, we show that TGFalpha, a known activator of Ras signaling, can drive cell proliferation and at the same time induce the expression of the Notch target Hes-1 in the neuroblastoma cell line SK-N-BE(2)c. The up-regulation of Hes-1 occurred both at the transcriptional and protein levels and by use of EGFR and MEK inhibitors we could show that the Hes-1 response was dependent on activation of the MAP kinase ERK.
|
16120441 |
2005 |
Central neuroblastoma
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
Here, we show that TGFalpha, a known activator of Ras signaling, can drive cell proliferation and at the same time induce the expression of the Notch target Hes-1 in the neuroblastoma cell line SK-N-BE(2)c. The up-regulation of Hes-1 occurred both at the transcriptional and protein levels and by use of EGFR and MEK inhibitors we could show that the Hes-1 response was dependent on activation of the MAP kinase ERK.
|
16120441 |
2005 |