Brain Neoplasms
|
0.300 |
Biomarker
|
group |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
nervous system disorder
|
0.300 |
Biomarker
|
group |
CTD_human |
A 3-dimensional human embryonic stem cell (hESC)-derived model to detect developmental neurotoxicity of nanoparticles.
|
23203475 |
2013 |
Malignant neoplasm of brain
|
0.300 |
Biomarker
|
disease |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Benign neoplasm of brain, unspecified
|
0.300 |
Biomarker
|
disease |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Brain Tumor, Primary
|
0.300 |
Biomarker
|
disease |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Recurrent Brain Neoplasm
|
0.300 |
Biomarker
|
disease |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Primary malignant neoplasm of brain
|
0.300 |
Biomarker
|
disease |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Neoplasms, Intracranial
|
0.300 |
Biomarker
|
group |
CTD_human |
Inhibition of notch signaling blocks growth of glioblastoma cell lines and tumor neurospheres.
|
21127729 |
2010 |
Mucoepidermoid Carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Analyses of potential downstream targets of the fusion revealed differential expression of the cAMP/CREB (FLT1 and NR4A2) and Notch (HES1 and HES5) target genes in fusion-positive and fusion-negative MECs.
|
16444749 |
2006 |
Mucoepidermoid Carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Analyses of the Notch target genes HES5 and MASH1 in MEC tumors with and without the WAMTP1-MAML2 fusion revealed upregulation of HES5 and downregulation of MASH1 in fusion positive MECs compared to normal salivary gland tissue and MECs lacking the fusion.
|
14720503 |
2004 |
Hyperhomocysteinemia
|
0.020 |
Biomarker
|
disease |
BEFREE |
These results suggest that HHcy-enhanced brain damage is associated with increased autophagy and neuronal apoptosis in Apo E<sup>-/-</sup> mice, in which downregulation of hes1 and hes5 is involved.
|
29171783 |
2017 |
Non-Small Cell Lung Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Taken together, out data have delineated that HES5 might contribute to the proliferation of NSCLC by STAT3 signaling.
|
27878283 |
2017 |
Diabetic Retinopathy
|
0.010 |
Biomarker
|
disease |
BEFREE |
Main conclusions allow certifying that crucial pathways related to Wnt-MAPK signaling pathways or neuroinflammation are epigenetically controlled in the fibrotic disorders involved in retinal detachment, but results also reinforced the contribution of neurovascularization (ETS1, HES5, PRDM16) in diabetic retinopathy.
|
28924151 |
2017 |
Endometriosis
|
0.010 |
Biomarker
|
disease |
BEFREE |
Notch signaling receptors NOTCH1 and NOTCH4, ligands JAGGED2 and DLL4, as well as direct target genes HES5 and HEY1 were decreased in the eutopic endometrium of women and baboons with endometriosis.
|
25546156 |
2015 |
Multiple Myeloma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Multiple myeloma cell growth relies on intrinsic aggressiveness, due to a high karyotypic instability, or on the support from bone marrow (BM) niche.We and other groups have provided evidences that Notch signaling is related to tumor cell growth, pharmacological resistance, localization/recirculation in the BM and bone disease.This study indicates that high gene expression levels of Notch signaling members (JAG1, NOTCH2, HES5 and HES6) correlate with malignant progression or high-risk disease, and Notch signaling may participate in myeloma progression by increasing the BM levels of interleukin-6 (IL-6), a major player in myeloma cell growth and survival.
|
27463014 |
2016 |
Carcinogenesis
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Either Hes1 or Hes5 overactivation is likely to affect cell differentiation, thereby resulting in carcinogenesis.
|
21495212 |
2010 |
Arteriopathic disease
|
0.010 |
Biomarker
|
group |
BEFREE |
Treatment with GTPs upregulated the levels of Jagged1, Notch1, Hes5, p-STAT3, and MnSOD2, and downregulated xanthine oxidase (XO) expression in rats with preglomerular arteriopathy.
|
30416668 |
2018 |
Tumor Cell Invasion
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
HES5 promotes cell proliferation and invasion through activation of STAT3 and predicts poor survival in hepatocellular carcinoma.
|
26342546 |
2015 |
Hepatocarcinogenesis
|
0.010 |
Biomarker
|
disease |
BEFREE |
Therefore, we have characterized HES5 and investigated its role during hepatocarcinogenesis.
|
26342546 |
2015 |
Neuroblastoma
|
0.020 |
PosttranslationalModification
|
disease |
BEFREE |
The HES2 and HES5 gene promoters were found to be heavily methylated in most neuroblastoma lines, and HES gene expression could be induced through treatment with decitabine.
|
21744479 |
2012 |
Central neuroblastoma
|
0.020 |
PosttranslationalModification
|
disease |
BEFREE |
The HES2 and HES5 gene promoters were found to be heavily methylated in most neuroblastoma lines, and HES gene expression could be induced through treatment with decitabine.
|
21744479 |
2012 |
Childhood Neuroblastoma
|
0.020 |
PosttranslationalModification
|
disease |
BEFREE |
The HES2 and HES5 gene promoters were found to be heavily methylated in most neuroblastoma lines, and HES gene expression could be induced through treatment with decitabine.
|
21744479 |
2012 |
Precursor B-cell lymphoblastic leukemia
|
0.010 |
PosttranslationalModification
|
disease |
BEFREE |
5-aza-2'-deoxycytidine treatment restored Hes5 expression and decreased promoter hypermethylation in most leukemia cell lines and primary B-ALL samples.
|
23637910 |
2013 |
Neoplasms
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Multiple myeloma cell growth relies on intrinsic aggressiveness, due to a high karyotypic instability, or on the support from bone marrow (BM) niche.We and other groups have provided evidences that Notch signaling is related to tumor cell growth, pharmacological resistance, localization/recirculation in the BM and bone disease.This study indicates that high gene expression levels of Notch signaling members (JAG1, NOTCH2, HES5 and HES6) correlate with malignant progression or high-risk disease, and Notch signaling may participate in myeloma progression by increasing the BM levels of interleukin-6 (IL-6), a major player in myeloma cell growth and survival.
|
27463014 |
2016 |
Neoplasms
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Analyses of the Notch target genes HES5 and MASH1 in MEC tumors with and without the WAMTP1-MAML2 fusion revealed upregulation of HES5 and downregulation of MASH1 in fusion positive MECs compared to normal salivary gland tissue and MECs lacking the fusion.
|
14720503 |
2004 |