|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In this study, we used mouse medulloblastoma models to explore the relationship of tumor pathophysiology and dysregulated expression of the NOTCH pathway transcription factor ATOH1, which is present in aggressive medulloblastoma subtypes driven by aberrant Sonic Hedgehog/Patched (SHH/PTCH) signaling.
|
28490517 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Heterozygosity of Atoh1 reduced tumor occurrence and prolonged survival.
|
29168692 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
MCPyV sT, when coexpressed with ATOH1, is thus sufficient to initiate development of epidermis-derived MCC-like tumors in mice.<i></i>.
|
28512245 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This notion was confirmed in multivariate analysis suggesting that ATOH1 expression is a potential independent predictor for tumor relapse in MCC patients (P = 0.028).
|
27624714 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Genome-wide expression analyses and binding experiments indicate that Brg1 specifically coordinates with key transcription factors including Gli1, Atoh1 and REST to regulate the expression of both oncogenes and tumor suppressors that are required for medulloblastoma identity and proliferation.
|
27065321 |
2016 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In cultured primary human colon carcinomas, Hath1 was up-regulated in 7 out of 10 tumors upon DBZ treatment.
|
23409082 |
2013 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We conclude that the nuclear expression of Atoh1 was inversely correlated with the differentiation and primary tumor stage of lung cancers.
|
23030416 |
2013 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
However, its inhibition had no tumour suppressor effect in the context of acute β-catenin activation probably due to the downregulation of Atoh1.
|
21205878 |
2011 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
ATOH1 antagonizes tumor formation and growth by regulating proliferation and apoptosis, likely via activation of the Jun N-terminal kinase signaling pathway.
|
19243219 |
2009 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Given that Atoh1 is also a putative target of Hh signaling, we conclude that the Hic1 and Ptch1 tumor suppressors cooperate to silence Atoh1 expression during a critical phase in GCP differentiation in which malignant transformation may lead to medulloblastoma.
|
18347096 |
2008 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In addition, we found ATOH1 expression in 9 (16%) out of 56 analyzed adenocarcinomas and these tumors showed neuroendocrine features as shown by dopa decarboxylase mRNA expression and immunostaining for neuroendocrine markers.
|
17549667 |
2007 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In addition, a significant correlation of high CXCR4 mRNA levels and presence of the neurotrophin receptor p75NTR or expression of ATOH1 and GLI1 suggests that CXCR4 is a reliable marker for tumors derived from the cerebellar external granular layer.
|
15880586 |
2005 |