|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In HNSCC patients, coexpression of GLI1 and SMO in primary tumors correlated with metastasis.
|
31408253 |
2020 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This results in the translocation of SMO to cilia, downstream gene expression, resistance of CSCs to chemotherapeutic agents, and enhances tumor formation in mice.
|
31253779 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The smoothened (SMO) receptor, an essential signal transducer in the Hedgehog pathway, was targeted with antagonists to suppress the tumor.
|
29175550 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Hh transcriptional repressor GLI3 and signaling activator SMO were the top 2 genes for discriminating among samples with active Hh signaling in human breast cancer subtypes and Hh-inhibitor resistant tumors.
|
29034935 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In the MCV-negative tumors, MET, NOTCH1, FGFR3, and SMO were overexpressed and JAK3 and NPM1 were under-expressed compared to the MCV-positive tumors.
|
28359267 |
2017 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Meningiomas with an SMO mutation presented with significantly larger tumor volume (70.6 ± 36.3 cm<sup>3</sup>) compared with AKT1-mutated (18.2 ± 26.8 cm<sup>3</sup>) and wild-type (22.7 ± 23.9 cm<sup>3</sup>) meningiomas, respectively.
|
27885953 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Overexpression of upstream (PTCH1 and SMO) and downstream (GLI1, CCND1 and BCL2) genes in the SHH pathway leads to the constitutive activation of this pathway in KOT and AB and may suggest a mechanism for the development of these types of tumors.
|
24930892 |
2014 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
SMO expression in colorectal cancer may interact with tumor CIMP status to affect patient prognosis, although confirmation by future studies is needed.
|
25023548 |
2014 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Analysis of SIM2s-MCF10DCIS.com tumors showed that SIM2s promoted a more differentiated tumor phenotype including the expression of a broad range of luminal markers (CSN2 (β-casein), CDH1 (E-cadherin), and KER18 (keratin-18)) and suppressed genes associated with stem cell maintenance and a basal phenotype (SMO (smoothened), p63, SLUG (snail-2), KER14 (keratin-14) and VIM (vimentin)).
|
22777354 |
2013 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
A 3-bp insertion (69_70insCTG) in SMO, predicting an additional leucine residue in the signal peptide segment of SMO protein was also identified in LO68 cells and a MMe tumour.
|
23826113 |
2013 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
SMOH mutations were identified in four of the 42 BCCs (10%) while two tumours demonstrated mutations in SUFUH, including one missense mutation and one silent mutation.
|
15656799 |
2005 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Since PAOh1/SMO is an analogue-inducible enzyme that produces H2O2 as a metabolic product, it may play a significant role in determining the sensitivity of various human tumors to specific polyamine analogues.
|
12827295 |
2003 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
It now appears that constitutive activation of Hedgehog signalling, by inactivating mutations in PTCH1 or activating mutations in the coreceptor SMOH, is required and possibly sufficient for basal cell carcinoma development and also contributes to the formation of a variety of other tumour types, including medulloblastoma and rhabdomyosarcoma.
|
11130178 |
2000 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
No mutations were found in either SHH or SMO in any tumor.
|
10564585 |
2000 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Mutational analysis identified four BCCs with somatic missense mutations in SMOH affecting codon 535 (TGG==>TTG: Trp==>Leu) in three tumors and codon 199 (CGG==>TGG: Arg==>Trp) in one tumor.
|
9581815 |
1998 |