Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
A covalent CDK7-specific inhibitor (THZ1) impairs AR-mediated MED1 recruitment to chromatin, and can suppress enzalutamide resistance <i>in vitro</i> and induce tumor regression in a castration-resistant prostate cancer xenograft model, suggesting a novel therapeutic approach for advanced prostate cancer.<i>See related article by Rasool et al., p. 1538</i>.
|
31676563 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
At the <i>in vivo</i> level, overexpression of miR-1291 inhibited the growth of xenograft tumors and significantly inhibited the expression of MED1 protein.
|
30867757 |
2019 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
MED1 mutation in its ER-interacting LxxLL motifs was sufficient to delay tumor onset and to impair tumor growth, metastasis, and cancer stem-like cell formation in this model.
|
29187405 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Using ZR-75-1 or BT-474 to generate in vivo tumor xenografts in BALB/c athymic mouse models, we showed that a combination of both drugs resulted in a stronger inhibition of tumor growth (P<0.05) and a greater decrease in the levels of activated MED1 (p-MED1) expressed in tumor issues compared with the use of either drug as a single agent.
|
28045951 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
89.5% of the HER2-amplified tumors were GRB7 and STARD3 co-amplified, whereas 68.4% of the HER2-amplified tumors had additional MED1 amplifications.
|
26910888 |
2016 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, gene expression analysis uncovered networks highlighting S100A8, MMP1, and MED1 as promising candidate genes involved in high-grade and LVI-positive tumors.
|
25391423 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In summary, these results suggest that miR-205 is an epigenetically regulated tumor suppressor that targets MED1 and may provide a potential biomarker in prostate cancer management.
|
22869146 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Importantly, knockdown of MED1 further potentiated tumor growth inhibition by fulvestrant.
|
23936234 |
2013 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Notably, ectopic MED1 overexpression in prostate cancer xenografts significantly promoted tumor growth in nude mice.
|
23538858 |
2013 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Med1-MB cells maintained constitutively active Hh target gene transcription, and consistently formed tumors within one month after injection into mouse cerebella.
|
24026530 |
2013 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Tissue microarray analysis of human breast cancers revealed that MED1 expression positively correlates most strongly with HER2 status of the tumors.
|
22964581 |
2012 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Med1-depleted cells displayed an increase in metastasis in a xenograft tumor model and in an in vivo metastasis assay.
|
22342682 |
2012 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Analysis using a microarray membrane with 113 cancer-related genes, western blot and specific tests, demonstrated that RB18A/MED1 knockdown significantly inhibits tissue inhibitor of metalloproteinase-3 expression, and increases uPAR expression, two genes well known to be involved in melanoma cell invasion, through modifications of the tumor microenvironment.
|
19243021 |
2009 |
Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
In colorectal cancer patients, when MED1 methylation was present, both tumor and matched mucosa were affected equally (mean frequency of methylation 24%) and there was no correlation between methylation and tumor stage.
|
19127118 |
2009 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
MBD4/MED1 is a newly identified mismatch repair gene, which is mutated in colon, endometrial, and pancreatic high-frequency microsatellite instability (MSI-H) tumors.
|
12430186 |
2002 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Mutagenesis caused by these deamination events is a frequent mechanism of genetic instability in cancer; thus, based on the biochemical activity of its gene product, MED1 is a candidate tumor suppressor gene.
|
11267993 |
2001 |