|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
A two-fold increase in E2F4 gene expression was observed in the breast tumors compared with in their respective controls (P=0.022); of these tumors, ~72% were under-methylated.
|
29805583 |
2018 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Finally, an E2F4 activation signature was strongly associated with resistance to aromatase inhibitors in the ACOSOG Z1031B neoadjuvant trial and with an increased risk of relapse in adjuvant-treated ER<sup>+</sup> tumors in METABRIC.<b>Conclusions:</b> In tumors resistant to prolonged neoadjuvant letrozole, we identified a gene expression signature of E2F4 target activation.
|
29581135 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
E2F4 activity stratification was highly predictive of patient outcome, and our results remained robust even when controlling for many factors including patient age, tumor size, grade, estrogen receptor (ER) status, lymph node (LN) status, whether the patient received adjuvant therapy, and the patient's other prognostic indices such as Adjuvant! and the Nottingham Prognostic Index scores.
|
25440089 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
E2F4's role in colorectal, gastric and hepatic carcinogenesis is tumor-promoting.
|
23745020 |
2013 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
E2F4 protein expression is also decreased in 24 of 26 sBL tumor samples from patients compared with control tissues.
|
22475873 |
2012 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Tumors considered platinum resistant were associated with lower E2F4 and E2F7 expression (P = 0.012 and 0.009, respectively) compared with platinum-sensitive tumors.
|
17200349 |
2007 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Furthermore, the identification of E2F4 and p130/p107 complexes as basal repressors of BRCA1 expression may facilitate the development of strategies based on disruption of these interactions to rescue BRCA1 expression in human tumors.
|
17106239 |
2006 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
However, there was a correlation between increased nuclear expression of E2F-4 and tumours with higher histological grade (p = 0.04) and positive lymph node disease (p = 0.02), suggesting that it may have an oncogenic rather than a tumour suppressor role.
|
15609312 |
2005 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
There was a correlation between increased nuclear expression of E2F-4 and indicators of poor prognosis including larger tumour size (p = 0.000), grade 3 lesions (p = 0.033), lymph node stage (p = 0.037), and poorer Nottingham prognostic index group (p = 0.003).
|
15221934 |
2004 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Although E2F-4 acts mainly as a repressor in the early part of the cell cycle, E2F-1 has the ability to function as both an oncogene and a tumor suppressor gene.
|
12373148 |
2002 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Some genes (e.g., E2F4) were overexpressed in tumor epithelial cells and some (e.g., Daxx) were increased in tumor stroma.
|
11358857 |
2001 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Microsatellite alterations were studied involving microsatellite instability (MSI) and loss of heterozygosity (LOH) at tumour suppressor loci, representative of the mutator pathway and the suppressor pathway, respectively, as well as mutations of target genes (TGF-beta RII, BAX, hMSH3, and E2F-4).
|
11439366 |
2001 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
A five-repeats expansion of the coding E2F4(CAG)n run was found in the only malignant melanoma of soft parts examined, which also showed instability at two dinucleotide loci, and in a superficial spreading melanoma, which was stable at the mononucleotide and dinucleotide repeats but was the only tumour that manifested instability at the SCA1(CAG)n repeat.
|
11468517 |
2001 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These experiments indicated that repression of E2F-responsive promoters following HPV E6/E7 repression was mediated by activation of the Rb tumor suppressor pathway and the assembly of repressing E2F4-Rb DNA binding complexes.
|
10982822 |
2000 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The E2F4 and hMSH3 genes were mutated in all tumor types.
|
10717241 |
2000 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We also evaluated the simple nucleotide repeats in the transforming growth factor type II receptor, insulin-like growth factor type II receptor, BAX, and E2F-4 genes, which are frequently mutated in tumors with microsatellite instability.
|
10213220 |
1999 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
This tumor also carried a deletion mutation in the serine (AGC) repeat of the E2F4 gene.
|
9824204 |
1998 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Additional investigations revealed that E2F4 mutations are common (11 of 17 cases, 65%, mostly deletions) in a subset of human colorectal cancers with extensive MI+ phenotype, with respect to the proportion of loci affected and that most of these E2F4-mutated tumors (9 of 11, 82%) were accompanied by frameshift mutations in a polyadenine stretch within the seventh exon of the hMSH3 gene, a known mismatch repair gene that is responsible for repair of mismatch loops of two to four nucleotides.
|
9485005 |
1998 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These data suggest that E2F-4 is a target of defective DNA repair in these tumors.
|
9192806 |
1997 |