|
Colorectal Carcinoma
|
0.700 |
GeneticVariation
|
disease |
UNIPROT |
|
|
|
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.700 |
SusceptibilityMutation
|
disease |
CLINVAR |
|
|
|
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.700 |
Biomarker
|
disease |
HPO |
|
|
|
|
Insulin Resistance
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
|
Decreased waist to hip ratio
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
|
Adenomatous Polyposis Coli
|
0.050 |
AlteredExpression
|
disease |
BEFREE |
In colon carcinoma cells, loss of APC leads to the accumulation of betacatenin in the nucleus, where it binds to and activates the Tcf-4 transcription factor (reviewed in [1] [2]).
|
10021369 |
1999 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Our results, taken together with the recent findings that c-myc transcription is negatively regulated by APC and our earlier data on transcriptional activation of eIF-4E expression by c-Myc suggest that eIF-4E is a downstream target of the APC/beta-catenin/Tcf-4 pathway, and is strongly involved in colon tumorigenesis.
|
10229202 |
1999 |
|
Colorectal Carcinoma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Frequent frameshift mutations of the TCF-4 gene in colorectal cancers with microsatellite instability.
|
10485457 |
1999 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
These results suggest that TCF-4 frameshift mutations are selected for and play a role in colorectal MSI-H tumorigenesis.
|
10485457 |
1999 |
|
Adenomatous Polyposis Coli
|
0.050 |
Biomarker
|
disease |
BEFREE |
A proportion of APC wild-type colon carcinomas and melanomas also contains constitutive nuclear Tcf-4/beta-catenin complexes as a result of dominant mutations in the N terminus of beta-catenin that render it insensitive to downregulation by APC, GSK3 beta, and Axin/Conductin.
|
10549354 |
2000 |
|
melanoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
A proportion of APC wild-type colon carcinomas and melanomas also contains constitutive nuclear Tcf-4/beta-catenin complexes as a result of dominant mutations in the N terminus of beta-catenin that render it insensitive to downregulation by APC, GSK3 beta, and Axin/Conductin.
|
10549354 |
2000 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Two of 22 (9%) MSI-H primary gastric cancers and none of 23 MSI-H endometrial primary tumors and cell lines were found to have a 1 bp deletion in the TCF-4 repeat.
|
10597289 |
1999 |
|
Endometrial Carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Variable mutation frequencies in coding repeats of TCF-4 and other target genes in colon, gastric and endometrial carcinoma showing microsatellite instability.
|
10597289 |
1999 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Thus, loss of the TCF-4 capacity to interact with COOH-terminal binding protein could be an important event during colorectal carcinogenesis by modifying Wnt signaling.
|
10919662 |
2000 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
However, there was also a higher level of nuclear beta-catenin in tumour compared to normal tissue, but nuclear Tcf-4 protein was constitutively expressed in tumour and normal tissue and showed no differences.
|
11396184 |
2001 |
|
Colorectal Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
The Tcf-4 transcription factor gene was reported to be one of the targets of microsatellite instability (MSI) in colorectal cancers in with MSI.
|
11528255 |
2001 |
|
Gastrointestinal Neoplasms
|
0.010 |
GeneticVariation
|
group |
BEFREE |
We carried out a sequencing analysis of the Tcf-4 gene in 41 Japanese patients with gastrointestinal tumors with MSI as well as in cancer cell lines.
|
11528255 |
2001 |
|
Malignant neoplasm of gastrointestinal tract
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Genetic alterations in the human Tcf-4 gene in Japanese patients with sporadic gastrointestinal cancers with microsatellite instability.
|
11528255 |
2001 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Subsequently, accumulated beta-catenin protein translocates to nuclei with T-cell factor-4, and upregulates transcriptional activity of the target genes involved in carcinogenesis.
|
11696170 |
2001 |
|
Colorectal Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Using HT-29 CRC cell lines having inducible wild-type APC (wt-APC) or transfected dominant-negative TCF-4, we show that wt-APC down-regulates survivin expression via APC/beta-catenin/TCF-4 signaling.
|
11751382 |
2001 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Finally, genetic aberrations of several components of the beta-catenin pathways, eg, Frizzled (Frz), AXIN, and TCF-4, may potentially contribute to colorectal carcinogenesis.
|
11839557 |
2002 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Frameshift mutations in a (A)9 tract of the TCF-4 gene were detected in 44% (22 out of 50) of MSI-H tumors, but not in any of the 20 MSI-L tumors or 40 MSS tumors.
|
11876551 |
2001 |
|
Colorectal Neoplasms
|
0.490 |
GeneticVariation
|
group |
LHGDN |
Functional MDR1 polymorphisms (G2677T and C3435T) and TCF4 mutations in colorectal tumors with high microsatellite instability.
|
11980438 |
2002 |
|
Colorectal Carcinoma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
T-cell factor-4 frameshift mutations occur frequently in human microsatellite instability-high colorectal carcinomas but do not contribute to carcinogenesis.
|
12036905 |
2002 |
|
Colorectal Neoplasms
|
0.490 |
AlteredExpression
|
group |
BEFREE |
TCF-4 and beta-catenin form a transcription complex, which is important for both maintenance of normal epithelium and development of colorectal tumors.
|
12036905 |
2002 |