|
Abnormal C-peptide level
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
|
Abnormal oral glucose tolerance
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
|
Abnormality of endocrine pancreas physiology
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
|
Abnormality of exocrine pancreas physiology
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
|
Acute kidney injury
|
0.100 |
Biomarker
|
disease |
HPO |
|
|
|
|
Acute lymphocytic leukemia
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
In this cohort of Taiwanese children, the relative frequencies of the 4 translocations of B-lineage ALL were 8% with ALL-type t(9;22)/BCR-ABL1, 4% with (1;19)/TCF-PBX1, 2% with t(4;11)/MLL-AF4, and 17.6% with t(12;21)/ETV6-RUNX1.
|
20930648 |
2010 |
|
Adenocarcinoma
|
0.040 |
AlteredExpression
|
group |
LHGDN |
Further evidence of hepatic transdifferentiation in hepatoid adenocarcinomas of the stomach: quantitative analysis of mRNA for albumin and hepatocyte nuclear factor-4alpha.
|
12701690 |
2003 |
|
Adenocarcinoma
|
0.040 |
AlteredExpression
|
group |
LHGDN |
The expression of hepatocyte nuclear factor-4alpha, a developmental regulator of visceral endoderm, correlates with the intestinal phenotype of gastric adenocarcinomas.
|
17393984 |
2006 |
|
Adenocarcinoma
|
0.040 |
Biomarker
|
group |
BEFREE |
Adenocarcinomas in the H-IIP group tended to be negative for thyroid transcription factor-1 (TTF-1) and positive for hepatocyte nuclear factor-4α (HNF-4α).
|
27757985 |
2017 |
|
Adenocarcinoma
|
0.040 |
AlteredExpression
|
group |
BEFREE |
Most TTF-1-negative pulmonary adenocarcinomas are mucinous lesions with the predominant expression of HNF4α and MUC5AC.
|
21348892 |
2011 |
|
Adenocarcinoma of lung (disorder)
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
Metaplastic cells adjacent to non-TRU-type ADCs ectopically expressed HNF-4α, a marker for non-TRU-type ADCs.
|
28952142 |
2018 |
|
Adenocarcinoma of lung (disorder)
|
0.030 |
Biomarker
|
disease |
BEFREE |
These findings suggest that GATA6 might interact with HNF4α and contribute to the development of mucinous-type LAs.
|
29469192 |
2018 |
|
Adenocarcinoma of lung (disorder)
|
0.030 |
Biomarker
|
disease |
BEFREE |
In summary, this is the first study to describe a subpopulation of ciliated cells that express HNF4α as a potential normal counterpart for non-TRU LADCs and suggests that bronchiolar metaplastic lesions that strongly express HNF4α are a precancerous lesion for non-TRU LADCs.
|
30848476 |
2019 |
|
Adenocarcinoma of pancreas
|
0.010 |
Biomarker
|
disease |
BEFREE |
However, the role of HNF4α in pancreatic adenocarcinoma (PDAC) has not been studied extensively and remains unclear.
|
30867652 |
2019 |
|
Adenocarcinoma, Endometrioid
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Dysregulation of beta-catenin levels and localization and constitutive activation of beta-catenin/TCF (T cell factor)-regulated gene expression occur in many cancers, including the majority of colorectal carcinomas and a subset of ovarian endometrioid adenocarcinomas.
|
19843521 |
2010 |
|
Adenomatous Polyposis Coli
|
0.090 |
GeneticVariation
|
disease |
BEFREE |
CTNNB1 and APC are part of the Wnt signaling pathway and mutations in either gene result in stabilization of the beta-catenin protein and allow nuclear translocation and binding of beta-catenin to the T-cell factor/lymphoid enhancer factor (TCF/Lef) family of transcription factors, resulting in activation of target genes which may underlie desmoid tumor biology and clinical behavior.
|
17952864 |
2008 |
|
Adenomatous Polyposis Coli
|
0.090 |
GeneticVariation
|
disease |
BEFREE |
Many colon cancers suffer mutations in either the adenomatous polyposis coli or beta-catenin genes that lead to stabilization of beta-catenin and activation of downstream T-cell factor (Tcf) target genes.
|
11389074 |
2001 |
|
Adenomatous Polyposis Coli
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Constitutive activation of beta-catenin-TCF-mediated transcription resulting from mutations in adenomatous polyposis coli (APC), beta-catenin, or Axin is believed to be a critical step in tumorigenesis among divergent types of cancers.
|
15574752 |
2004 |
|
Adenomatous Polyposis Coli
|
0.090 |
Biomarker
|
disease |
BEFREE |
There are at least five mechanisms by which APC can regulate the formation of the β-catenin/TCF complex: This paper presents a computational model for the Wnt pathway that explicitly includes the above five roles of APC in regulating β-catenin/TCF formation.
|
30110600 |
2018 |
|
Adenomatous Polyposis Coli
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Mutational inactivation in the tumor suppressor adenomatous polyposis coli (APC), as well as activation of beta-catenin, causes the accumulation of beta-catenin, which in turn associates with the T cell factor/lymphoid enhancer factor (TCF/LEF) family of transcription factors and activates transcription of their target genes.
|
14660579 |
2004 |
|
Adenomatous Polyposis Coli
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Loss of APC function results in accumulation of beta-catenin and activation of beta-catenin/TCF-dependent transcription.
|
16885356 |
2006 |
|
Adenomatous Polyposis Coli
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
TGFbeta now stimulated the constitutive TCF transcriptional activation activity associated with the beta-catenin/Wnt pathway in the APC knocked-down cells.
|
18774639 |
2008 |
|
Adenomatous Polyposis Coli
|
0.090 |
GeneticVariation
|
disease |
BEFREE |
In many cancers, inactivation of the adenomatous polyposis coli (APC) or Axin tumor suppressor proteins or activating mutations in beta-catenin lead to elevated beta-catenin levels, enhanced binding of beta-catenin to T cell factor (TCF) proteins, and increased expression of TCF-regulated genes.
|
12086873 |
2002 |
|
Adenomatous Polyposis Coli
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Using a luciferase-based Wnt-TCF transcription factor assay, it was shown that APC levels were inversely associated with TCF/LEF activity.
|
23129580 |
2013 |
|
Adult Acute Lymphocytic Leukemia
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
In this cohort of Taiwanese children, the relative frequencies of the 4 translocations of B-lineage ALL were 8% with ALL-type t(9;22)/BCR-ABL1, 4% with (1;19)/TCF-PBX1, 2% with t(4;11)/MLL-AF4, and 17.6% with t(12;21)/ETV6-RUNX1.
|
20930648 |
2010 |