|
Body Height
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Harmonizing Genetic Ancestry and Self-identified Race/Ethnicity in Genome-wide Association Studies.
|
31564439 |
2019 |
|
Lean body mass
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Genomics of body fat percentage may contribute to sex bias in anorexia nervosa.
|
30593698 |
2019 |
|
Neoplasms
|
0.050 |
GeneticVariation
|
group |
BEFREE |
Genomic, transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) breast cancer cohorts were used to examine statistical associations between tumor mutational burden (TMB) and the survival of patients whose tumors were assigned to previously-described prognostic immune subclasses reflecting favorable, weak or poor immune-infiltrate dispositions (FID, WID or PID, respectively).
|
30386679 |
2018 |
|
Neoplasms
|
0.050 |
Biomarker
|
group |
BEFREE |
Interestingly, RINF localizes to 5q31.3, a small region often deleted in myeloid leukemia (acute myeloid leukemia [AML]/myelodysplasia [MDS]) and suspected to harbor one or several tumor suppressor gene.
|
19182210 |
2009 |
|
Neoplasms
|
0.050 |
Biomarker
|
group |
BEFREE |
These observations together suggest that CXXC5 may act as a tumor suppressor by promoting TGF-β signaling via a positive feedback loop, and reveal a strategy for HCC to bypass TGF-β-mediated cytostasis by disrupting the positive feedback regulation.
|
29036306 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.040 |
Biomarker
|
disease |
BEFREE |
Finally, CXXC5 knockdown in human AML cell lines caused significantly increased expression of the potential tumor suppressor gene TSC22 and genes encoding the growth factor receptor KIT, the cytokine Angiopoietin 1 and the selenium-containing glycoprotein Selenoprotein P. Thus, high CXXC5 expression seems to affect several steps in human leukemogenesis, including intracellular events as well as extracellular communication.
|
25605239 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.040 |
Biomarker
|
disease |
BEFREE |
Interestingly, RINF localizes to 5q31.3, a small region often deleted in myeloid leukemia (acute myeloid leukemia [AML]/myelodysplasia [MDS]) and suspected to harbor one or several tumor suppressor gene.
|
19182210 |
2009 |
|
Leukemia, Myelocytic, Acute
|
0.040 |
Biomarker
|
disease |
BEFREE |
CXXC5/RINF knockdown in AML cell lines caused increased susceptibility to chemotherapy-induced apoptosis, and regulation of apoptosis also seemed to differ between primary human AML cells with high and low RINF expression.
|
23988457 |
2013 |
|
Malignant neoplasm of breast
|
0.030 |
Biomarker
|
disease |
BEFREE |
Genomic, transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) breast cancer cohorts were used to examine statistical associations between tumor mutational burden (TMB) and the survival of patients whose tumors were assigned to previously-described prognostic immune subclasses reflecting favorable, weak or poor immune-infiltrate dispositions (FID, WID or PID, respectively).
|
30386679 |
2018 |
|
Malignant neoplasm of breast
|
0.030 |
Biomarker
|
disease |
BEFREE |
However, the role of CXXC5 in breast cancer requires further investigation.
|
29928427 |
2018 |
|
Leukemogenesis
|
0.030 |
Biomarker
|
disease |
BEFREE |
Some genes, such as CXXC5, ETS1 and VAV3 have previously been implied to have a role in leukemogenesis.
|
28626218 |
2017 |
|
Breast Carcinoma
|
0.030 |
Biomarker
|
disease |
BEFREE |
Genomic, transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) breast cancer cohorts were used to examine statistical associations between tumor mutational burden (TMB) and the survival of patients whose tumors were assigned to previously-described prognostic immune subclasses reflecting favorable, weak or poor immune-infiltrate dispositions (FID, WID or PID, respectively).
|
30386679 |
2018 |
|
Breast Carcinoma
|
0.030 |
Biomarker
|
disease |
BEFREE |
However, the role of CXXC5 in breast cancer requires further investigation.
|
29928427 |
2018 |
|
Osteoporosis
|
0.020 |
Biomarker
|
disease |
BEFREE |
Recently, the Dvl-CXXC5 interaction has been identified as an excellent target for osteoporosis treatment.
|
27932247 |
2017 |
|
Osteoporosis
|
0.020 |
Biomarker
|
disease |
BEFREE |
Based on the structural analysis of binding modes of MD-simulated Dvl PDZ domain with CXXC5 peptide and crystal Dvl PDZ domain with synthetic peptide-ligands, we generated two different pharmacophore models and applied pharmacophore-based virtual screening to discover potent inhibitors of the Dvl-CXXC5 interaction for the anabolic therapy of osteoporosis.
|
29627878 |
2018 |
|
Adult Acute Myeloblastic Leukemia
|
0.020 |
Biomarker
|
disease |
BEFREE |
Interestingly, RINF localizes to 5q31.3, a small region often deleted in myeloid leukemia (acute myeloid leukemia [AML]/myelodysplasia [MDS]) and suspected to harbor one or several tumor suppressor gene.
|
19182210 |
2009 |
|
Adult Acute Myeloblastic Leukemia
|
0.020 |
Biomarker
|
disease |
BEFREE |
The gene CXXC5 on 5q31 is frequently deleted in acute myeloid leukemia (AML) with del(5q), suggesting that inactivation of CXXC5 might play a role in leukemogenesis.
|
25805812 |
2015 |
|
Childhood Acute Myeloid Leukemia
|
0.020 |
Biomarker
|
disease |
BEFREE |
The gene CXXC5 on 5q31 is frequently deleted in acute myeloid leukemia (AML) with del(5q), suggesting that inactivation of CXXC5 might play a role in leukemogenesis.
|
25805812 |
2015 |
|
Childhood Acute Myeloid Leukemia
|
0.020 |
Biomarker
|
disease |
BEFREE |
Interestingly, RINF localizes to 5q31.3, a small region often deleted in myeloid leukemia (acute myeloid leukemia [AML]/myelodysplasia [MDS]) and suspected to harbor one or several tumor suppressor gene.
|
19182210 |
2009 |
|
Tumor Cell Invasion
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
Overall, our experiment demonstrated a novel function of CXXC5 in the regeneration of impaired cementum caused by <i>P. gingivalis</i> invasion and suggested that MAPK signaling network balances the facilitation effects of CXXC5 in cementoblast differentiation.
|
31360111 |
2019 |
|
Tumor Cell Invasion
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
Moreover, knockdown of PSMB2 or CXXC5 suppresses HCC cell proliferation and invasion.
|
29780166 |
2018 |
|
Liver carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Our findings shed new light on TGF-β signaling regulation and demonstrate the function of CXXC5 in HCC development.
|
29036306 |
2018 |
|
MYELODYSPLASTIC SYNDROME
|
0.020 |
Biomarker
|
group |
BEFREE |
We have previously described the essential role of the retinoid-inducible nuclear factor (RINF) during differentiation of hematopoietic cells and suggested its putative involvement in myeloid leukemia and preleukemia.
|
21325450 |
2011 |
|
MYELODYSPLASTIC SYNDROME
|
0.020 |
Biomarker
|
group |
BEFREE |
Interestingly, RINF localizes to 5q31.3, a small region often deleted in myeloid leukemia (acute myeloid leukemia [AML]/myelodysplasia [MDS]) and suspected to harbor one or several tumor suppressor gene.
|
19182210 |
2009 |
|
Alopecia
|
0.010 |
Biomarker
|
disease |
BEFREE |
Overall, these findings suggest that the CXXC5-Dishevelled interaction is a potential target for the treatment of hair loss.
|
28595998 |
2017 |