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 |
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 |
Neoplasms
|
0.050 |
AlteredExpression
|
group |
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 |
Neoplasms
|
0.050 |
AlteredExpression
|
group |
BEFREE |
RINF expression was significantly higher in all tumor forms (primary breast, and thyroid cancers and metastatic melanomas) as compared with normal control tissues (P < 0.001 for each comparison).
|
21325450 |
2011 |
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 |
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 |
AlteredExpression
|
disease |
BEFREE |
Inactivation of CXXC5 is associated with different leukemic pathways and defines an AML subgroup with better outcome.
|
25805812 |
2015 |
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 |
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 |
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 |
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 |
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 |
Leukemogenesis
|
0.030 |
AlteredExpression
|
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 |
Leukemogenesis
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
In gene-expression profiling, lower CXXC5 expression was associated with upregulation of cell-cycling genes and co-downregulation of genes implicated in leukemogenesis (WT1, GATA2, MLL, DNMT3B, RUNX1).
|
25805812 |
2015 |
Malignant neoplasm of breast
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
Notably, high levels of RINF was strongly associated with TP53 wild-type status (P = 0.002) possibly indicating that high levels of RINF could substitute for TP53 mutations as an oncogenic mechanism during the malignant development of some cases of breast cancer.
|
21325450 |
2011 |
Breast Carcinoma
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
Notably, high levels of RINF was strongly associated with TP53 wild-type status (P = 0.002) possibly indicating that high levels of RINF could substitute for TP53 mutations as an oncogenic mechanism during the malignant development of some cases of breast cancer.
|
21325450 |
2011 |
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 |
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 |
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 |
AlteredExpression
|
disease |
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 |