|
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 |
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 |
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 |
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 |
|
Mammary Neoplasms
|
0.020 |
AlteredExpression
|
group |
BEFREE |
CXXC5 is a gene encoding a retinoid-inducible nuclear factor, whose overexpression in breast tumours, metastatic malignant melanomas and papillary thyroid carcinoma has been recently reported.
|
29027288 |
2017 |
|
Mammary Neoplasms
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Our data indicate that (i) RINF overexpression is associated with the malignant phenotype in solid tumors and (ii) RINF overexpression represents an independent molecular marker for poor prognosis in breast tumors.
|
21325450 |
2011 |
|
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 |
|
Malignant Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
Previous studies revealed that CXXC5 is associated with various malignant tumours.
|
29928427 |
2018 |
|
Herpes Simplex Infections
|
0.010 |
Biomarker
|
group |
BEFREE |
Consequently, CXXC5-deficient mice had compromised early IFN response and became highly vulnerable to infection by herpes simplex virus and vesicular stomatitis virus.
|
28416650 |
2017 |
|
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 |
|
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 |
|
Tumor Progression
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
CXXC5 expression in prostate cancer: implications for cancer progression.
|
29027288 |
2017 |
|
Carcinogenesis
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Our findings suggest that CXXC5 may play a role in the process of prostate carcinogenesis.
|
29027288 |
2017 |
|
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 |
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 |
|
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 |
|
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 |
|
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 |