|
Juvenile Myelomonocytic Leukemia
|
0.600 |
CausalMutation
|
disease |
CLINVAR |
|
|
|
|
Juvenile Myelomonocytic Leukemia
|
0.600 |
Biomarker
|
disease |
GENOMICS_ENGLAND |
|
|
|
|
Juvenile Myelomonocytic Leukemia
|
0.600 |
Biomarker
|
disease |
CTD_human |
|
|
|
|
Juvenile Myelomonocytic Leukemia
|
0.600 |
Biomarker
|
disease |
HPO |
|
|
|
|
Leukemia, Myelocytic, Acute
|
0.340 |
GeneticVariation
|
disease |
BEFREE |
In adult myeloid leukemias we found significant associations between the variant allele of PML_rs9479 and decreased AML risk (OR = 0.61 (0.38-0.97), and between variant alleles of IRF8_ rs10514611 and ARHGAP26_rs187729 and increased CML risk (OR = 2.4 (1.12-5.15) and 1.63 (1.07-2.47), respectively).
|
24886876 |
2014 |
|
Leukemia, Myelocytic, Acute
|
0.340 |
AlteredExpression
|
disease |
BEFREE |
GRAF transcript was significantly lower in AML group compared to controls (3.30 vs 56.06, P<0.001).
|
21074269 |
2011 |
|
Leukemia, Myelocytic, Acute
|
0.340 |
AlteredExpression
|
disease |
BEFREE |
The aim of this study was to investigate the expression level of GRAF gene in those patients with myeloid malignancies including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS) and chronic myeloid leukemia (CML).
|
20704716 |
2010 |
|
Leukemia, Myelocytic, Acute
|
0.340 |
PosttranslationalModification
|
disease |
BEFREE |
In contrast to normal tissues, which tested negative for GRAF promoter methylation, 11 of 29 (38%) bone marrow samples from patients with acute myeloid leukaemia or myelodysplastic syndrome were positive.
|
16404424 |
2006 |
|
Leukemia, Myelocytic, Acute
|
0.340 |
CausalMutation
|
disease |
CGI |
|
|
|
|
MYELODYSPLASTIC SYNDROME
|
0.330 |
PosttranslationalModification
|
group |
BEFREE |
GTPase regulator associated with focal adhesion kinase (GRAF), a putative tumor suppressor gene, was revealed with mutations and promoter methylation in AML and myelodysplastic syndrome.
|
21074269 |
2011 |
|
MYELODYSPLASTIC SYNDROME
|
0.330 |
AlteredExpression
|
group |
BEFREE |
The aim of this study was to investigate the expression level of GRAF gene in those patients with myeloid malignancies including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS) and chronic myeloid leukemia (CML).
|
20704716 |
2010 |
|
MYELODYSPLASTIC SYNDROME
|
0.330 |
PosttranslationalModification
|
group |
BEFREE |
In contrast to normal tissues, which tested negative for GRAF promoter methylation, 11 of 29 (38%) bone marrow samples from patients with acute myeloid leukaemia or myelodysplastic syndrome were positive.
|
16404424 |
2006 |
|
MYELODYSPLASTIC SYNDROME
|
0.330 |
CausalMutation
|
group |
CGI |
|
|
|
|
Psychotic Disorders
|
0.300 |
Biomarker
|
group |
PSYGENET |
Here, we report a newly diagnosed anti-Ca/ARHGAP26-IgG-positive patient who presented with recurrent psychotic symptoms but no cerebellar ataxia.
|
26298328 |
2015 |
|
Myelomonocytic leukemia
|
0.300 |
CausalMutation
|
disease |
CGI |
|
|
|
|
Body Height
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Characterizing rare and low-frequency height-associated variants in the Japanese population.
|
31562340 |
2019 |
|
Hepatitis C
|
0.100 |
GeneticVariation
|
disease |
GWASCAT |
Impact of IFNL4 Genetic Variants on Sustained Virologic Response and Viremia in Hepatitis C Virus Genotype 3 Patients.
|
31260374 |
2019 |
|
White Blood Cell Count procedure
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Eosinophil count procedure
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Systolic Pressure
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Coronary Artery Disease
|
0.100 |
GeneticVariation
|
disease |
GWASCAT |
Identification of 64 Novel Genetic Loci Provides an Expanded View on the Genetic Architecture of Coronary Artery Disease.
|
29212778 |
2018 |
|
Coronary Artery Disease
|
0.100 |
GeneticVariation
|
disease |
GWASDB |
Large-scale association analysis identifies new risk loci for coronary artery disease.
|
23202125 |
2013 |
|
Somatic mutation
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
|
Neoplasms
|
0.060 |
Biomarker
|
group |
BEFREE |
Rho GTPase-activating protein 26 (ARHGAP26) is a negative regulator of the Rho family that converts the small GTP-binding protein RhoA (GTP-RhoA) to its inactive GDP-bound form and is a putative tumor suppressor gene associated with cell growth and migration.
|
31004081 |
2019 |
|
Neoplasms
|
0.060 |
Biomarker
|
group |
BEFREE |
Consistent with the tumor suppressive role of claudins shown in mice, in humans, claudin-low breast cancer has been described as a distinct entity with a poor prognosis, and claudin-18-Rho GTPase activating protein 26 (CLDN18-ARHGAP26) fusion protein as a driver gene aberration in diffuse-type gastric cancer due to effects on RhoA.
|
31332482 |
2019 |