Dental caries
|
0.100 |
GeneticVariation
|
disease |
GWASCAT |
Genome-wide analysis of dental caries and periodontitis combining clinical and self-reported data.
|
31235808 |
2019 |
Red Blood Cell Count measurement
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
Duration of sleep
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
GWAS identifies 14 loci for device-measured physical activity and sleep duration.
|
30531941 |
2018 |
Low density lipoprotein cholesterol measurement
|
0.100 |
GeneticVariation
|
phenotype |
GWASDB |
Large-scale gene-centric meta-analysis across 32 studies identifies multiple lipid loci.
|
23063622 |
2012 |
Triglycerides measurement
|
0.100 |
GeneticVariation
|
phenotype |
GWASDB |
Large-scale gene-centric meta-analysis across 32 studies identifies multiple lipid loci.
|
23063622 |
2012 |
Serum LDL cholesterol measurement
|
0.100 |
GeneticVariation
|
phenotype |
GWASDB |
Large-scale gene-centric meta-analysis across 32 studies identifies multiple lipid loci.
|
23063622 |
2012 |
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
This study demonstrated that miR-129-5p could function as a tumor suppressor in the progression and development of PC by targeting PBX3, providing a reliable prognostic factor and a new therapeutic strategy for PC.
|
31518383 |
2019 |
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
The EWSR1-PBX3 gene fusion has been previously identified in three cases of ME tumors of bone and soft tissue, and in a case of retroperitoneal leiomyoma.
|
30834570 |
2019 |
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
One of the possible mechanisms responsible for the tumour-promoting actions is that ANRIL sponging miR-144 to derepress PBX3.
|
31609763 |
2019 |
Neoplasms
|
0.090 |
AlteredExpression
|
group |
BEFREE |
Clinical associations were analyzed in independent tissue collections and gene expression datasets of colorectal cancers with recorded follow-up data.<b>Results:</b> PBX3 was expressed in tumor cells with high WNT activity undergoing EMT at the leading tumor edge of colorectal cancers, whereas stromal cells were PBX3 negative.
|
29391352 |
2018 |
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
In summary, our findings demonstrated that miR-495 functions as a tumor suppressor in human melanoma via directly targeting PBX3.
|
29670366 |
2018 |
Neoplasms
|
0.090 |
AlteredExpression
|
group |
BEFREE |
The expression levels of PBX3 were analyzed in CC cell lines and tumor specimens by real-time polymerase chain reaction (RT-PCR), Western blotting, and immunohistochemical staining.
|
29225475 |
2017 |
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
PBX3 (Pre-B cell leukemia homeobox 3), a putative target gene of miR-320, has been reported to be upregulated in various tumors and promote tumor cell growth through regulating MAKP/ERK pathway.
|
28934982 |
2017 |
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
Downregulated DEGs included TFs, such as the proto‑oncogene SPI1, pre‑B‑cell leukemia homeobox 3 (PBX3) and lymphoid enhancer‑binding factor 1 (LEF1), as well as tumor suppressors (TSs), such as capping actin protein, gelsolin like (CAPG) and tumor protein p53‑inducible nuclear protein 1 (TP53INP1).
|
28791367 |
2017 |
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
A xenograft LN229 model was used to confirm that PBX3 depletion decreased tumor growth in vivo.
|
28856521 |
2017 |
leukemia
|
0.070 |
Biomarker
|
disease |
BEFREE |
Furthermore, pre-leukemia transcription factor 3 (PBX3) was a direct target gene of miR-144-3p.
|
28111340 |
2017 |
leukemia
|
0.070 |
GeneticVariation
|
disease |
BEFREE |
We found that Pbx3 deletion significantly prolonged the survival of leukemic mice and decreased the leukemia burden by decreasing the capacity of LSCs and promoting LSC apoptosis.
|
28411381 |
2017 |
Childhood Leukemia
|
0.070 |
Biomarker
|
disease |
BEFREE |
Furthermore, pre-leukemia transcription factor 3 (PBX3) was a direct target gene of miR-144-3p.
|
28111340 |
2017 |
Childhood Leukemia
|
0.070 |
GeneticVariation
|
disease |
BEFREE |
We found that Pbx3 deletion significantly prolonged the survival of leukemic mice and decreased the leukemia burden by decreasing the capacity of LSCs and promoting LSC apoptosis.
|
28411381 |
2017 |
leukemia
|
0.070 |
Biomarker
|
disease |
BEFREE |
Finally, kinetics and severity of disease in transplantation assays indicated that Pbx3/Meis1 dimers are rate-limiting factors for Hoxa9-induced leukemia.
|
25911551 |
2015 |
Childhood Leukemia
|
0.070 |
Biomarker
|
disease |
BEFREE |
Finally, kinetics and severity of disease in transplantation assays indicated that Pbx3/Meis1 dimers are rate-limiting factors for Hoxa9-induced leukemia.
|
25911551 |
2015 |
leukemia
|
0.070 |
Biomarker
|
disease |
BEFREE |
Collectively, our data suggest that PBX3 is a critical cofactor of HOXA9 in leukemogenesis, and targeting their interaction is a feasible strategy to treat presently therapy resistant CA-AML (eg, MLL-rearranged leukemia) in which HOXA/PBX3 genes are overexpressed.
|
23264595 |
2013 |
leukemia
|
0.070 |
Biomarker
|
disease |
BEFREE |
Together the data support a key role for HOXA/TALE in cytogenetically normal acute myeloid leukemia and demonstrate that targeting of clinically significant HOXA/PBX3 elements may provide therapeutic benefit to patients with this subtype of leukemia.
|
23539541 |
2013 |
Childhood Leukemia
|
0.070 |
Biomarker
|
disease |
BEFREE |
Collectively, our data suggest that PBX3 is a critical cofactor of HOXA9 in leukemogenesis, and targeting their interaction is a feasible strategy to treat presently therapy resistant CA-AML (eg, MLL-rearranged leukemia) in which HOXA/PBX3 genes are overexpressed.
|
23264595 |
2013 |
Childhood Leukemia
|
0.070 |
Biomarker
|
disease |
BEFREE |
Together the data support a key role for HOXA/TALE in cytogenetically normal acute myeloid leukemia and demonstrate that targeting of clinically significant HOXA/PBX3 elements may provide therapeutic benefit to patients with this subtype of leukemia.
|
23539541 |
2013 |