|
Body Height
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Waist-Hip Ratio
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
Genetic deletion of Ezh1/2 in a mouse AML model induced cell cycle progression of quiescent LSCs and differentiation to LSCs, eventually eradicating AML LSCs.
|
28951561 |
2018 |
|
Neoplasms
|
0.020 |
GeneticVariation
|
group |
BEFREE |
Two hotspots of EZH1 mutations were only found in RAS-negative follicular-patterned tumors.
|
29723601 |
2018 |
|
Thyroid Gland Follicular Adenoma
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
Recurrent EZH1 mutations are a second hit in autonomous thyroid adenomas.
|
27500488 |
2016 |
|
Thyroid Gland Follicular Adenoma
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
EZH1 mutations were detected in 3% of follicular adenoma and in 20% of Hürthle cell adenoma, and one minimally invasive Hürthle cell carcinoma.
|
29723601 |
2018 |
|
Glioma
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Survival analysis then revealed a five-PcG gene signature one protective gene (enhancer of zeste homolog 1) and four risky genes (EZH2, PHD finger protein 19, DNMT3A and DNMT3B), which may identify patients with high risk of poor prognosis of glioma.
|
28454437 |
2017 |
|
Nodule
|
0.010 |
GeneticVariation
|
phenotype |
BEFREE |
Somatic mutation of BRAF (22/32) is only detected in PTC, while mutations in SPOP (4/38), ZNF148 (6/38) and EZH1 (3/38) are found enriched in adenomatoid nodule.
|
28580939 |
2017 |
|
Thyroid Neoplasm
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Thyroid tumors with EZH1 mutations reported in the literature were benign in most cases.
|
29723601 |
2018 |
|
Adenocarcinoma, Oxyphilic
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
EZH1 mutations were detected in 3% of follicular adenoma and in 20% of Hürthle cell adenoma, and one minimally invasive Hürthle cell carcinoma.
|
29723601 |
2018 |
|
Follicular adenoma
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
EZH1 mutations were detected in 3% of follicular adenoma and in 20% of Hürthle cell adenoma, and one minimally invasive Hürthle cell carcinoma.
|
29723601 |
2018 |
|
Papillary thyroid carcinoma
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Somatic mutation of BRAF (22/32) is only detected in PTC, while mutations in SPOP (4/38), ZNF148 (6/38) and EZH1 (3/38) are found enriched in adenomatoid nodule.
|
28580939 |
2017 |
|
Hurthle Cell Tumor
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
EZH1 mutations were detected in 3% of follicular adenoma and in 20% of Hürthle cell adenoma, and one minimally invasive Hürthle cell carcinoma.
|
29723601 |
2018 |
|
Thyroid Gland Oncocytic Adenoma
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
EZH1 mutations were detected in 3% of follicular adenoma and in 20% of Hürthle cell adenoma, and one minimally invasive Hürthle cell carcinoma.
|
29723601 |
2018 |
|
Oncovirus infection
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Inactivation of chromatin-associated genes (ARID1A, SMARCA4/BRG1, SMARCB1/SNF5, KDM6A/UTX, BAP1, KMT2D/MLL2) and oncovirus infection (HTLV-1, EBV) trigger EZH1/2 perturbation and H3K27me3 deposition.
|
31747604 |
2019 |
|
Malignant Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
EZH1/2 function mostly within canonical PRC2 and exhibit proliferation-dependent redundancy that shapes mutational signatures in cancer.
|
30867289 |
2019 |
|
Malignant Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
Dual inhibition of enhancer of zeste homolog 1/2 overactivates WNT signaling to deplete cancer stem cells in multiple myeloma.
|
30343511 |
2019 |
|
Malignant Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
Notably, this combination also exhibited strong synergy in prostate cancer cells.<b>Conclusions:</b> Our results identify dual inhibition of EZH2 and EZH1 together with proteasome inhibition as a promising epigenetics-based therapy for PRC2-dependent cancers.<i>Clin Cancer Res; 23(16); 4817-30.©2017 AACR</i>.
|
28490465 |
2017 |
|
Malignant Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
A solid cancer panel assay demonstrated that some cancer cell lines are sensitive to EZH1/2 dual inhibitor in vitro and in vivo.
|
28741798 |
2017 |
|
Primary malignant neoplasm
|
0.040 |
Biomarker
|
group |
BEFREE |
Notably, this combination also exhibited strong synergy in prostate cancer cells.<b>Conclusions:</b> Our results identify dual inhibition of EZH2 and EZH1 together with proteasome inhibition as a promising epigenetics-based therapy for PRC2-dependent cancers.<i>Clin Cancer Res; 23(16); 4817-30.©2017 AACR</i>.
|
28490465 |
2017 |
|
Primary malignant neoplasm
|
0.040 |
Biomarker
|
group |
BEFREE |
Dual inhibition of enhancer of zeste homolog 1/2 overactivates WNT signaling to deplete cancer stem cells in multiple myeloma.
|
30343511 |
2019 |
|
Primary malignant neoplasm
|
0.040 |
Biomarker
|
group |
BEFREE |
EZH1/2 function mostly within canonical PRC2 and exhibit proliferation-dependent redundancy that shapes mutational signatures in cancer.
|
30867289 |
2019 |
|
Primary malignant neoplasm
|
0.040 |
Biomarker
|
group |
BEFREE |
A solid cancer panel assay demonstrated that some cancer cell lines are sensitive to EZH1/2 dual inhibitor in vitro and in vivo.
|
28741798 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.030 |
Biomarker
|
disease |
BEFREE |
Our analysis implicated <i>BCL2</i> expression level as an important indicator of venetoclax responsiveness and provided a rationale for its targeting in specific leukemia subtypes and multiple myeloma, linked several polycomb group proteins that could be targeted by small molecules (SFMBT1, CBX7, and EZH1) with chronic lymphocytic leukemia, and supported <i>CDK6</i> as a disease-specific target in acute myeloid leukemia.
|
30940663 |
2019 |
|
Multiple Myeloma
|
0.030 |
Biomarker
|
disease |
BEFREE |
Polycomb repressive complex 2 (PRC2) components, EZH2 and its homolog EZH1, and PI3K/Akt signaling pathway are focal points as therapeutic targets for multiple myeloma.
|
31571328 |
2019 |