|
Malignant Neoplasms
|
0.050 |
Biomarker
|
group |
BEFREE |
This function of HELLS in maintenance of genome stability is likely to contribute to its role in cancer biology and demonstrates that different chromatin remodelling activities are required for efficient repair in specific genomic contexts.
|
31802118 |
2020 |
|
Primary malignant neoplasm
|
0.050 |
Biomarker
|
group |
BEFREE |
This function of HELLS in maintenance of genome stability is likely to contribute to its role in cancer biology and demonstrates that different chromatin remodelling activities are required for efficient repair in specific genomic contexts.
|
31802118 |
2020 |
|
Red cell distribution width determination
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
RDW - Red blood cell distribution width result
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Neoplasms
|
0.070 |
AlteredExpression
|
group |
BEFREE |
GSCs preferentially expressed HELLS compared with their differentiated tumor progeny and nonmalignant brain cells.
|
30779712 |
2019 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
Conclusion: Our data reveal that HELLS is a key epigenetic driver of HCC; by altering the nucleosome occupancy at the NFR and enhancer, HELLS epigenetically suppresses multiple tumor suppressor genes to promote HCC progression.
|
30516846 |
2019 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
In conclusion, LSH promotes tumor growth of HCC through transcriptional regulation of CENPF expression.
|
31066149 |
2019 |
|
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
Cell proliferation assay, cell migration and invasion assays, plate colony formation assay, immunofluorescence assay, Operetta® high-content screening and analysis, Western blot analysis and Co-Immunoprecipitation (Co-IP) assay, RNA immunoprecipitation assay and tumor growth assay was used to address the potential interplay of between GINS4 and LSH, and the functional of GINS4.
|
31253190 |
2019 |
|
Malignant Neoplasms
|
0.050 |
Biomarker
|
group |
BEFREE |
These findings suggest that LSH is a novel regulator of p53 through the proteasomal pathway, thereby providing an alternative mechanism of p53 involvement in lipid metabolism in cancer.
|
31594538 |
2019 |
|
Primary malignant neoplasm
|
0.050 |
Biomarker
|
group |
BEFREE |
These findings suggest that LSH is a novel regulator of p53 through the proteasomal pathway, thereby providing an alternative mechanism of p53 involvement in lipid metabolism in cancer.
|
31594538 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.030 |
Biomarker
|
disease |
BEFREE |
The expression of chromatin modifier lymphoid-specific helicase (LSH) and GINS4 was assessed in tumor and normal tissue from 79 patients with NSCLC with clinical characteristics.
|
31253190 |
2019 |
|
Tumor Progression
|
0.030 |
PosttranslationalModification
|
phenotype |
BEFREE |
The chromatin modifier lymphoid-specific helicase (LSH) is essential for DNA methylation and cancer progression as a transcriptional repressor.
|
31594538 |
2019 |
|
Malignant neoplasm of lung
|
0.030 |
Biomarker
|
disease |
BEFREE |
GINS4 facilitates lung cancer progression by promoting key characteristics of tumor potential, and LSH epigenetically interacts with and stabilizes GINS4 transcripts.
|
31253190 |
2019 |
|
Carcinoma of lung
|
0.030 |
Biomarker
|
disease |
BEFREE |
GINS4 facilitates lung cancer progression by promoting key characteristics of tumor potential, and LSH epigenetically interacts with and stabilizes GINS4 transcripts.
|
31253190 |
2019 |
|
Primary malignant neoplasm of lung
|
0.030 |
Biomarker
|
disease |
BEFREE |
GINS4 facilitates lung cancer progression by promoting key characteristics of tumor potential, and LSH epigenetically interacts with and stabilizes GINS4 transcripts.
|
31253190 |
2019 |
|
Glioblastoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Collectively, targeting HELLS may permit the functional disruption of the relatively undruggable MYC and E2F3 transcription factors and serve as a novel therapeutic paradigm for glioblastoma.
|
30779712 |
2019 |
|
Glioma
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
The potential clinical significance of HELLS was reinforced by improved survival of tumor-bearing mice upon targeting HELLS and poor prognosis of glioma patients with elevated HELLS expression.
|
30779712 |
2019 |
|
Neoplasm Metastasis
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
In contrast, depletion of HELLS reduced HCC growth and metastasis both in vitro and in vivo.
|
30516846 |
2019 |
|
Adult Glioblastoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Collectively, targeting HELLS may permit the functional disruption of the relatively undruggable MYC and E2F3 transcription factors and serve as a novel therapeutic paradigm for glioblastoma.
|
30779712 |
2019 |
|
Childhood Glioblastoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Collectively, targeting HELLS may permit the functional disruption of the relatively undruggable MYC and E2F3 transcription factors and serve as a novel therapeutic paradigm for glioblastoma.
|
30779712 |
2019 |
|
Glioblastoma Multiforme
|
0.020 |
Biomarker
|
disease |
BEFREE |
Collectively, targeting HELLS may permit the functional disruption of the relatively undruggable MYC and E2F3 transcription factors and serve as a novel therapeutic paradigm for glioblastoma.
|
30779712 |
2019 |
|
Liver carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
In contrast, depletion of HELLS reduced HCC growth and metastasis both in vitro and in vivo.
|
30516846 |
2019 |
|
Liver carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Therefore, LSH may be a novel predictor for prognosis and a potential therapeutic target for HCC.
|
31066149 |
2019 |
|
Burkitt Lymphoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
The levels of Ki67, LSH, 5-hmC, and E2F1 were all increased in germinal center B-cell lymphomas when compared with those in normal lymph nodes, and LSH was highly expressed in diffuse large B-cell lymphomas (DLBCLs) and Burkitt lymphomas (BLs) that were positive for Epstein-Barr virus (EBV) infection, indicating that LSH is linked to EBV infection in DLBCL and BL.
|
30964110 |
2019 |
|
Medulloblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Elucidation of HELLS as one of the downstream effectors of the SHH pathway may lead to novel targets for precision therapeutics with the promise of better outcomes for SHH medulloblastoma patients.
|
31541170 |
2019 |