|
Obesity
|
0.400 |
GeneticVariation
|
disease |
GWASCAT |
Evaluation of 29 SNPs (P < 1 × 10(-5)) in an additional 971 severely obese children and 1,990 controls identified 4 new loci associated with severe obesity (LEPR, PRKCH, PACS1 and RMST).
|
23563609 |
2013 |
|
Obesity
|
0.400 |
GeneticVariation
|
disease |
GWASDB |
Evaluation of 29 SNPs (P < 1 × 10(-5)) in an additional 971 severely obese children and 1,990 controls identified 4 new loci associated with severe obesity (LEPR, PRKCH, PACS1 and RMST).
|
23563609 |
2013 |
|
Obesity
|
0.400 |
Biomarker
|
disease |
CTD_human |
Evaluation of 29 SNPs (P < 1 × 10(-5)) in an additional 971 severely obese children and 1,990 controls identified 4 new loci associated with severe obesity (LEPR, PRKCH, PACS1 and RMST).
|
23563609 |
2013 |
|
Body mass index
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Age at menarche
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
GWASCAT |
Large-scale association analysis in Asians identifies new susceptibility loci for prostate cancer.
|
26443449 |
2015 |
|
Kallmann Syndrome
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
A novel deletion in RMST implicates the loss of function of a lncRNA as a unique cause of KS and suggests it plays a critical role in the ontogeny of GnRH neurons and puberty.
|
31628846 |
2020 |
|
Malignant Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
Using random forest technology in a sequential analysis, we (1) identified eligibility for each of four therapies among 13,365 patients: esophagectomy alone (n = 6649), neoadjuvant therapy (n = 4706), esophagectomy and adjuvant therapy (n = 998), and neoadjuvant and adjuvant therapy (n = 1022); (2) performed survival analyses incorporating interactions of patient and cancer characteristics with therapy; (3) determined optimal therapy as that predicted to maximize lifetime within 10 years (restricted mean survival time; RMST) for each patient; and (4) compared lifetime gained from optimal versus actual therapies.
|
31442498 |
2019 |
|
Cerebrovascular Disorders
|
0.010 |
Biomarker
|
group |
BEFREE |
In conclusion, RMST promoted OGD-induced microglial M1 polarization by competitively interacting with hnRNPK via TAK1-mediated NF-κB pathway, which will provide a basis for understanding the pathogenesis of cerebrovascular diseases.
|
31329361 |
2019 |
|
Primary malignant neoplasm
|
0.010 |
Biomarker
|
group |
BEFREE |
Using random forest technology in a sequential analysis, we (1) identified eligibility for each of four therapies among 13,365 patients: esophagectomy alone (n = 6649), neoadjuvant therapy (n = 4706), esophagectomy and adjuvant therapy (n = 998), and neoadjuvant and adjuvant therapy (n = 1022); (2) performed survival analyses incorporating interactions of patient and cancer characteristics with therapy; (3) determined optimal therapy as that predicted to maximize lifetime within 10 years (restricted mean survival time; RMST) for each patient; and (4) compared lifetime gained from optimal versus actual therapies.
|
31442498 |
2019 |
|
Cardiovascular Diseases
|
0.010 |
Biomarker
|
group |
BEFREE |
RMST provides an intuitive and explicit way to express the effect of pravastatin therapy on CHD-free and overall survival in older adults free of cardiovascular disease.
|
30251369 |
2018 |
|
Coronary heart disease
|
0.010 |
Biomarker
|
disease |
BEFREE |
Pravastatin-treated individuals lived RMST 2,088.1 days), on average, 18.7 more days free of CHD over 6 years than those receiving usual care (RMST 2,069.4 days), but this difference was not statistically significant (difference 18.7 days, 95% CI=-10.4-47.8 days, p=.21).
|
30251369 |
2018 |
|
Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
RMST played a role of tumor suppressor in TNBC through inhibiting cell proliferation, invasion and migration, enhancing cell apoptosis, and regulating cell cycle.
|
29215701 |
2018 |
|
Tumor Progression
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
CCK-8 and colony formation assay unveiled that RMST could slow down the proliferation of TNBC cells to influence the tumor progression.
|
29215701 |
2018 |
|
Middle Cerebral Artery Occlusion
|
0.010 |
Biomarker
|
disease |
BEFREE |
RMST silencing protected against MCAO-induced ischemic brain injury in vivo and OGD-induced primary hippocampal neuron injury in vitro.
|
29258823 |
2018 |
|
Ischemic stroke
|
0.010 |
Biomarker
|
disease |
BEFREE |
Collectively, this study provides evidence that lncRNA is involved in the pathogenesis of ischemic brain injury, and suggests a promising approach of RMST inhibition in treating ischemic stroke.
|
29258823 |
2018 |
|
Tumor Cell Invasion
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
RMST overexpression could also restrain the invasion and migration abilities of TNBC cells.
|
29215701 |
2018 |
|
Triple Negative Breast Neoplasms
|
0.010 |
Biomarker
|
disease |
BEFREE |
CCK-8 and colony formation assay unveiled that RMST could slow down the proliferation of TNBC cells to influence the tumor progression.
|
29215701 |
2018 |
|
Triple-Negative Breast Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
CCK-8 and colony formation assay unveiled that RMST could slow down the proliferation of TNBC cells to influence the tumor progression.
|
29215701 |
2018 |
|
Malignant neoplasm of breast
|
0.010 |
Biomarker
|
disease |
BEFREE |
To the best of our knowledge, it was the first report that RMST was involved in breast cancer.
|
27380926 |
2016 |
|
Breast Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
To the best of our knowledge, it was the first report that RMST was involved in breast cancer.
|
27380926 |
2016 |