| Gene | Score gda | Association Type | Type | Original DB | Sentence supporting the association | PMID | PMID Year | ||||
|---|---|---|---|---|---|---|---|---|---|---|---|
|
0.070 | AlteredExpression | disease | BEFREE | There were no other significant associations between PD-L1, FGFR1, PIK3CA, PTEN, and p16 expression and total/local severity of emphysema or presence of COPD/GOLD stage. | 31481045 | 2019 | ||||
|
0.070 | AlteredExpression | disease | BEFREE | Immunostaining for p16 revealed an enhanced expression of this marker in patients with COPD compared with that in controls. | 31019774 | 2019 | ||||
|
0.070 | GeneticVariation | disease | BEFREE | We examined real-world differences in 30-day readmission and exacerbation rates between Medicare beneficiaries with COPD treated with a nebulized long-acting beta<sub>2</sub>-agonist (arformoterol tartrate [ARF]) and beneficiaries treated with a nebulized short-acting beta<sub>2</sub>-agonist (SABA) for maintenance therapy after hospital discharge. | 31630815 | 2019 | ||||
|
0.070 | Biomarker | disease | BEFREE | Our findings suggest that p16 is not the only key player associated with CS-induced cellular senescence phenotypes (SIPS and SASP), decline in lung function, and airspace enlargement in COPD/emphysema. | 29447461 | 2018 | ||||
|
0.070 | AlteredExpression | disease | BEFREE | The expression levels of P16 and P21 were also higher in the airway epithelia of COPD model rats; however, the levels of P16 and P21 in the groups treated with all concentrations of <i>O. sinensis</i> were obviously lower than those in the COPD model group based on real-time quantitative PCR and western blotting. | 29808102 | 2018 | ||||
|
0.070 | Biomarker | disease | BEFREE | Methylation status of CDKN2A and MGMT was significantly higher in COPD and LC patients compared with CTR group (p < 0.0001). | 22818553 | 2012 | ||||
|
0.070 | GeneticVariation | disease | BEFREE | Furthermore, T-box (TBX) genes and cyclin-dependent kinase inhibitor 2A (CDKN2A), which are in a direct transcriptional regulatory relationship, emerged as preeminent participants in the etiology of COPD by means of senescence. | 22829758 | 2012 |