On multivariate analysis, high levels of CXCR4 were associated with distant recurrence (P < 0.001) but not with locoregional recurrence.
In a multivariate analysis, high levels of miR-21 (P = 0.007, HR = 2.24; 95% CI = 1.25-4.02), pT stage, lymph node metastasis, and serum CEA level were independent prognostic factors for unfavorable RFS (Table 3).
In the multivariate analysis, high-level TUBB3 expression was an independent prognostic factor for poor PFS (HR 2.74, 95% CI 1.91-3.91, P = 0.001).
On multivariate analysis, high-level CCR7 staining predicted relapse-free (hazard ratio 3.0, 95% confidence intervals 1.1 8.0, P=0.026) and disease-specific (hazard ratio 10.2, 95% confidence intervals 2.1 48.6, P=0.004) survival.
Finally, in our multivariate analysis, higher levels of CRP and levels of anti-CCP antibodies remained associated with the cIMT, independent of age and disease duration, suggesting that the possible damage to vascular endothelium in the carotid arteries is a subclinical but active process in RA.
In multivariate analysis, high MAGE level was significantly associated with incidence of MACE (hazard ratio 2.419 [95% CI 1.273 9.100]; P = 0.017) even after adjusting for Global Registry of Acute Coronary Events risk score, but admission glucose and HbA1c was not.
In univariate and multivariate analysis, high TMPRSS4 levels were associated with both DFS and OS (Liang et al, 2013).
In both Cox univariate and multivariate analysis, high cytosolic levels of uPA or PAI-1 were significantly associated with increased rates of relapse and death.
In the multivariate analysis, high p21 expression level at the pre-treatment biopsy was significantly associated with poor DFS (p = 0.001, HR 6.14; 95% CI 2.03, 18.55).
In the multivariate analysis, high IL-17 levels were associated with increased probability of survival, while high levels of G-CSF were associated with increased risk of mortality at 28 days (P < 0.05; Figure 1).
Interestingly, in the multivariate analysis, high serum PTH and FGF23 levels associated with aortic valve calcification.
