BackgroundAlthough an elevated hemoglobin A1c (HbAc1) level is an independent predictor of worse survival in patients with both digestive cancer and diabetes mellitus, its relationship to short-term prognosis in these patients has not been addressed. This study assessed this relationship in gastrointestinal cancer (GIC) patients with type 2 diabetes mellitus (T2DM).MethodsA retrospective review of patients with GIC with or without T2DM from 2004 to 2014 was performed. Patients with T2DM were grouped according to HbA1c level, either normal (mean < 7.0%) or elevated (mean ≥ 7.0%). Age- and sex-matched GIC patients without T2DM served as controls.ResultsOne hundred and eighteen patients aged 33 - 81 years with T2DM met the study eligibility criteria; 51 were in the normal HbA1c group, and 67 were in the elevated HbA1c group. The 91 patients in the non-T2DM group were randomly selected and matched to the T2DM group in terms of admittance date, age, and sex. There was a trend toward a higher 180-day mortality rate in the T2DM group compared with the non-T2DM group (15.3% vs. 7.7%, P = 0.095) and in the elevated HbA1c group compared with the normal HbA1c group (19.4% vs. 9.8%, P = 0.151); however, the differences were not significant. The duration of the hospital stay was longer in patients with T2DM than in those without T2DM (13.2 vs. 8.9 days, P < 0.05) and in patients with elevated versus normal HbA1c levels (14.5 vs. 11.4 days, P < 0.05). Diabetic GIC patients with elevated HbA1c levels had significantly more total postoperative complications than those with normal HbA1c levels (25.4% vs. 9.8%, P < 0.05). In multivariate regression analyses, short-term adverse outcomes were strongly associated with elevated HbA1c levels (odds ratio (OR): 5.276; 95% confidence level (CI): 1.73 - 16.095; P < 0.05) and no strict antidiabetic treatment (OR: 7.65; 95% CI: 2.49 - 23.54; P < 0.001).ConclusionAn elevated level of HbA1c significantly correlated with and was an independent predictor of short-term adverse outcomes in GIC patients with T2DM.
Hepatocellular carcinoma (HCC) is a common high-mortality cancer, mainly due to diagnostic difficulties during its early clinical stages. In this study, we aimed to identify genes that are important for HCC diagnosis and treatment, and we investigated the underlying mechanism of prognostic differences. Differentially expressed genes (DEGs) were identified by using the limma package, and receiver operating characteristic curve analysis was performed to identify diagnostic markers for HCC. Bioinformatics and clinical specimens were used to assess epithelial cell transforming 2 (ECT2) in terms of expression, prognostic value, pathways, and immune correlations. In vitro experiments were used to investigate the underlying mechanism and function of ECT2, and the results were confirmed through in vivo experiments. The integrated analysis revealed 53 upregulated DEGs, and one candidate biomarker for diagnosis (ECT2) was detected. High expression of ECT2 was found to be an independent prognostic risk factor for HCC. ECT2 expression showed a strong correlation with tumor-associated macrophages. We found that ECT2 overexpression increased the migration and proliferation of HCC cells. It also promoted the expression of PLK1, which subsequently interacted with PTEN and interfered with its nuclear translocation, ultimately enhancing aerobic glycolysis and promoting M2 macrophage polarization. M2 macrophages suppress the functions of NK cells and T cells, and this was confirmed in the in vivo experiments. Overall, ECT2 may promote the polarization of M2 macrophages by enhancing aerobic glycolysis and suppressing the functions of immune cells. ECT2 could serve as a candidate diagnostic and prognostic biomarker for HCC.
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