The purpose of this study was to conduct a comprehensive study of the clinical correlation between the alpha-fetoprotein (AFP) level at diagnosis and pathological grades, progression, and survival of patients with hepatocellular carcinoma (HCC). A total of 78,743 patients in Surveillance, Epidemiology, and End Results Program (SEER)-registered HCC was analyzed. The AFP test results for patients with HCC were mainly recorded as AFP-negative and AFP-positive. Logistic regression analysis revealed that the AFP level at diagnosis was an independent risk factor of pathological grade (odds ratio [OR], 2.559; 95% confidence interval [CI], 2.075–3.157; P < 0.001), TNM-7 stage (OR, 2.794; CI, 2.407–3.242; P < 0.001), and tumor size (OR, 1.748; 95% CI, 1.574–1.941; P < 0.001). Multivariable Cox regression analyses identified AFP level as an independent predictor of survival risk of patients with HCC who did not undergo surgery (hazard ratio [HR], 1.660; 95% CI, 1.534–1.797; P < 0.001), and those who underwent surgery (HR, 1.534; 95% CI, 1.348–1.745; P < 0.001). The AFP level at diagnosis was an independent risk predictor associated with pathological grade, progression, and survival. Further, surgery may not significantly reverse the adverse effects of AFP-positive compared with AFP-negative.

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Marital status is an independent prognostic factor for survival in several cancers. To determine if that is also true for pancreatic cancer after surgical treatment, we examined 13,370 cases of pancreatic cancer reported to the Surveillance, Epidemiology, and End Results (SEER) database between 1988 and 2012. We found that patients who were widowed at the time of diagnosis were more likely to be female, a high percentage were elderly, a high ratio were diagnosed in early years, and a high proportion of tumors were located at the head of the pancreas (P < 0.05). Marital status was confirmed to be an independent prognostic factor in both univariate and multivariate analyses (P < 0.05). In those with localized disease, 5-year pancreatic cancer cause-specific survival was 6.5% lower in widowed patients than married ones (38.6% vs. 32.1%), though this difference was not significant in a multivariate analysis (P = 0.084). In those with regional disease or distant metastasis, univariate and multivariate analyses indicated marital status to be an independent prognostic factor (P < 0.05). Thus marital status is an important prognostic factor in pancreatic cancer, and widowed patients are at greater risk of death than others.

BackgroundHepatocellular carcinoma (HCC) is the third leading cause of cancer-related mortality worldwide. Recurrence and metastasis after curative resection remain critical obstacles in HCC treatment. CD146 predicted poor prognosis of a variety of cancers including melanoma, breast tumors, prostate cancer, and gastric cancer. However, the role of CD146 in HCC has not yet been systematically explored.MethodsTo investigate the role of CD146 in HCC, we evaluated its expression in HCC tissues and HCC cell lines using real-time PCR and western blotting (WB). Second, we established HCC cell lines that stably overexpressed and interfered CD146 and explored the function of CD146 in HCC in vitro and in vivo. Third, we conducted microarray analysis to investigate the potential mechanism by identifying differentially expressed genes. Last, follow ups were conducted to help uncover the connection of CD146 expression and the prognosis of HCC patients.ResultsWe found that CD146 was overexpressed in HCC tissues and that high CD146 expression predicted poor overall survival time and shorter recurrence period in HCC patients. In vitro and in vivo experiments indicated that CD146 promoted migration and invasion of HCC cell lines. Further study indicated that CD146 promoted epithelial mesenchymal transition (EMT), IL-8 upregulation, and STAT1 downregulation. CD146 was upregulated in HCC tissues and cell lines.ConclusionsCD146 promoted metastasis of HCC cells and predicted poor prognosis of HCC patients. CD146 induced EMT, and IL-8 upregulation and STAT1 downregulation may be the potential underlying mechanism. The exact mechanism still needs further investigation.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-016-0313-3) contains supplementary material, which is available to authorized users.