Significant predictors for HCC were identified using multiple Cox regression analysis in study cohort: treatment age ≥60 years (hazard ratio [HR]: 2.04, 95% confidence interval [CI] = 1.3-3.7), pretreatment bilirubin ≥1.1 mg/dL (HR: 1.99, 95% CI = 1.08-3.67), α-fetoprotein ≥7.9 ng/mL (HR: 2.44, 95% CI = 1.16-5.32), no sustained virological response (SVR; HR: 1.91, 95% CI = 1.05-3.45), and baseline cirrhosis (HR: 4.45, 95% CI = 2.07-9.73).
In multiple regression analysis, <i>RASSF1A</i> and <i>E-Cadherin</i> were predictors of HCC within cirrhosis cases, but only <i>E-Cadherin</i> was an independent risk factor for prediction of HCC in cases with low AFP (<i>P</i> = 0.01).<b>Conclusions</b>: The presence of hypermethylated serum <i>RASSF1A, E-Cadherin</i> and <i>RUNX3</i> is linked to HCC in patients with HCV-related cirrhosis.
Finally, we confirmed that the area under the receiver operating characteristic curve (AUC = 0.944) for the combination of AFP and VTN increased more so than for a single glycopeptide (AUC = 0.889 for AFP and 0.792 for VTN) with respect to discriminating between HCC and cirrhosis serum.
Subgroup analysis of CR achievement illuminated that DEB-TACE+RFA disclosed better CR achievement in patients with history of cirrhosis (P <.001), tumor located in right liver (P = .003), bilobar disease (P = .013), tumor size <3.3 cm (P = .001), no portal vein invasion (P = .001), no hepatic vein invasion (P <.001), Child-pugh stage A (P <.001), Barcelona Clinic Liver Cancer (BCLC) stage 0, A-B (P <.001), abnormal alpha-fetoprotein (AFP) (P = .001) and normal AFP (P = .016).
On multivariate analysis, baseline AFP > 5.5 was associated with the presence of cirrhosis (P =0.001), coexisting non-alcoholic steatohepatitis (NASH) (P = 0.035), and GT 1 (P = 0.029).
When samples were grouped according to the serum level of AKR1B10 (≥232.7pg/ml), serum AKR1B10 positively correlated to serum AFP (χ<sup>2</sup>=6.295, P=0.012), ALT (χ<sup>2</sup>=18.803, P=0.000), AST (χ<sup>2</sup>=33.421, P=0.000), tumor nodule number (χ<sup>2</sup>=6.777, P=0.009), cirrhosis (χ<sup>2</sup>=43.458, P=0.000), and tumor size (χ<sup>2</sup>=6.042, P=0.014) in the Chi-square test.
Among the patients who developed HCC, non-SVR patients had significantly higher total bilirubin, higher FIB-4, lower pre-treatment platelet count, higher pre-treatment AFP levels and higher proportion of cirrhosis than SVR patients before occurrence of HCC.
Liver fibrosis (cirrhosis; P = 0.0005), age (≥ 49 years; P = 0.0048), platelet count (≤ 115 × 10/mm<sup>3</sup> ; P = 0.0007), α-fetoprotein (≥ 8.0 ng/mL; P = 0.030), type IV collagen (≥ 200 ng/mL; P = 0.043), fibrosis-4 index (≥ 4.14; P = 0.0006), and human leukocyte antigen (HLA)-DQA1/DRB1-SNP (AA genotype; P = 0.0092) were significantly associated with HCC development according to the log-rank test.
The aim of this study was to determine the role of AFP in HCC surveillance among patients with cirrhosis.<b>Methods:</b> The study population consisted of 392 patients with cirrhosis.
Especially, plasma circSMARCA5 presented a high accuracy (AUC = 0.847, 0.706) for detecting HCC with serum AFP below 200 ng/ml from those hepatitis and cirrhosis with AFP below 200 ng/ml.
These tests enable an algorithm which could improve the performance of the standard surveillance protocol recommended (imaging with or without AFP), limited to patients with cirrhosis.
The panel distinguished HCC from cirrhosis and normal controls, with an area under the receiver operating curve (AUC) of 0.82; this was significantly better than that of AFP (AUC: 0.75).
Additionally, subgroup analysis showed that high THBS4 levels were only associated with poor overall survival for alpha-fetoprotein >40 ng/mL (P = 0.028) and cirrhosis (P = 0.002).
In this pilot study, we assessed serum microRNA (miRNA) expression to distinguish cirrhosis and HCC, alone and in combination with the aminotransferase-to-platelet ratio (APRI), Fibrosis 4 (FIB-4), and alpha-fetoprotein (AFP).
Subgroup analyses showed that a positive ΔCTC was associated with lower survival and higher recurrence among patients with low alpha-fetoprotein levels and cirrhosis (all p < 0.05).
This multicenter study evaluated the Milan, Hangzhou, and AFP model-based criteria for prediction of early recurrence of HCC in patients with cirrhosis who had undergone LT. MATERIAL AND METHODS From the China Liver Transplant Registry (CLTR) database, we analyzed data of 589 HCC patients who had undergone LT between Jan 2015 and Jan 2019.
Lack of reduction in serum alpha-fetoprotein during treatment with direct antiviral agents predicts hepatocellular carcinoma development in a large cohort of patients with hepatitis C virus-related cirrhosis.
The WFA<sup>+</sup> -M2BP marker was superior to AFP in differentiating early-stage HCC (BCLC stages 0 and A) from cirrhosis with AUROC of 0.80 (95% CI, 0.68-0.91; P < 0.001) and 0.73 (95% CI, 0.60-0.86; P = 0.002), respectively.
This panel had a higher diagnostic performance than did α-fetoprotein (AFP) in differentiating HCC from a high-risk population of cirrhosis, such as an area under the receiver-operating characteristic curve of 0.930, 0.892, and 0.807 for the panel versus 0.657, 0.725, and 0.650 for AFP in the discovery set, test set, and cohort 1 of the validation set, respectively.
The area under the curve (AUC) of LysoPC [18:2 (9Z,12Z)], LysoPC (P-16:0), asparaginyl-proline and vaccenic acid in the comparison between HCC and cirrhosis were all increased compared with that of AFP, indicating a more improved diagnosis ability.
In addition, elevated NLR was associated with the presence of tumor vascular invasion (OR 2.35; 95% CI 1.93-2.86), multiple tumors (OR 1.38; 95% CI 1.15-1.66), alpha-fetoprotein ≥ 400 ng/mL (OR 1.51; 95% CI 1.15-1.98), presence of HbsAg (+) (OR 0.68; 95% CI 0.51-0.90), and cirrhosis (OR: 0.59; 95% CI 0.44-0.80).
Compared with 164 non-HCC SVR patients, 22 who developed HCC were older at SVR (P = 0.032), had a higher incidence of diabetes (P = 0.013) and higher pre-antiviral treatment alpha-fetoprotein (AFP) levels (P = 0.016), more had fibrosis stage 3 and cirrhosis (P = 0.0009) and hepatitis B core antibody (anti-HBc) positivity (P = 0.006).
Aim of this work: To determine the numbers of Myeloid-derived suppressor cells (MDSCs) in peripheral blood and ascitic fluid in cirrhosis and HCC and their relation to IFN-γ and α-fetoprotein (α-FP).