Nucleos(t)ide analogs (NUCs) are recommended when both are fulfilled in the absence of hepatocellular carcinoma (HCC) or cirrhosis; (1) elevated serum hepatitis B virus (HBV)-DNA (≥20,000 IU/mL for hepatitis B e antigen-positive chronic hepatitis B [CHB] or ≥2000 IU/mL for hepatitis B e antigen-negative CHB) and (2) serum alanine aminotransferase ≥2× upper limit of normal.<sup>1</sup> Therefore, many patients still remain untreated.
Polymeric immunoglobulin receptor (PIGR) was significantly elevated in both cohorts by 170% in NAFLD and 298% in cirrhosis and was further validated in mouse models.
Because the function of HSCs is known to be modulated by retinoids, we investigated the expression profile of retinoic acid receptor beta (RAR-β) in patients with cirrhosis and HCC, as well as the effects of RAR-β activation in HSCs.
A significant decrease was found in the hepatic expression of the SHH, IHH, and TGF-β1 pathways along with the expression of TAZ in tissue specimens with simple steatosis in comparison with patients affected by NASH cirrhosis and controls.
In the present study, tissue samples from normal liver, cirrhosis and HCC were subjected to differentially gene expression analysis, weighted gene correlation network analysis to identify the twenty hub genes (TOP2A, CDC20, PTTG1, CDCA5, CCNB2, PRC1, KIF20A, SF3B4, HSP90AB1, FOXD2, PLOD3, CCT3, SETDB1, VPS45, SPDL1, RACGAP1, MED24, KIAA0101, ZNF282, and USP21) in the pathological progression from cirrhosis to HCC.
Further, the levels of miR-21 and miR-222 were increased in cirrhosis and HCC but were decreased in FNH and the expression of miR-17-5p, miR-18a, miR-195 and miR-210 was decreased in FNH as compared with cirrhosis and/or HCC.
Outcome variables were: a) liver fibrosis (Metavir score) [fibrosis stage (F0, F1, F2, F3 and F4) and advanced fibrosis and cirrhosis (F ≥ 3 and F4, respectively)]; b) non-invasive indexes [FIB-4, APRI, and their cut-offs (FIB-4 ≥ 3.25 and APRI≥1.5)]; c) inflammation-related biomarkers (leptin, HGF, NGF, sFasL, sFas, MIF, HA, Ang-2, TIMP1, MMP1 and MMP2).
In the present study, tissue samples from normal liver, cirrhosis and HCC were subjected to differentially gene expression analysis, weighted gene correlation network analysis to identify the twenty hub genes (TOP2A, CDC20, PTTG1, CDCA5, CCNB2, PRC1, KIF20A, SF3B4, HSP90AB1, FOXD2, PLOD3, CCT3, SETDB1, VPS45, SPDL1, RACGAP1, MED24, KIAA0101, ZNF282, and USP21) in the pathological progression from cirrhosis to HCC.
Immunohistochemical staining of human liver disease tissue arrays showed that HMGCS2 is abundantly expressed in normal liver tissues but is downregulated in cirrhosis and HCC tissues.
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).
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).
Our data showed that the levels of MEF2A, C, and D proteins were high in liver tissues from patients with cirrhosis and increased during culture-induced activation of primary H-HSCs.
High levels of TRAIL, adiponectin and, sclerostin after bile duct ligation, suggest that these factors may have some roles in bone loss after cirrhosis.
HNF1A mutations in carcinomas were associated with negative viral hepatitis status (p = .004), mutually exclusive with catenin beta-1 (CTNNB1) hotspot mutations, and trended to occur more in females (p = .06) and without cirrhosis (p = .03).