epidermal-growth-factor and Hepatitis-C

The epidermal growth factor (EGF) rs4444903 polymorphism is associated with aberrant expression of EGF, which was a characteristic of cirrhotic liver diseases, induces highly malignant hepatocellular carcinoma (HCC). Numerous studies have uncovered the association of this polymorphism with the risk of liver disease, but with inconsistent findings.. Therefore, this meta-analysis was performed to evaluate whether EGF rs4444903 polymorphism conferred susceptibility to liver disease. Totally 18 eligible articles were identified by searching PubMed, Google, CNKI and EMBASE up to December 1, 2020.. Our results indicated that there was no significant difference in the minor G allele frequency of rs4444903 polymorphism between HBV/HCV carriers and healthy controls. In other words, EGF rs4444903 polymorphism was not associated with the risk of HBV/HCV. Interestingly, this polymorphism increased the risk of liver cirrhosis in the controls with HCV infection. Additionally, EGF rs4444903 polymorphism is associated with the increased risk of HCC under the five models. Subgroup analysis by ethnicity shows that rs4444903 polymorphism intensifies the risk of HCC among Asians and Caucasians. Strong correlation is also reported in controls with cirrhosis or HCV infection and studies using PCR-RFLP genotyping.. The study supports that EGF rs4444903 polymorphism is a genetic contributor to liver cirrhosis and HCC in the overall population. Nevertheless, this conclusion must be confirmed by larger studies with more diverse ethnic populations.

Topics: Carcinoma, Hepatocellular; Epidermal Growth Factor; Genetic Predisposition to Disease; Hepatitis B virus; Hepatitis C; Humans; Liver Cirrhosis; Liver Neoplasms

Topics: Animals; Apoptosis; Carcinoma, Hepatocellular; Epidermal Growth Factor; fas Receptor; Heparin-binding EGF-like Growth Factor; Hepatitis C; Humans; Intercellular Signaling Peptides and Proteins; Liver Diseases; Mice; Signal Transduction

Topics: Animals; Apoptosis; Epidermal Growth Factor; Fas Ligand Protein; fas Receptor; Heparin-binding EGF-like Growth Factor; Hepatitis C; Humans; Intercellular Signaling Peptides and Proteins; Liver; Liver Neoplasms; Membrane Glycoproteins

Novel direct-acting antivirals (DAAs) have completely changed the panorama of hepatitis C due to their high efficacy and optimal safety profile. Unfortunately, an unexpectedly high rate of early recurrence of hepatocellular carcinoma has been reported within weeks of starting treatment, but the mechanism is not known.. We monitored the serum level of vascular endothelial growth factor (VEGF) and changes in the pattern of circulating interleukins in 103 chronic hepatitis C patients during antiviral treatment with DAA-regimens. VEGF, epidermal growth factor (EGF), and several interleukins were assessed at baseline, during treatment, and after treatment. The biological effect of DAA-treated patient serum on human umbilical vein endothelial cell (HUVEC) proliferation was also confirmed.. After 4 weeks of therapy, VEGF increased approximately 4-fold compared to baseline, remained elevated up to the end of treatment, and returned to the pre-treatment level after the end of therapy. In contrast, interleukin-10 and tumor necrosis factor-alpha significantly decreased during therapy, which was coincident with HCV clearance. The levels of both remained low after treatment. The addition of serum from patients collected during therapy induced HUVEC proliferation; however, this disappeared after the end of therapy.. DAA administration induces an early increase in serum VEGF and a change in the inflammatory pattern, coinciding with HCV clearance. This may alter the balance between inflammatory and anti-inflammatory processes and modify the antitumor surveillance of the host. Fortunately, such modifications return reverse to normal after the end of treatment.

Topics: Adult; Aged; Aged, 80 and over; Antiviral Agents; Cell Proliferation; Epidermal Growth Factor; Female; Hepacivirus; Hepatitis C; Human Umbilical Vein Endothelial Cells; Humans; Inflammation; Interleukin-10; Male; Middle Aged; Neoplasms; Tumor Necrosis Factor-alpha; Vascular Endothelial Growth Factor A

Topics: Antiviral Agents; Epidermal Growth Factor; Hepacivirus; Hepatitis C; Humans; Inflammation; Ligands

Earlier, we reported a highly statistically significant association between T-helper 1 (Th1) and Th2 cytokine genotypes and hepatocellular carcinoma (HCC) risk among natives of southern Guangxi, China, a hyperendemic region for HCC. Epidermal growth factor (EGF) plays a critical role in malignant transformation of hepatocytes and tumor progression. A polymorphism in the EGF gene (61A > G) results in elevation of EGF in liver tissues and blood. Epidemiological data are sparse on the possible association between EGF genetic polymorphism and HCC risk.. The EGF 61A > G polymorphism, multiple Th1 and Th2 genotypes, and environmental risk factors for HCC were determined on 117 HCC cases and 225 healthy control subjects among non-Asians of Los Angeles County, California, a low-risk population for HCC, and 250 HCC cases and 245 controls of southern Guangxi, China.. Following adjustment for all known or suspected HCC risk factors, non-Asians in Los Angeles who possessed at least one copy of the high activity 61*G allele of the EGF gene showed a statistically non-significant, 78% increased risk of HCC compared with those possessing the EGF A/A genotype. This EGF-HCC risk association significantly strengthened among heavy users of alcohol [odds ratio (OR) = 3.44, 95% confidence interval (CI) = 0.93-12.76, P = 0.065)], and among individuals carrying the high-risk Th1/Th2 genotypes for HCC (OR = 3.34, 95% CI = 1.24-9.03, P = 0.017). No association between EGF genotype and HCC risk was observed among Chinese in southern Guangxi, China.. Genetic polymorphism in the EGF gene resulting in elevated level of EGF, may contribute to HCC risk among low-risk non-Asians in Los Angeles.

Topics: Adult; Aged; Alcohol-Related Disorders; Carcinoma, Hepatocellular; Case-Control Studies; China; Epidermal Growth Factor; Female; Genotype; Hepatitis B; Hepatitis C; Humans; Incidence; Liver Neoplasms; Los Angeles; Male; Middle Aged; Polymorphism, Single Nucleotide; Prevalence; Risk Factors; Smoking; Th1 Cells; Th2 Cells