Study of Serum Soluble Programmed Death Ligand 1 as a Prognostic Factor in Hepatocellular Carcinoma in Egyptian Patients

2019 ◽  
Vol 19 (11) ◽  
pp. 896-905 ◽  
Author(s):  
Fatma El-Gebaly ◽  
Sabry Abou-saif ◽  
Mahmoud Elkadeem ◽  
Amal Helmy ◽  
Sherief Abd-Elsalam ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cirrhosis ◽  
Vascular Invasion ◽  
Study Groups ◽  
Prognostic Indicator ◽  
High Serum ◽  
Soluble Form ◽  
Tumor Immune Evasion ◽  
Programmed Death ◽  
Increased Risk

Background: The expression of programmed cell death ligands on tumor cells has a role in the suppression of antitumor immunity, resulting in tumor immune evasion. Objective: In this study, we evaluated the prognostic value of the soluble form of programmed death-ligand1 (sPD-L1) in Egyptian hepatocellular carcinoma (HCC) patients. Methods: This prospective cohort study was performed between November 2016 to November 2018 on 85 individuals (25 HCC patients, 25 HCC with vascular invasion and/or extrahepatic metastasis, 25 patients with liver cirrhosis, 10 healthy controls). The levels of sPD-L1 were determined in all subjects and compared in different groups and stages of cirrhosis and HCC. The association between sPD-L1 levels and overall survival (OS) was assessed. Results: Significant statistical difference in sPD-L1 was detected between different study groups. The cut-off value for normal sPD-L1 was defined by high sPD-L1 levels determined in a healthy control cohort. It was 2.522 ng/ml. In HCC patients, cut-off value was 7.42 ng/ml (sensitivity 88%, specificity 100%). In HCC with vascular invasion or metastasis, cut–off value was 9.62 ng/ml (sensitivity 88%, specificity 88%). Patients with high serum sPD-L1 or serum bilirubin concentrations had an increased risk of mortality. Conclusion: High sPD-L1 level could be a possible prognostic indicator for a poor outcome in liver cirrhosis and HCC patients. The predictive value of sPD-L1 levels for a successful anti- PD1/PD-L1 therapy should be investigated in the future.

scholarly journals Follow-Up Liver Stiffness Measurements after Liver Resection Influence Oncologic Outcomes of Hepatitis-B-Associated Hepatocellular Carcinoma with Liver Cirrhosis

Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 425 ◽  
Author(s):  
Jung Lee ◽  
Hyun Lee ◽  
Seung Kim ◽  
Sang Ahn ◽  
Kwan Lee
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cirrhosis ◽  
Hepatitis B ◽  
Antiviral Therapy ◽  
Liver Stiffness ◽  
Late Recurrence ◽  
Oncologic Outcomes ◽  
Increased Risk ◽  
Hcc Recurrence

The severity of liver fibrosis can be noninvasively evaluated by measuring liver stiffness (LS) using transient elastography. This study aimed to evaluate the prognostic value of achieving low liver stiffness measurement (LSM) in patients with cirrhosis confirmed from the resected liver due to hepatocellular carcinoma (HCC). A total of 184 patients that received curative surgery for HCC related to the hepatitis B virus at Barcelona Clinic Liver Cancer stage 0–A, and had a METAVIR fibrosis score of 4 were investigated. LSM significantly decreased after antiviral therapy during follow-up (p = 0.001), and achieving LSM ≤8 kilopascal (kPa) suggested a reduced risk of late recurrence (>12 months) (hazard ratio (HR), 0.519; 95% confidence interval (CI), 0.307–0.877; p = 0.014). Older age at surgery (≥45 years) and multiple HCC nodules predicted an increased risk of late recurrence (HR, 3.270; 95% CI, 1.296–8.251; p = 0.012; and HR, 3.146; 95% CI, 1.396–7.089; p = 0.006). Decreased LSM also suggested decreased mortality (HR, 0.251; 95% CI, 0.086–0.756; p = 0.045) along with baseline low aspartate aminotransferase-to-platelet ratio index (APRI) score (<1.5) (HR, 0.251; 95% CI, 0.086–0.759; p = 0.041). Having early HCC recurrence (HR, 9.416; 95% CI, 3.566–24.861; p < 0.001) and microvascular tumor invasion (HR, 3.191; 95% CI, 1.188–8.568; p = 0.021) predicted increased mortality. Among HCC patients with liver cirrhosis under antiviral therapy, achieving low LSM (≤8 kPa) predicted reduced late HCC recurrence.

scholarly journals Segmental Distribution of Hepatocellular Carcinoma Correlates with Microvascular Invasion in Liver Explants Undergoing Transplantation

2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Yasir Al-Azzawi ◽  
Eva Rouanet ◽  
Ryan J. Hendrix ◽  
Lidia Spaho ◽  
Hesham Malik ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Transplantation ◽  
Vascular Invasion ◽  
Retrospective Chart Review ◽  
Microvascular Invasion ◽  
Poor Prognostic Factor ◽  
Vein Thrombosis ◽  
Increased Risk ◽  
Common Etiology ◽  
Segment 8

Introduction. Microvascular invasion (MVI) in hepatocellular carcinoma (HCC) patients is a poor prognostic factor after liver transplantation and/or resection. Any correlation between MVI and segmental location of HCC has yet to be studied. Our aim is to evaluate the segmental location of HCC and any correlation with the presence of MVI, portal vein thrombosis (PVT) in explanted livers, and the recurrence of HCC after transplantation. Another objective of the study is to assess the treatment history (ablation or transarterial chemoembolization (TACE)) and size of the tumor with respect to the risk of MVI. Methods. A single center, retrospective chart review, including 98 HCC patients, aged 18 years and older who had liver transplantation in our institute between 2012 and 2017. We reviewed the radiological images of the HCC tumors, the pathological findings of the explanted livers, and the follow-up imaging after transplantation. Results. 98 patients with the diagnosis of HCC underwent liver transplantation between 2012 and 2017. The mean age of the cohort was 63 ± 8.2. Males represented 75% and Caucasian race represented 75% of the cohort. The most common etiology of cirrhosis was chronic hepatitis C virus infection followed by alcohol abuse and nonalcoholic steatohepatitis (NASH) with percentages of 50%, 23%, and 10%, respectively. Microvascular invasion was found in 16% of the patients while PVT and the recurrence of HCC were found in 17% and 6 % of the cohort, respectively. MVI was found in 10 single HCC and 6 multifocal HCC. Right lobe HCC had more MVI when compared to the left and multilobar HCC, with percentages of 11%, 2%, and 3%, respectively. Localization of HCC in segment 8 was associated with the highest percentage of MVI when compared to all other segments. The risk of MVI in segment 8 HCC was 3.5 times higher than the risk from the other segments (p=0.002) while no vascular invasion was found in segments 1, 3, and 5. The risk of vascular invasion in untreated HCC is 3 times the risk in treated HCC (P=0.03). Conclusion. Our data indicate that the risk of microvascular invasion is highest in tumors localized to segment 8. The size and number of HCC tumors were not associated with an increased risk of microvascular invasion.

scholarly journals Aberrant p16INK4A methylation: Relation to viral related chronic liver disease and hepatocellular carcinoma

2014 ◽  
Vol 03 (01) ◽  
pp. 001-004 ◽  
Author(s):  
Fatma A. El-Mougy ◽  
Mohammed M. Youssef ◽  
Dalia A. Omran ◽  
Sahar A. Sharaf ◽  
Hany H. El-Sayed ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Healthy Volunteers ◽  
Study Groups ◽  
Suppressor Gene ◽  
High Serum ◽  
Aberrant Methylation ◽  
Chi Square ◽  
Exact Test ◽  
The Status ◽  
Cirrhotic Patients

Abstract Background: Hepatocellular carcinoma (HCC) is currently the fifth most common solid tumor worldwide and the third leading cause of cancer related deaths. Several studies have shown that the tumor suppressor gene p16INK4A is frequently downregulated by aberrant methylation of the 5′-cytosine-phosphoguanine island within the promoter region. Aim: To find out the frequency of methylated p16INK4A in the peripheral blood of HCC and cirrhotic patients and to evaluate its role in hepatocarcinogenesis. Patients and Methods: This study was performed on 58 subjects: 30 HCC patients, 20 cirrhotic patients, and eight healthy volunteers. Methylation of p16INK4A was examined using methylation specific polymerase chain reaction (PCR) (MSP). Comparison of quantitative variables between the study groups was done using Mann-Whitney U test for independent samples when not normally distributed. For comparing categorical data, Chi-square (χ2 ) test was performed. Exact test was used instead when the expected frequency was less than 5. Results: Methylation of p16INK4A was found in 6.7% of HCC patients, 5% of liver cirrhosis (LC) patients, and none of the healthy volunteers; 66.67% of the p16INK4A-methylated cases (2/3) were positive for anti-hepatitis C virus (HCV) antibodies (one of them had HCC). All HCC cases with aberrant p16INK4A methylation show very high serum alpha fetoprotein (AFP) level (9,080; 30,000 μg/mL). There were no significant associations between the status of p16INK4A methylation and tumor size. Conclusion: Hypermethylation of p16INK4A was found to be infrequent among Egyptian patients with HCC.

Effect of MCP-1 and CCR2 Genes Polymorphism on Development of Hepatocellular Carcinoma in HCV- Infected Patients in Sohag Governorate, Egypt

2020 ◽  
Vol EJMM29 (4) ◽  
pp. 125-134
Author(s):  
Asmaa Nasr El-Din ◽  
Ghada M. Galal ◽  
Ahmed Abudeif ◽  
Marwa S. Hashem ◽  
Abeer Sheneef
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cirrhosis ◽  
Real Time ◽  
Tumor Cells ◽  
Real Time Pcr ◽  
Primary Tumor ◽  
High Serum ◽  
Tumor Associated Macrophage ◽  
Common Cancer ◽  
The World

Background: HCC is the most common primary tumor of the liver .It is the fifth common cancer in men and the eighth common in women and is the second leading cause of cancer-related death in the world. The MCP-1 is a chemokine and a potent chemotactic factor for monocytes. MCP-1 expression in tumor cells is significantly linked to the extent of tumor-associated macrophage infiltration. Objectives: to detect the effect of MCP-1 and CCR2 Genes Polymorphism in development of HCC in HCV- related liver cirrhosis patients. Methodology: MCP-1-2518 A/G and CCR2 (V64Ile) genes polymorphism was assessed by real time PCR in 35 HCC patients and 30 HCV related LC. Serum MCP-1 was measured by ELISA. Results: For MCP-1 -2518 A G gene, HCC patients had a higher frequency of AG and GG genotypes than of AA genotype compared to other groups. For CCR2 (V64Ile), HCC patients had a higher frequency of GA and AA genotypes than GG genotype compared to other groups. Conclusion: There is a significant association between CCR2 (V64Ile) polymorphism, high serum MCP-1 level and HCC development in HCV- related liver cirrhosis patients.

The role of chemokine CC ligand 20 in patients with liver cirrhosis and hepatocellular carcinoma

2012 ◽  
Vol 27 (2) ◽  
pp. 125-131 ◽  
Author(s):  
Hanan H. Soliman ◽  
Hala Nagy ◽  
Nesreen Kotb ◽  
Mohamed A. Alm El-Din
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cirrhosis ◽  
Predictive Value ◽  
Serum Levels ◽  
Study Groups ◽  
Cross Sectional Study ◽  
Cross Sectional ◽  
Asymptomatic Patients ◽  
Group I

Background and aim To evaluate the role of chemokine CC ligand 20 (CCL20) as a biomarker for hepatocellular carcinoma (HCC). Patients and methods Ninety patients in four groups were enrolled in this prospective cross-sectional study: 30 with HCC (group I), 30 with liver cirrhosis (group II), 15 with hepatitis C virus infection (group III), and 15 healthy blood donors as controls. Alpha fetoprotein (AFP), CCL20 and vascular endothelial growth factor (VEGF) were measured in all groups. Results Serum levels of CCL20 were significantly different among the study groups (F=230.979, p<0.001). The highest level was found in HCC patients (57.305 ± 6.386 pg/mL) followed by patients with cirrhosis (45.999 ± 5.165 pg/mL) compared with 22.781 ± 5.986 pg/mL and 18.585 ± 3.554 pg/mL in asymptomatic patients with HCV infection and controls, respectively. In HCC patients, CCL20 significantly correlated with VEGF (r=0.559, p=0.001), AFP (r=0.814, p<0.001), Child score (r=0.748, p<0.001), and tumor size (r=0.825, p<0.001). The cutoff value of CCL20 for the detection of HCC in HCV-infected patients was 54 pg/mL with 93.1% accuracy, 89.6% negative predictive value, 92.6% positive predictive value, 83.3% sensitivity, and 93.3% specificity. In patients with cirrhosis, CCL20 significantly correlated with VEGF (r=0.455, p=0.011), AFP (r=0.975, p<0.001), and Child score (r=0.977, p<0.001). Conclusion CCL20 may be used for the detection of HCC in HCV-infected patients with comparable specificity and higher sensitivity than AFP.

scholarly journals Relation between GSTP1 polymorphism and oxidative stress in patients with hepatocellular carcinoma

2020 ◽  
Vol 32 (1) ◽  
Author(s):  
Shaimaa Gamal Hassan Elofey ◽  
Nevine F. Shafik ◽  
Noha Hassan Radwan ◽  
Osman Mohammed Mansour ◽  
Rasha Mahmoud Allam ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Normal Control ◽  
Predictive Value ◽  
Area Under The Curve ◽  
High Serum ◽  
Assessment Model ◽  
Control Group ◽  
Increased Risk ◽  
Sensitivity Specificity

Abstract Background Glutathione can reduce the oxidative stress by converting the unstable to stable molecules and its status in hepatocellular carcinoma (HCC) is correlated with tumor growth and metastasis. Glutathione S-transferase Pi (GSTP1) is reported to detoxify the xenobiotic substrates by catalyzing their conjugation to reduced glutathione (GSH) and its over-expression was demonstrated in the early stages of HCC, while loss of GSTP1 has been suggested to increase the risk of deoxyribonucleic acid (DNA) damage and mutation. The aim of this study is to assess the relationship of GSTP1 polymorphism Ile105Val (rs1695 A > G) with HCC risk, and to investigate the oxidative stress status of HCC patients by measuring the antioxidant glutathione (GSH) levels. This study was conducted on 99 newly diagnosed HCC patients and 80 apparently healthy individuals as a normal control group. All participants were subjected to the measurement of plasma GSH levels according to Ellman’s method, and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) for the detection of GSTP1 polymorphismIle105Val (rs1695 A > G). Results The occurrence of either the mutant homozygous or the mutant heterozygous genotype of GSTP1 was significantly higher in HCC patients, while the occurrence of the wild genotype was significantly higher among the normal control subjects. Mutant GSTP1 genotype, older age, male gender, and high serum alanine aminotransferase (ALT) were associated with increased risk of development of HCC. The best sensitivity, specificity, PPV (positive predictive value), NPV (negative predictive value), and overall diagnostic performance for plasma GSH at a cutoff level of 2003.5 μM/mg were 57.6%, 52.5%, 60%, and 40%. The area under the curve for GSH was 0.562. Conclusion Mutant GSTP1 genotype was an independent prognostic factor for increased HCC risk which can be used in a risk assessment model for HCC. Plasma GSH presents insufficient sensitivity and specificity for HCC.

scholarly journals Cancer-Associated Thrombosis in Cirrhotic Patients with Hepatocellular Carcinoma

Cancers ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 450 ◽  
Author(s):  
Alberto Zanetto ◽  
Elena Campello ◽  
Luca Spiezia ◽  
Patrizia Burra ◽  
Paolo Simioni ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cirrhosis ◽  
Common Knowledge ◽  
Significant Risk ◽  
Fibrinogen Concentration ◽  
Increased Risk ◽  
Venous Thromboembolic ◽  
Systemic Factors ◽  
Frequent Site ◽  
Cancer Associated Thrombosis

It is common knowledge that cancer patients are more prone to develop venous thromboembolic complications (VTE). It is therefore not surprising that patients with hepatocellular carcinoma (HCC) present with a significant risk of VTE, with the portal vein being the most frequent site (PVT). However, patients with HCC are peculiar as both cancer and liver cirrhosis are conditions that can perturb the hemostatic balance towards a prothrombotic state. Because HCC-related hypercoagulability is not clarified at all, the aim of the present review is to summarize the currently available knowledge on epidemiology and pathogenesis of non-malignant thrombotic complications in patients with liver cirrhosis and HCC. They are at increased risk to develop both PVT and non-splanchnic VTE, indicating that both local and systemic factors can foster the development of site-specific thrombosis. Recent studies have suggested multiple and often interrelated mechanisms through which HCC can tip the hemostatic balance of liver cirrhosis towards hypercoagulability. Described mechanisms include increased fibrinogen concentration/polymerization, thrombocytosis, and release of tissue factor-expressing extracellular vesicles. Currently, there are no specific guidelines on the use of thromboprophylaxis in this unique population. There is the urgent need of prospective studies assessing which patients have the highest prothrombotic profile and would therefore benefit from early thromboprophylaxis.

Close Association between High Serum ALT and More Rapid Recurrence of Hepatocellular Carcinoma in Hepatectomized Patients with HCV-Associated Liver Cirrhosis and Hepatocellular Carcinoma

Intervirology ◽  
2000 ◽  
Vol 43 (1) ◽  
pp. 20-26 ◽  
Author(s):  
Kazuo Tarao ◽  
Yasushi Rino ◽  
Shoji Takemiya ◽  
Setsuo Tamai ◽  
Shinichi Ohkawa ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cirrhosis ◽  
Close Association ◽  
High Serum
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