Indeed, recurrence was clinicopathologically associated with two host factors, serum albumin levels and HCV infection in our training cases (Table 1), suggesting that multicentric recurrence was dominant for the patients with chronic liver damages.18 Therefore, the assessment of noncancerous background tissue should reflect clinical outcomes that are not restricted to tumor progression.19, 20 BYL719 ic50 Our retrospective study indicated that the noncancerous gene expression of CYP1A2, CNDP1, and OAT was significantly associated with recurrence

(Table 1). The variable-selection procedure revealed the noncancerous CYP1A2 gene as the best predictive model for the recurrence of HCC, but not including the cancer-derived genes (Table 1).

Further prospective, multicenter study validated that noncancerous CYP1A2 expression was identified as a unique biomarker for the prediction of recurrence after the curative resection of early-stage HCC (Table 3). Using tissue microarrays, CYP1A2 showed significant negative correlation with the cumulative recurrence-free rates (Fig. 3). CYP1A2 is a major form of hepatic cytochorme P450 oxidative system, which is involved in drug metabolism and cholesterol synthesis.17 Decreased expression of hepatic CYP1A2 was known to be significantly correlated with fibrotic progression of hepatitis C patients21 and pathological progress of nonalcoholic Everolimus cell line fatty liver disease.22 Barker et al. reported previously that CYP1A2 was down-regulated dramatically by oxidative stress in hepatocytes, indicating CYP1A2 as a specific surrogate marker of hepatic oxidative damage.23 According to knockout mice analysis by Shertzer et al., oxidative stress was significantly elevated in the liver microsomes of CYP1A2-knockout mice, compared to those

of wild-type or CYP1A1-knockout mice.24 In this regard, CYP1A2 may be considered not only a biomarker of oxidative stress, but also an antioxidant enzyme. The other noncancerous candidates, CNDP1 medchemexpress and OAT, might also be associated with oxidative stress by the modulation of amino acids carnosine15 and ornithine.16 Oxidative stress is known to induce DNA damage, and accumulation of such genetic damage can eventually lead to hepatocarcinogenesis.25 To evaluate the biological pathways associated with CYP1A2 expression, we utilized GSEA on the gene-expression profiles of the noncancerous liver tissues.14 GSEA can directly analyze the changes of gene-expression levels as continuous variables.26 According to our GSEA assessment, the gene sets of peroxisome and oxidoreductase activity were significantly correlated with CYP1A2 expression levels (Fig. 4). The peroxisome is an organelle that participates not only in the generation of reactive oxygen species, but also in cell rescue from the damaging effects of such oxidative radicals.

Acceptability Cabozantinib solubility dmso of such screening influenced by knowledge, perception and attitude of the people. The study was conducted to determine the knowledge, perception and attitude of Indonesia people toward CRC screening. Aim: this study are assessing the knowledge perception

and attitudes with regard to colorectal cancer screening. Method: Cross sectional study with an interview-based population survey carried out in adult ages 30-79 years old, the instrument was structured questionnaires consisting 9 chapters. This survey collected from health center in Depok and hospital in Sumatera and Java. Result: the result from 809 respondents collected indicates that there are 478 (59, 1%) female, 459 (56,7%) age >=50 years old, 611 (75,5%) high educated, 681 (84,2%) married, 458(56,6%) worked and 440 (54,4%) had income this website > 1 million, 76 (9.4%) done cancer colorectal screening, 25 (26.6%) good knowledge, 34 (7.6%) had a positive perception and 76 (17.1%)

positive attitude and 74 (13,9%) respondent from hospital. Chi square analysis, respondent whom less knowledge have odds ratio 34,3

(95% CI ,12,7-92,5; P<0,0001) and respondent from hospital done CRC screening have odds ratio 22,34 (95% CI 5,442-91,22; P<0,0001). Conclusion: The knowledge, perception and attitude on colorectal cancer screening test still low in Indonesian people. Key Word(s): 1. CRC screening; 2. knowledge; 3. perception; attitude Presenting Author: RUPAM MCE BHATTACHARYYA Additional Authors: G. LONGCROFT-WHEATON, P. BHANDARI Affiliations: Queen Alexandra Hospital, Portsmouth, United Kingdom Introduction: ESD enables en-bloc resection reducing recurrence rates, but is technically challenging with high complication rates and hence not widely practiced in the West. We have used a novel Knife Assisted Resection (KAR) technique. We aim to evaluate the outcome of KAR in treatment of large and refractory colonic polyps and identify polyp features that predict complications and recurrence after KAR. Methods: Cohort study of patients referred to our centre.

Acceptability Selleck Opaganib of such screening influenced by knowledge, perception and attitude of the people. The study was conducted to determine the knowledge, perception and attitude of Indonesia people toward CRC screening. Aim: this study are assessing the knowledge perception

and attitudes with regard to colorectal cancer screening. Method: Cross sectional study with an interview-based population survey carried out in adult ages 30-79 years old, the instrument was structured questionnaires consisting 9 chapters. This survey collected from health center in Depok and hospital in Sumatera and Java. Result: the result from 809 respondents collected indicates that there are 478 (59, 1%) female, 459 (56,7%) age >=50 years old, 611 (75,5%) high educated, 681 (84,2%) married, 458(56,6%) worked and 440 (54,4%) had income GDC-0973 datasheet > 1 million, 76 (9.4%) done cancer colorectal screening, 25 (26.6%) good knowledge, 34 (7.6%) had a positive perception and 76 (17.1%)

positive attitude and 74 (13,9%) respondent from hospital. Chi square analysis, respondent whom less knowledge have odds ratio 34,3

(95% CI ,12,7-92,5; P<0,0001) and respondent from hospital done CRC screening have odds ratio 22,34 (95% CI 5,442-91,22; P<0,0001). Conclusion: The knowledge, perception and attitude on colorectal cancer screening test still low in Indonesian people. Key Word(s): 1. CRC screening; 2. knowledge; 3. perception; attitude Presenting Author: RUPAM MCE公司 BHATTACHARYYA Additional Authors: G. LONGCROFT-WHEATON, P. BHANDARI Affiliations: Queen Alexandra Hospital, Portsmouth, United Kingdom Introduction: ESD enables en-bloc resection reducing recurrence rates, but is technically challenging with high complication rates and hence not widely practiced in the West. We have used a novel Knife Assisted Resection (KAR) technique. We aim to evaluate the outcome of KAR in treatment of large and refractory colonic polyps and identify polyp features that predict complications and recurrence after KAR. Methods: Cohort study of patients referred to our centre.

PKCs mediate effects by phosphorylating their substrates. Myristoylated alanine-rich C kinase substrate (MARCKS) is one such substrate and plays a key role in cytoskeletal dynamics.11, 12 MARCKS BAY 73-4506 research buy is an F-actin crosslinking protein and is phosphorylated by cPKCα, PKCδ, and PKCϵ in vitro.13, 14 Phosphorylation of MARCKS by PKCδ and PKCϵ has been shown to be involved in exocytosis and endocytosis

in nonhepatic cells. Thus, MARCKS phosphorylation by PKCδ is involved in airway mucin secretion15, 16 and gut peptide secretion.17 MARCKS phosphorylation by PKCϵ has been shown to stimulate vesicle translocation in chromaffin cells18 and basolateral fluid-phase endocytosis in T84 cells.19 Phosphorylation of MARCKS by PKCs results

in the retrieval of MARCKS from the plasma membrane (PM) to the cytosol and in F-actin disassembly.18 It may be noted that actin plays an important role in hepatobiliary transporter translocation20-22 and that TLC induces F-actin accumulation around bile canaliculi.23 Phosphorylation of MARCKS by PKCs requires the translocation of PKCs to MARCKS located in the PM, and as a result, MARCKS phosphorylation and the consequent effect are dependent on subcellular targeting of PKC.24, 25 These studies raise the possibility that TLC-induced endocytic retrieval of Mrp2 may result from PKCϵ-dependent MARCKS phosphorylation. In the present study, we determined whether TLC-induced MRP2 retrieval is mediated via PKCϵ and whether the effect of PKCϵ is mediated Erlotinib cell line via MARCKS phosphorylation. The results of our studies with dominant-negative (DN)–PKCϵ and phosphorylation-deficient (PD)–MARCKS in HuH7 cells stably transfected with sodium taurocholate cotransporting polypeptide (HuH-NTCP cells) are consistent with the following signaling pathway: TLC PKCϵ MARCKS phosphorylation MRP2 retrieval. 8-(4-Chlorophenylthio)–cyclic

adenosine monophosphate (CPT-cAMP), wortmannin, and the antibody for human MRP2 were purchased from Sigma-Aldrich (St. Louis, MO). The commercial sources of other antibodies were Cell Signaling [phosphorylated MCE公司 myristoylated alanine-rich C kinase substrate (pMARCKS) and hemagglutinin (HA)], Calbiochem (actin), Clontech [green fluorescent protein (GFP)], Upstate (PKCϵ), and BD Transduction Laboratories (E-cadherin). Sulfosuccinimidyl-6-(biotin-amido)hexanoate was purchased from Pierce (Rockford, IL). Streptavidin beads were purchased from Novagen (Madison, WI). Lipofectamine 2000 was obtained from Invitrogen (Carlsbad, CA). Plasmid constructs for wild-type (WT)–MARCKS and PD-MARCKS (with the effector domain phosphorylation sites at S152, S156, and S163 replaced by alanine) were kind gifts from Dr. Saito.26 Kinase-dead DN-PKCϵ plasmids were purchased from Addgene (Cambridge, MA).

PKCs mediate effects by phosphorylating their substrates. Myristoylated alanine-rich C kinase substrate (MARCKS) is one such substrate and plays a key role in cytoskeletal dynamics.11, 12 MARCKS Transmembrane Transporters modulator is an F-actin crosslinking protein and is phosphorylated by cPKCα, PKCδ, and PKCϵ in vitro.13, 14 Phosphorylation of MARCKS by PKCδ and PKCϵ has been shown to be involved in exocytosis and endocytosis

in nonhepatic cells. Thus, MARCKS phosphorylation by PKCδ is involved in airway mucin secretion15, 16 and gut peptide secretion.17 MARCKS phosphorylation by PKCϵ has been shown to stimulate vesicle translocation in chromaffin cells18 and basolateral fluid-phase endocytosis in T84 cells.19 Phosphorylation of MARCKS by PKCs results

in the retrieval of MARCKS from the plasma membrane (PM) to the cytosol and in F-actin disassembly.18 It may be noted that actin plays an important role in hepatobiliary transporter translocation20-22 and that TLC induces F-actin accumulation around bile canaliculi.23 Phosphorylation of MARCKS by PKCs requires the translocation of PKCs to MARCKS located in the PM, and as a result, MARCKS phosphorylation and the consequent effect are dependent on subcellular targeting of PKC.24, 25 These studies raise the possibility that TLC-induced endocytic retrieval of Mrp2 may result from PKCϵ-dependent MARCKS phosphorylation. In the present study, we determined whether TLC-induced MRP2 retrieval is mediated via PKCϵ and whether the effect of PKCϵ is mediated Selleck ABT 888 via MARCKS phosphorylation. The results of our studies with dominant-negative (DN)–PKCϵ and phosphorylation-deficient (PD)–MARCKS in HuH7 cells stably transfected with sodium taurocholate cotransporting polypeptide (HuH-NTCP cells) are consistent with the following signaling pathway: TLC PKCϵ MARCKS phosphorylation MRP2 retrieval. 8-(4-Chlorophenylthio)–cyclic

adenosine monophosphate (CPT-cAMP), wortmannin, and the antibody for human MRP2 were purchased from Sigma-Aldrich (St. Louis, MO). The commercial sources of other antibodies were Cell Signaling [phosphorylated 上海皓元 myristoylated alanine-rich C kinase substrate (pMARCKS) and hemagglutinin (HA)], Calbiochem (actin), Clontech [green fluorescent protein (GFP)], Upstate (PKCϵ), and BD Transduction Laboratories (E-cadherin). Sulfosuccinimidyl-6-(biotin-amido)hexanoate was purchased from Pierce (Rockford, IL). Streptavidin beads were purchased from Novagen (Madison, WI). Lipofectamine 2000 was obtained from Invitrogen (Carlsbad, CA). Plasmid constructs for wild-type (WT)–MARCKS and PD-MARCKS (with the effector domain phosphorylation sites at S152, S156, and S163 replaced by alanine) were kind gifts from Dr. Saito.26 Kinase-dead DN-PKCϵ plasmids were purchased from Addgene (Cambridge, MA).

A jejunal Roux limb is required for anastomosis of the other graft duct. (iv) The two graft ducts are connected to one single large recipient duct in two anastomoses.

The recipient duct is partially sutured in its middle part and specifically fashioned to accommodate two graft ducts separately. This “2-to-1 reconstruction” is used when the distance between the two graft ducts is bigger than the diameter of the smaller duct opening and when there is only one recipient duct opening, with a size big enough for two graft ducts. Technical flaw has been considered a factor in the formation of BAS. A study reported a 2.5-time reduction of the rate of BAS after LDLT to 7% (with only 2.5% of the BAS cases requiring intervention) with the routine use of microsurgical BR.[24, 43] This reflects that technical flaw may be a contributing factor in the formation of http://www.selleckchem.com/products/abt-199.html BAS. The involvement of microvascular surgeons may also be beneficial. In addition, choice of suture for anastomosis could be another factor but research is needed to verify see more which suture material is better.[43, 44] However, not all transplant centers have the same availability of expertise. Endoscopic retrograde cholangiography (ERC) with balloon dilatation

is the most common treatment for BAS after DDA.[22, 45] The success rate of the treatment can be as high as 73.2%.[22] Among various factors that decide success of treatment, morphology of stricture is the most influential

one, and pouched strictures are the most difficult type. Hsieh et al.[23] reported that ERC with balloon dilatation followed by maximal stent placement resulted in a 100% success rate in the treatment of BAS after DDA on an intention-to-treat analysis. However, this result is not reproducible and is not applicable in certain situations. Sometimes the graft bile 上海皓元 duct above the stricture is not distended enough or the stricture is too tight for stent insertion. In fact, the endoscopic means cannot produce a good result for a long and tight stricture.[3] It has been suggested that ERC should be performed by the operating surgeon since the surgeon has a better understanding of the biliary systems of the graft and the recipient[22] (Fig. 3). Careful study of the donor cholangiograms at the time of endoscopy is also very useful in detecting biliary anomalies. Percutaneous transhepatic biliary drainage (PTBD) with dilatation is often adopted after endoscopic treatment fails.[5] This invasive treatment carries some risk. If the intrahepatic ducts are not distended enough, cannulation will be difficult and the risk of vascular injury is higher. A 2.2% risk of hepatic artery injury has been reported.[46] The rendezvous technique is an approach combining PTBD and ERC. This technique has the advantage of getting rid of the external draining catheter.

Others have also reported associations with qHBeAg and clinical responses or virological breakthrough in patients treated with LAM and PEG-IFN.17, 19-21 Most recently, a thorough investigation that included both qHBsAg and qHBeAg was conducted to identify their relationship with intrahepatic markers of HBV replication, and it suggested potential practical implications for these quantitative serological markers.24

Our study is the first to report serial qHBeAg values in patients on ETV therapy. We have shown that a decline in qHBeAg is highly predictive for SR with sensitivity and specificity values as high as 75.0% and 89.8%, respectively. Selleck AT9283 In other words, if a 10-fold drop in qHBeAg is encountered with 6 months of ETV therapy, there is a good chance of SR in such patients. Recent investigations have alluded to a potentially interesting aspect of qHBsAg as antigen expression in the natural course of HBV infection. Two independent groups found that the level of qHBsAg Crizotinib mouse was higher in the immune-tolerant and immune-clearance phases

than in the low-replicative phase and in patients with HBeAg(−) disease.22, 23 These discrepancies in qHBsAg across different phases of CHB infection and in correlation between qHBsAg and HBV DNA provide evidence that different pathways exist for HBsAg and HBV DNA production as well as that HBV may integrate into the host genome. In addition, similar published results have demonstrated 上海皓元 a good correlation in HBeAg(+) patients (r = 0.69, P < 0.001), whereas the association between HBsAg production and HBV replication broke down in HBeAg(−) patients (r = 0.28, P = 0.012); this was assumed to occur when HBsAg was produced from a source other than cccDNA.24 These reports suggest that the correlation between qHBsAg and HBV DNA without antiviral treatment is more significant in the higher HBV replicative phase

than in the low-replicative phase. As expected, our study on patients receiving ETV demonstrated a significant correlation between HBV DNA and qHBsAg only in HBeAg(+) patients. This correlation coefficient peaked at 6 months and gradually decreased over time. A possible explanation for this is that the proportion of patients with undetectable or lower HBV DNA levels increased with ETV therapy, and this led to a similar status for the low-replicative phase. Moreover, a modest decline of qHBsAg during ETV therapy could not catch up with the rapid reduction of HBV DNA, and the result was the disproportional status of these two parameters. This explanation, however, warrants further validation because the dynamic relation between qHBsAg and HBV DNA should be understood in the context of overproduction of defective HBsAg particles and the role of integrated HBV DNA.30 Some limitations of this study need consideration. First, only Korean patients with genotype C HBV were included in this study. Although homogeneity in a study population is in some ways favorable, it limits generalization.

Others have also reported associations with qHBeAg and clinical responses or virological breakthrough in patients treated with LAM and PEG-IFN.17, 19-21 Most recently, a thorough investigation that included both qHBsAg and qHBeAg was conducted to identify their relationship with intrahepatic markers of HBV replication, and it suggested potential practical implications for these quantitative serological markers.24

Our study is the first to report serial qHBeAg values in patients on ETV therapy. We have shown that a decline in qHBeAg is highly predictive for SR with sensitivity and specificity values as high as 75.0% and 89.8%, respectively. RG7204 solubility dmso In other words, if a 10-fold drop in qHBeAg is encountered with 6 months of ETV therapy, there is a good chance of SR in such patients. Recent investigations have alluded to a potentially interesting aspect of qHBsAg as antigen expression in the natural course of HBV infection. Two independent groups found that the level of qHBsAg see more was higher in the immune-tolerant and immune-clearance phases

than in the low-replicative phase and in patients with HBeAg(−) disease.22, 23 These discrepancies in qHBsAg across different phases of CHB infection and in correlation between qHBsAg and HBV DNA provide evidence that different pathways exist for HBsAg and HBV DNA production as well as that HBV may integrate into the host genome. In addition, similar published results have demonstrated 上海皓元医药股份有限公司 a good correlation in HBeAg(+) patients (r = 0.69, P < 0.001), whereas the association between HBsAg production and HBV replication broke down in HBeAg(−) patients (r = 0.28, P = 0.012); this was assumed to occur when HBsAg was produced from a source other than cccDNA.24 These reports suggest that the correlation between qHBsAg and HBV DNA without antiviral treatment is more significant in the higher HBV replicative phase

than in the low-replicative phase. As expected, our study on patients receiving ETV demonstrated a significant correlation between HBV DNA and qHBsAg only in HBeAg(+) patients. This correlation coefficient peaked at 6 months and gradually decreased over time. A possible explanation for this is that the proportion of patients with undetectable or lower HBV DNA levels increased with ETV therapy, and this led to a similar status for the low-replicative phase. Moreover, a modest decline of qHBsAg during ETV therapy could not catch up with the rapid reduction of HBV DNA, and the result was the disproportional status of these two parameters. This explanation, however, warrants further validation because the dynamic relation between qHBsAg and HBV DNA should be understood in the context of overproduction of defective HBsAg particles and the role of integrated HBV DNA.30 Some limitations of this study need consideration. First, only Korean patients with genotype C HBV were included in this study. Although homogeneity in a study population is in some ways favorable, it limits generalization.

Here, we couple a simple primary production model with nondestructive estimates of taxon-specific biomass on subtidal reefs off Santa Barbara, California to produce a 4-year time series of net primary production by intact assemblages of understory macroalgae in giant kelp forests off Santa Barbara, California, USA. Daily bottom irradiance varied significantly throughout the year, and algal assemblages MK-2206 price were on average exposed to saturating irradiance for only 1.3–4.5 h per day, depending on the time of year. Despite these variable light-limiting conditions, biomass rather than irradiance explained the vast majority of variation observed in daily NPP at all times of the year. Measurements of peak

biomass in spring and summer proved

to be good predictors of NPP for the entire year, explaining as much as 76% of the observed click here variation. In contrast, bottom irradiance was a poor predictor of NPP, explaining <10% of the variation in NPP when analyzed seasonally and ~2% when evaluated annually. Our finding that annual NPP by macroalgal assemblages can be predicted from a single, nondestructive measurement of biomass should prove useful for developing time series data that are necessary to evaluate natural and anthropogenic changes in NPP by one of the world's most productive ecosystems. "
“The biosynthesis of nutritionally important polyunsaturated fatty 上海皓元医药股份有限公司 acids (PUFAs) in phytoplankton is influenced by environmental temperature. We investigated the potential of climate warming to alter lipid dynamics of Scenedesmus obliquus (Turpin) Kütz. by comparing lipid and fatty acid (FA) profiles as well as FA metabolism (using [1-14C] acetate) at 20°C and 28°C. We documented an overall decline (53%–37%) in the proportion of n-3 PUFA (in particular, of α-linolenic acid [ALA; 18:3n-3]), and a concomitant increase in saturated fatty

acids (SAFAs) in total lipids (TLs) at 28°C, consistent with enhanced incorporation of radioactivity from [1-14C] acetate into total 16:0, 18:1, and decreased incorporation into 18:2 and 18:3 FA (from 36% to 22% of the total) at 28°C. Glycerophospholipids were also affected by warming; ALA and stearidonic acids (SDAs; 18:4n-3) both decreased (by 13% and 15%, respectively) in phosphatidylcholine (PC) and (by 24% and 20%, respectively) in phosphatidylethanolamine (PE). The characteristic FA in phosphatidylglycerol (PG; 16:1n-13t) increased (by 22%) at 28°C. The activities of desaturases, which add double bonds to FA moieties, comprised the major suite of reactions affected by the temperature increase in TL and polar lipid (PL) classes. Climate modelers predict an increase in the number of extreme heat days in summer at temperate latitudes, with parallel projected increases in water temperatures of shallow water bodies. Our results suggest that the overall decrease in the essential n-3 FA ALA in S.

(B) The number of apoptotic cells (Annexin

V+ cells) was not significantly affected in PLC/PRF/5 and HLE cells by modulating the expression of the miR-216a/217 cluster. The Annexin V+ cells decreased from 2.44% to 1.32% by overexpression of miR-216a/217 in PLC/PRF/5 cells and increased from 0.99% to 2.92% following the knockdown of miR-216a/217 in HLE cells (P>0.05). Figure S5. Expression of SMAD7 (A), PTEN (B), JAK2 (C) and CADM1 (TSLC1) (D) was shown by dot plot analysis, Barasertib in vitro by searching a HCC Gene Expression database established in our laboratory using Affymetrix Human Genome U133 plus 2.0 Arrays (Affymetrix, Santa Clara, CA, USA) comprising of HCC tumor and adjacent histologically normal liver tissue (1). Figure S6. Potential targeting region of miR-216a/217 predicted for PTEN-3′UTR (A and B) and SMAD7-3′UTR (C and D) using RNAhybrid 2.2. (A-D) The predicted target sequences and mutations generated for the 3′-UTR of PTEN and SMAD7 mRNA are shown. (E) Images to show the morphological changes observed for PLC/PRF/5-miR-216a/217 cells following transfection with wild-type plasmids containing SAMD7 (i and ii) or PTEN (iii and iv)

compared to control vectors, the morphological changes were indicative of mesenchymal-epithelial transition (MET). HIF inhibitor Figure S7. (A and B) TGF-β1 treatment induced the up-regulation of miR-216a/217 in HepG2 cells. (C and D) Addition of LY2109761, a selective TGF-β receptor type I/II dual inhibitor, inhibited TGF-β1-induced miR-216a/217 expression in HCC cells. (E) Low concentration of LY2109761 (< 1 μM) have insignificant effect on the viability of the PLC/PRF/5 cells.

Figure S8. (A) Kaplan-Meier survival analysis between HCC patients with early-recurrent and non-recurrent disease. Significant difference in disease-free survival (P<0.0001) was observed between HCC patients with early-recurrent and non-recurrent disease. (B) Immunohistochemical studies of the expression MCE of P-Akt in matched normal, early-recurrent and non-recurrent HCC liver tissue samples (20X). Of note, more than 50% of the early-recurrent HCC tissues studied by IHC exhibited elevated P-Akt staining in 25-75% of the tumor tissues examined and revealed that a significant difference in the staining of P-Akt between the early recurrent and non-recurrent HCC tissues (S8B). Figure S9. Expression of CADM1 (TSLC1) (A) and SMAD7 (B) is down-regulated in liver cancer compared with normal liver tissues (indicated by red arrows) by searching the IST Online system (http://www.medisapiens.com/ist-online-overview/). “
“Background and Aim:  Hepatocellular carcinoma (HCC) is a common human cancer worldwide. The levels of serum clusterin in HCC patients and its potential diagnostic significance is not clear. We aimed to evaluate the clinical use of serum clusterin levels as a surveillance tool for HCC with hepatitis B virus (HBV) related cirrhosis.