2. The serum levels of ULBP-2, MIC-1 were associated with progression of pancreatic cancer.3. ULBP-2 was superior to CA 199 in discriminating patients with early-stage PC from healthy controls. MIC-1 was superior to CA19-9 in diagnosing early-stage PC.4. MIC-1 is associated with pancreatic cancer cachexia.5. The combination of ULBP-2, MIC-1 and

CA 199 performed better than each marker alone in distinguishing PC patients from healthy individuals. Key Word(s): 1. Pancreatic cancer; 2. ULBP-2; 3. MIC-1; 4. Serum biomarker; Presenting Author: DEBI (PAPU) PRASAD Corresponding Author: DEBI (PAPU) PRASAD Affiliations: COUNTY MANUKAU DHB Objective: IPMN are rare tumours of the pancreas Staurosporine price and no successful treatments option other than surgery available. We report an interesting case being managed with NAC infusion through percutaneous transhepatic biliary drain (PTBD). Methods: 55 yr old man presented with history of painless jaundice and weight loss. USS and CT scan showed 5 cm head of pancreas mass with biliary and pancreatic Ensartinib duct dilatation. Deemed

malignant and inoperable. So patient had an ERCP and stent placement. Bilirubin subsequently improved from 374 to 93. On CT 10 months later the mass had decreased (?Benign) in size. Repeat ERCP with stent was done. He subsequently presented with obstructive jaundice. CT scan showed gross dilatation of the biliary tree and the pancreatic duct. ERCP was done with stent placement and interestingly no stricture was found but large amount of mucins causing

blockage of the pancreatic duct. Main duct IPMN was diagnosed on ERCP and by CT criteria. Patient subsequently had PTBD with external internal system but LFTs did not improve. The Right PTBD was draining minimal viscous fluid. Results: NAC as a mucolytic agent facilitates drainage by decreasing viscosity and has been tried in Cystic Fibrosis and other bronchopulmonary disease. We decided to use NAC to help clearing the mucin and improving drainage. NAC 600 mg was diluted with NS (12 mg/ml) and was given every three hour via biliary drain. Drain was clamped Palmatine for 2 hours post infusion and then opened. This was to allow time for NAC to act and not to overdistend the PTBD system. Patient reported thinning of drainage fluid and his bilirubin improved. Subsequently he was discharged home and now self administering NAC. He reported increase in energy level and weight and bilirubin continued to improve (125 to 39). However this could not clear the CBD very well resulting in increase in bilirubin everytime the PTC got blocked. Currently he is having change of the PTC every 6 to 8 weeks. Conclusion: Issues of interest: NAC helps in assisting drainage of biliary system in IPMN. Large control study needed to clarify on optimal dosing and whether continuous infusion would help it more. Key Word(s): 1. IPMN; 2. NAC Infusion; 3. Infusion; 4.

Because the activation of Kupffer cells seems critical to the development of liver injury due to alcohol, agents aimed at preventing the activation have been studied. Because calcium is essential to activation, a calcium channel blocker was administered to rats given high enteral doses of alcohol. Nimodipine significantly reduced both biochemical abnormalities and histologic changes in these alcohol-fed

rats.27 Another approach was to stimulate phagocytic activity of murine Kupffer cells. Tuftsin, a natural immunomodulator peptide, was shown to stimulate phagocytosis.28 In still another approach with some promise, LPS-neutralizing antibody was found to ameliorate acute hepatocyte injury produced by galactosamine.29 Consistent with the fact that TNF is a major mediator of LPS injury, soluble TNF receptor was demonstrated to provide protection against CCl4 liver injury in rats.30 Although selleckchem oral antibiotics had been shown in the 1960s and 1970s to protect against acute liver injury and the cirrhosis of choline deficiency, investigators more recently demonstrated that polymyxin and neomycin offered the same protection to the high-dose alcohol-fed rat model.31 IL-10, which is an anti-inflammatory

cytokine that inhibits TNFα production, prevented lethality from endotoxin in galactosamine-sensitized mice, offering another possible modifier of toxic liver injury.32 Another protector against galactosamine lethality is high-dose alanine, which confers protection even up to 12 hours after toxic challenge. It resulted in increased hepatic adenosine triphosphate content probably RAD001 manufacturer due to high-dose alanine’s promotion of ATP synthesis. It was felt that this impressive protection and C-X-C chemokine receptor type 7 (CXCR-7) low toxicity might be an effective therapy in humans.33 An important contribution to our knowledge of the mechanism of alcohol-induced liver injury in rats resulted from studies of dietary intervention. It was shown that the feeding of medium-chain triglycerides inhibited both free radical production and TNFα production in the ethanol-treated animals.34 Another study investigated dietary saturated fatty acids in the

ethanol rat model and found that this dietary intervention reversed the inflammatory and fibrotic changes despite continued alcohol administration.35 Both these studies would seem to open exciting possibilities of a nutritional approach to the problem of alcohol-induced damage. A study in 2002 on the effect of LPS-binding protein in early alcohol liver injury in mice showed significant modification of the injury.36 The investigators concluded that the LPS-binding protein enhanced LPS-induced signal transduction, most likely in Kupffer cells. Another protective agent described in 2003 was edaravone, which prevented liver injury and mortality in endotoxin-treated rats. It is another potent and novel free radical scavenger that might be used in treating alcoholic hepatitis.

The sections were washed twice, after all incubation steps, in phosphate-buffered

saline for 5 minutes. Then slides were microwave-oven heated three times for 5 minutes in Tris/ethylenediaminetetra-acetic acid pH 9.0 buffer (heat-induced epitope retrieval), and washed with phosphate-buffered saline. Sections were subsequentially incubated in the presence of the primary antibody overnight at −4°C. The specimens were then incubated with the LSAB HRP detection kit (Universal DakoCytomation Torin 1 purchase LSAB+ System HRP) at room temperature, according to the manufacturer’s instructions. As a chromogen, 3-amino-9-ethylcarbazole was used for 5 minutes at room temperature with subsequent nuclear counterstaining with hematoxylin. Normal mouse serum was

used instead of primary antibodies as a negative control. A four-grade semiquantitative scoring this website system (in other words, score 0-3), performed by one pathologist (C.T.) unaware of other variables, was adopted for the evaluation of CYP2R1 and CYP27A1 immunohistochemical expression. The score was graded according to the intensity of the staining: score 0 was defined as the absence of significant reactivity, scores 1 and 2 as slight and moderate reactivity, respectively, and score 3 as intense reactivity. Because a slight degree of variation could be observed in the immunohistochemical expression of CYP2R1 and CYP27A1 among different areas of the same sample, the most intense reactivity observed in the biopsy specimen was recorded as the summary score. Casein kinase 1 Immunohistochemical analysis of CYP450 was performed for control purposes using a specific primary monoclonal antibody (clone 1A2, Abcam, MA) and evaluated by the same four-grade semiquantitative scoring system adopted for CYP27A1 and CYP2R1 assessment. Patients were treated with pegylated interferon α-2a (Pegasys, Roche, Basel, Switzerland) 180 μg /week or pegylated interferon 2b (Peg-Intron, Schering) 1.5 μg/kg/week plus ribavirin

at a dosage of 1000 or 1200 mg/day according to body weight (1000 mg/day for a body weight of <75 kg, 1200 mg/day for a body weight of >75 kg) for 48 weeks. Patients were withdrawn from treatment if they did not achieve a virological response, defined as undetectable serum HCV RNA by polymerase chain reaction, within 24 weeks after start of treatment.24 Sustained virological response (SVR) was defined as negative serum HCV RNA at polymerase chain reaction 6 months after stopping antiviral therapy. Continuous variables were summarized as mean ± standard deviation, and categorical variables as frequency and percentage. The Student t test and analysis of variance were used when appropriate. Multiple linear regression analysis was performed to identify independent predictors of 25(OH)D serum levels as a continuous dependent variable.

Disclosures: Olivier Chazouillères – Consulting: APTALIS, MAYOLY-SPINDLER The following people have nothing to disclose: Véronique D. Barbu, Isabelle Jéru, Christophe Corpechot, Eric Fernandez, Laure Muller, Fabienne Dufernez, Yannick Marie, Zhenyu Xu, Chantal Housset Background and Aim: Fenofibrate is a novel therapy for Primary Biliary Cirrhosis (PBC). We sought to perform a systematic review and a meta-analysis of studies that assessed

the efficacy of fenofibrate in the treatment of PBC patients. Methods: electronic database search was performed for relevant studies. Database searched included MG-132 chemical structure PubMed, Scopus, and ScienceDirect. In addition, search of abstracts presented in the main scientific meetings in the field and articles in press was performed. Random effect model was used to pool the effect size across studies for changes in means of alkaline phosphatase, GGT, bilirubin and IgM levels before and after treatment and the overall rate of having complete response to fenofibrate therapy. Publication bias, heterogeneity testing and sensitivity analysis were also performed.

Results: Six studies with 102 patients (90% female) met the inclusion criteria. All studies were case CHIR 99021 crossover where patients who had no or incomplete response to UDCA had fenofibrate added at a dose of 100-200 mg daily. Treatment duration ranged from Oxymatrine 8-100 weeks. Treatment with fenofibrate was associated with a significant decrease in the pooled mean alkaline phosphatase (−114 IU/L, 95% CI:−152 to −76, p<0.0001); a significant decrease in GGT level (−92 IU/L, 95%CI:−149 to −43; p=0.0004); significant decrease in total bilirubin (−0.11mg/dl;95%CI:−0.18 to −0.08; p=0.0008), and a significant decrease in IgM level (−88mg/dl; 95%CI:−119 to −58; p<0.0001);. The pooled complete response rate was 69% (95% CI: 53-82%; p=0.024). The odds ratio of achieving complete response while on fenofi-brate was 2.43 (95% CI: 1.44-4.1, p=0.0009). Conclusions: Fenofibrate therapy at doses of 100-200 mg daily appears to be an effective

adjunctive therapy in PBC patients who had no or incomplete response to UDCA. There is a critical need for larger scale randomized trial to confirm its efficacy and define its position in the treatment paradigm of PBC. Disclosures: Cynthia Levy – Consulting: Lumena, Gilead, Evidera The following people have nothing to disclose: Alla Grigorian, Houssam E. Mardini, Christophe Corpechot, Raoul Poupon Background: Primary biliary cirrhosis (PBC) is a chronic, cholestatic liver disease that can lead to cirrhosis & liver failure. Ursodeoxycholic acid (UDCA) improves transplant-free survival, but up to 40% may not achieve adequate biochemical response. Fibrates may decrease alkaline phosphatase (ALP), but no study has examined their impact on transplant-free survival.

More than 60% of new immigrants to the US come from countries of increased hepatitis B endemicity (hepatitis B surface antigen [HBsAg] prevalence of ≥2%). Most HBV-infected persons from these countries become infected at birth or during early childhood, when the risk for chronic HBV infection is greatest; 25% of persons with chronic HBV remain at risk of premature death from hepatitis B–related liver disease (e.g., hepatocellular carcinoma).3 In the US, estimates of HBV prevalence are

derived from the National Health and Nutrition Examination Survey (NHANES). However, this survey underrepresents some populations with high hepatitis B virus (HBV) prevalence. For example, NHANES data do not identify respondents born in most Asian or any African countries or report racial/ethnic Gefitinib categories that indicate origins in these countries.4, 5 These limitations in data collection mask hepatitis B–related health disparities contributing to the “silent epidemic” of viral hepatitis in the US.6, 7 Seeking to fill the void in national health surveys, Kowdley et al. reviewed the medical literature published since 1980 to gather

data for general population groups (e.g., pregnant women and military recruits) and then pooled these data to obtain the prevalence of chronic hepatitis B (HBsAg+) by country. To estimate the number of persons residing in the US by country of origin, prevalence data were brought together with data from the US Census American Community Survey, a household survey that collects various data, including country check details of birth (http://www.census.gov/acs/www/).8 The authors acknowledge limitations to their approach: chronic HBV seroprevalence data were scarce for many countries (one-third

of countries had conducted fewer than six surveys), often varied substantially from one survey within a country to another, and most (72%) data were obtained from surveys conducted prior to 2000. CBA, community-based organization; CDC, Centers for Disease Control and Prevention; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; NHANES, National Health and Nutrition Examination Survey; US, United States. Compared with the results of another recently published study, the findings of Kowdley et al. appear also to be conservative. Bringing together Centers for Disease Control and Prevention (CDC) and World Health Organization data to estimate HBV prevalence, Mitchell et al.9 estimated chronic hepatitis B prevalence among persons who immigrated during 1974-2008 to be 4.6%, higher than the 3.45% estimate derived by Kowdley et al. The Mitchell analysis revealed that the number of imported cases of hepatitis B increased over time (30,000 in 1988 to 62,000 in 2006). Data from these indirect approaches suggest that NHANES underestimates the number of persons with hepatitis B in the US.

The analysis of all included trials showed that therapy with IL-2Ra was not associated with an increased incidence of malignancies, bacterial or viral infection, or adverse events in general, indicating that IL2-Ra are safe and without significant side effects for at least 12 months after liver transplantation. Longer follow-up has been reported for registry data and corroborates this analysis.46 The main limitation PXD101 mouse of this review is the low number of randomized controlled trials, even compared to kidney transplantation,7 which makes it difficult to acquire enough data for meaningful results. After a first unsystematic review we decided to include not only randomized

trials but also nonrandomized controlled trials in this review. Very few studies only compared IL-2Ra to placebo or no treatment and many more studies explored the effects of reduced or delayed concomitant immunosuppression. Therefore, we decided to include those studies in the analysis by selleck screening library allocating them

to predefined comparisons. Furthermore, we included and pooled studies that used a different type of IL2-Ra, had different concomitant medication (CNI and MMF), or had different follow-up times. Because all these differences may be sources of heterogeneity, it was planned to perform joint analyses and also to explore differences of effect by performing subgroup analyses and meta-regression. Due to the paucity of data on secondary outcomes we were only able to extensively analyze the primary endpoints. Another problem was the insufficient detailed reporting of outcomes; this was most evident regarding the side effects of immunosuppression. Not only did few studies give data on complications and side effects, but also these were reported in insufficient detail or were measured or grouped differently in the various trials. We endeavored to overcome this limitation by grouping data on side effects into broader categories, but this may further limit the interpretation

of the results. External and internal validity Liothyronine Sodium of the trials and the results of this meta-analysis are difficult to assess because important methodological details were omitted in the trial reports. Although we attempted to minimize publication bias by searching for and including data from different databases, conference abstracts, and non-English language sources, the inclusion of such data further hindered assessment of validity. Nonetheless, this review and meta-analysis was conducted at an appropriate time because enough data has accumulated for a first inspection by meta-analytical methods. We do not expect more data to accumulate over the next years unless further trials are demanded of the proprietors of commercially available IL-2Ra preparations by the regulatory authorities. Fifteen patients would need to be treated to prevent one acute rejection (NNT [number needed to treat] = 15) and 29 patients would need to be treated to prevent one steroid-resistant rejection (NNT = 29).

These catfishes produce stridulatory sounds by their pectoral spines and low-frequency sounds by vibrating their swim bladders (Fine & Ladich, 2003; Ladich & Fine, 2006). We thank S. Papes, W. Lechner and A. Zebedin for help with initial sound recordings and seahorses’ feeding; M. Pollirer and the Department of Marine Biology for providing sea water; and M. Stachowitsch for professional scientific English proofreading.

EPZ-6438 ic50 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior provided a PhD scholarship to T.P.R.O in Brazil and in Vienna (CAPES/PDEE), and Conselho Nacional de Desenvolvimento Científico e Tecnológico provided a research fellowship to I.L.R. All experiments were conducted at the University of Vienna with permission from the Austrian Federal Ministry for Science and Research (GZ 66.006/0023-II/10b/2008). “
“Cougars Puma concolor are described as ‘habitat generalists’, but little is known about which ecological factors drive their home range selection. For example, how do resource distributions and inter-species competition with dominant competitors (i.e. wolves, Canis lupus) over such resources, influence the distributions of cougars on the landscape? We tracked cougars using Very High Frequency (VHF; 2001 to 2005) and Global Positioning System (GPS; 2006 to 2011) technology in the Southern Yellowstone Ecosystem (SYE) mTOR inhibitor in northwestern

Wyoming, USA. We tested whether data type (VHF vs. GPS), cougar sex, access to forests Silibinin (refugia) or

hunt opportunity explained the size of 50% and 95% kernel density estimator (KDE) home ranges. Second, we quantified attributes of cougar home ranges and tested whether they were different from attributes of the overall study area, to address the ecological question: Do cougars select home ranges based on the availability of refugia, hunt opportunity or some combination of the two? Cougar sex and data type proved significant predictors of home range size for both 95% and 50% KDEs, and the amount of forest partly explained the size of 50% KDEs. Cougar home ranges derived from VHF data were 1.4–1.9 times larger than home ranges derived from GPS data; however, home range attributes determined from VHF and GPS data were remarkably equivalent. Female cougars selected home ranges with higher hunt opportunity than males, supporting the assumption that females primarily select home ranges with suitable prey to sustain themselves and their young. All cougars selected home ranges further from known wolf packs, providing evidence for newly established competition between resident cougars and recolonizing wolves, but did not select home ranges with greater access to landscape refugia. Our results provided evidence that cougars in the SYE select home ranges that provide high hunting opportunity and a spatial buffer that mitigates potential conflicts with a dominant competitor.

We previously reported that TJs impose a physical barrier and restrict viral access to receptors23 and that complex hepatocyte-like polarity limits HCV entry.18 To investigate whether binding of anti-CLDN1 antibodies to polarized human hepatoma cells perturbed TJ integrity, we assessed the ability of TJs to restrict the paracellular diffusion

of CMFDA from the BC lumen to the basolateral medium (barrier function) as described.18 As shown in Fig. 2, the capacity of BC lumens to retain CMFDA was similar in polarized HepG2 cells treated with rat anti-CLDN1 antibodies, rat control serum, or PBS, whereas CMFDA retention was reduced in interferon-γ–treated HepG2 cells (Fig. 2B). These data suggest that anti-CLDN1 antibodies have no effect on TJ integrity. To investigate whether anti-CLDN1 antibodies could inhibit HCV infection, Huh7.5.1 cells were infected with chimeric J6/CF-JFH1 firefly luciferase check details reporter virus (Luc-Jc1)26, 29 in the presence of anti-CLDN1 or control antibodies. Fig. 3A shows that anti-CLDN1 serum inhibits Luc-Jc1 infection of Huh7.5.1 cells in a dose-dependent manner, whereas the control preimmune serum had no inhibitory effect. Neutralization of HCVcc infection correlated with binding of antibodies to the target cell line (Fig. 3B). To confirm that inhibition of Luc-Jc1

infection was mediated by anti-CLDN1 antibodies, we purified IgG from rat anti-CLDN1 and preimmune serum. As shown in Fig. 3C, anti-CLDN1 IgG but not control IgG markedly inhibited Luc-Jc1 HCVcc infection in a dose-dependent manner. These data demonstrate that the inhibitory effect of anti-CLDN1 serum was mediated by anti-CLDN1 IgG and not by other substances present in the serum. Infection experiments using primary human hepatocytes and HCVpp packaged with envelope glycoproteins Oxymatrine from genotypes 1-4 demonstrated that anti-CLDN1 blocking activity was similar for infection with HCV-bearing envelope

proteins of other genotypes (Fig. 3D). Taken together, these findings demonstrate that antibodies directed against the CLDN1 extracellular loops inhibit HCV infection in HCV permissive cell lines and human hepatocytes. We previously demonstrated that CD81 and SR-BI act in concert to mediate HCV entry.26 To investigate whether the three host factors CLDN1, CD81, and SR-BI act in a cooperative manner, we added low concentrations of anti-receptor antibodies simultaneously prior to HCV infection. The use of antibody concentrations that submaximally blocked HCV infection allowed us to observe additive or synergistic effects. First, we determined the ability of combinations of two out of the three antibodies to neutralize HCVcc infection. Fig. 4 shows an additive effect of the concomitant blocking of both CD81 and CLDN1 (Fig. 4B), SR-BI and CLDN1 (Fig. 4C), or CD81 and SR-BI (Fig. 4D). This effect was not observed when control IgG or control serum was used in combination with anti-CLDN1 antibodies (data not shown).

Interferon-alpha is not a direct-acting antiviral but rather acts on cell-surface receptors to trigger signaling pathways that activate “interferon-stimulated genes,” which render the cell resistant to viral infection and less capable of supporting viral replication.21, 22 The basis of the antiviral activity of alpha interferon is complex and involves multiple, often redundant cellular pathways,

such as those involved in regeneration; cell turnover; apoptosis; and PD0325901 in vitro protein, lipid, and carbohydrate metabolism. Possibly the continuous stimulation of interferon-induced genes by long-term maintenance therapy is detrimental, particularly to cells and tissues without active viral replication. These effects may be diverse and, therefore, not manifested as a single adverse reaction. An alternative explanation for the difference in mortality between the treatment and control groups in the HALT-C Trial is the presence of an undefined confounding factor, such as baseline difference in the randomization groups, or difference in subsequent management. However, given the size of the trial, the success of randomization,6 and buy HM781-36B the uniformity of management in

the two groups, these differences are unlikely to have accounted for a statistical difference in mortality rates. Currently, hypotheses to explain excess mortality linked to interferon are not supported by clinical or experimental observations, but warrant further study. Thus, the HALT-C Trial was not able to show a benefit of long-term peginterferon maintenance on rates of clinical progression, histologic progression to cirrhosis, hepatic decompensation, HCC, or death.6 In this extended click here follow-up analysis, as in the analysis of the randomized trial, the mortality rate appeared to be higher among patients in the peginterferon treatment group. In other post-hoc analyses of the HALT-C Trial

cohort, long-term peginterferon therapy appeared to be associated with a lower rate of late HCC, diverging from the control group after 4 years of observation, but only in patients with cirrhosis at baseline.23 As shown in the current analysis, the lower rate of late HCC was not accompanied by a lower rate of death or liver transplantation. In summary, long-term observation of a large cohort of patients with chronic hepatitis C and advanced hepatic fibrosis revealed a high rate of death, particularly among those with cirrhosis at baseline. Approximately two-thirds of deaths were attributable to liver disease. An increase in mortality occurred in patients in the long-term peginterferon treatment group, but this increase in mortality was attributed to nonliver-related deaths and occurred largely among patients with precirrhotic advanced fibrosis at baseline. No pattern to this excess mortality was discernible; deaths were unrelated to direct effects of peginterferon treatment.

Conclusions: TPU0114 inhibits HCC cell proliferation and induces apoptosis, possibly through the suppression of Bcl-xl signaling. This novel compound could be effective in the eradication of both CSCs and non-CSCs by targeting anti-apoptotic signaling in human HCC. Disclosures: Mariko Yoshida – Grant/Research GSK126 Support:

Bayer Hikari Okada – Employment: Kanazawa University Shuichi Kaneko – Grant/Research Support: MDS, Co., Inc, Chugai Pharma., Co., Inc, Toray Co., Inc, Daiichi Sankyo., Co., Inc, Dainippon Sumitomo, Co., Inc, Ajinomoto Co., Inc, MDS, Co., Inc, Chugai Pharma., Co., Inc, Toray Co., Inc, Daiichi Sankyo., Co., Inc, Dainippon Sumitomo, Co., Inc, Ajinomoto Co., Inc, Bayer Japan The click here following people have nothing to disclose: Tomoyuki Hayashi, Taro Yamashita, Naoki Oishi, Kouki Nio, Takehiro Hayashi, Yasumasa Hara, Yoshimoto Nomura, Tomomi Hashiba, Koji Miyanouchi Purpose: Aberrant Wnt/Beta-catenin (Bcat) signaling occurs in hepatoblastoma (HB), the most common pediatric liver malignancy. The association of HBL with prematurity, polyposis and Beckman-Weidemann syndromes suggests a potential “second-hit” genetic basis. Methods: For hypothesis

generation and testing, 14 caucasian children who received liver transplantation (LTx) for unresectable HB, 16 parents and 1012 normal Caucasian controls (NC) were compared at >550000 genome-wide SNP loci. Validation involved expression of the candidate gene, DDEF1 in explants from LTx recipients, and immunohistochemistry (IHC) for DDEF1, and related pathway members, EGFR and B-cat in formalin-fixed-paraffin-embedded (FFPE) tissue from 37 children, 25 with surgical resection, 11 with LTx, one with biopsy only. Three children experienced metastatic disease. Results: Initially, 4392 SNPs with large differences learn more (P < .01) in minor allele frequencies (MAF) were selected for hypothesis testing in parents vs NC comparison. Five intronic

SNPs in the DDEF1 gene, rs1417008, rs3758028, rs16904252, rs16904237, and rs16904215 demonstrated significant differences in MAF when children with HB were compared with NC (p-value <1.397e-06). DDEF1 was upregulated (qRTPCR) in uninvolved tissue from 6 LTx explants compared with ten normal liver allografts (mean delta Ct 6.49 vs 7.29, p=0.016). Staining intensity was graded as 0-3 (0=no staining and 3=intense staining) for DDEF1, EGFR and B-cat in each of four different tumor components, fetal (F-32), embryonal (E-19), mesenchymal (M-4) and small cell undifferentiated (SCU-5). Intense DDEF1 staining occurred in >60% of embryonal and 40% of SCU. Intense nuclear beta-catenin and absent EGFR staining characterized all SCU tumor tissue.