There are some standardization issues related to VWF:CB that MK-8669 clinical trial may limit usefulness and cause confusion. Notably, efficacy of VWF:CB to diagnose and classify of VWD depends on methodology, including collagen used

and coating conditions [24–26]. An automated VWF:CB assay is currently not available. Limited uptake in the USA [21,26] may relate to the fact that there is no FDA approved method. Finally, several commercial and in-house methods have been described and evaluated, but require further standardization [24]. Good quality, accurate laboratory results are essential to facilitate diagnosis in patients with bleeding disorders. However, there is high variability of results reported in different centres, particularly for VWF activity assays. Improvements in accuracy and precision of laboratory assays can be achieved through standardization and external learn more quality assessment (EQA) [27]. An EQA programme was established on behalf of the World Federation of Hemophilia in 1993 [28]. Lyophilized

plasma samples from patients with haemostatic disorders and from normal subjects are distributed to laboratories in both emerging and established heamophilia centres, and the results compared with target values obtained, using the same samples, by up to 900 centres in the United Kingdom National External Quality Assessment Service (UK NEQAS) programme. Problems with diagnostic performance of individual laboratories can be identified, as well as methodological problems associated with specific assays. Interlaboratory variability for VWF activity is particularly MCE公司 marked. Figure 2 shows CVs for assays performed on the same samples by UK NEQAS participants, WFH participants, centres in emerging countries and centres in established countries (primarily International Hemophilia Training Centres). Whilst the precision amongst emerging centres

is comparable with established centres and NEQAS laboratories for screening tests, possibly reflecting their relative simplicity, emerging centres are less able to measure coagulation factors accurately. Troubleshooting and training in the form of regional workshops can help improve laboratory performance by identifying issues, such as calibration problems and poor assay design. A questionnaire in 2007 revealed that 40% of emerging centre laboratories only used a single dilution of test plasma in their assay, an approach previously demonstrated to give inferior results [29]. Furthermore, only 5% of centres used a locally determined reference range. It is interesting to note, however, that performance of emerging centres in the measurement of FVIII and fibrinogen in cryoprecipitate is equivalent to that of established centres (Table 1), which may reflect popular usage of cryoprecipitate for treatment of haemophilia A and VWD in developing countries [30,31].

Moreover, the Expression

of key co-stimulatory and co-regulatory molecules on DC and Treg were examined by flow cytomeric analysis. Results: our findings show that everolimus-treated liver transplant patients maintain a stable DC subset distribution and phenotype. Thus, expression of co-stimulatory and co-regulatory molecule (CD86, CD83, PD-L1 and ICOS-L) did not differ between the 2 groups. Moreover, expression on DC subsets of HLA-DR and human leukocyte antigen (HLA)-G, a non-classical HLA class I molecule, and of its receptor, the immunoglobulin (Ig)-like transcript (ILT)-4 did not this website differ between the mTOR and CNI groups. Notably, however, expression of the ectonucleoti-dase CD39 was significantly higher

on myeloid DC in patients taking everolimus compared with the CNI. Notably, http://www.selleckchem.com/products/ldk378.html in the ever-olimus group the incidence of Treg was significantly higher and the expression of Programmed death-1 (PD-1) on Treg was significantly lower as compared with CNI group. Conclusions: this preliminary study provides new information about how mTOR inhibitor-based immnosuppression may influence peripheral innate and adaptive immune cells in liver transplant patients. Our findings also point out possible new biomarkers of liver graft acceptance which could be monitored after transplantation. Disclosures: The following people have nothing to disclose: Antonino Castellaneta, Antonio Massaro, María Rendina, Francesca D’Errico, Sonia Carparelli, Angus W. Thomson, Alfredo Di Leo Background Progression of fibrosis after liver transplantation (LT) is associated with a worse outcome. One study suggested that abusive drinking after LT for pure alcoholic cirrhosis was associated 上海皓元 with liver fibrosis progression. Aims (1) to evaluate alcohol consumption in France after LT for alcoholic cirrhosis using

carbohydrate deficient transferrin (CDT); (2) To assess fibrosis progression using 2 non-invasive methods. Methods Liver fibrosis progression was assessed using FibroTest (FT, Biopredictive, France) and FibroScan (FS, Echosens, France) in all patients who underwent LT for pure alcoholic cirrhosis in our center, on the same day, once a year. Discordances between the 2 methods were resolved by consensus, after repeating the tests and analysing the files of each patients (clinical examination, biology, ultrasound exam). Excessive drinking was defined by a CDT>1.8%. Parameters of metabolic syndrome were assessed each year. Results Overall, 93 patients were transplanted in La Pitie-Salpetriere (Paris, France) for pure alcoholic cirrhosis, all other causes of hepatopathy being ruled out, between February 2000 and June 2012. Among them, 9 died within the first year after LT, and 9 were not evalu ated (lost of follow-up or residing in a foreign country).

[37, 38] Therefore, HBV pre-S deletion mutations may lead to defective host immunity against HBV infection and contribute to more progressive liver cell damage and finally hepatocarcinogenesis. HBV is the smallest human DNA virus with a partially double-stranded circular DNA.[39] The partially double-stranded DNA will transform into covalently closed circular DNA (cccDNA) in the nucleus of hepatocytes

after HBV infection. Such HBV cccDNA is responsible for persistent infection of hepatocytes. During HBV replication, pregenomic RNA can be transcribed from cccDNA to serve as the template of negative-strand DNA through reverse transcription, and then fully double-stranded DNA through DNA polymerase within the nucleocapsid, finally with the assembly of envelope protein to form mature HBV virions.[40] Several messenger MLN0128 order RNAs (mRNAs) can also be transcribed from cccDNA and then translate to viral proteins. selleck screening library HBsAg is presumably responsible for receptor binding. It is comprised of large, middle, and major (or small) proteins. Intracellular hepatitis B core antigen (HBcAg) is an inner nucleocapsid surrounding the viral DNA. HBcAg is the major target of cytotoxic

T cell. HBeAg is a circulating peptide derived (by peptide cleavage) from the core gene, then modified and secreted from liver cells. HBeAg usually serves as a marker of active viral replication. In addition, small HBsAg and truncated pre-S proteins can be generated from integrated HBV-DNA.[41-44] Therefore, several quantifiable viral factors can be used clinically, including HBV-DNA from the infectious particles and circulating viral proteins such as HBsAg and HBeAg. HBV-DNA quantification assays are available 上海皓元 and have been used in clinical practice for more than a decade. Several commercial assays based on molecular

biology techniques have been developed to detect and quantify HBV-DNA.[45] More recently, real-time polymerase chain reaction assays to detect and quantify HBV-DNA were recommended by the American Association for the Study of Liver Disease, the European Association for the Study of Liver, and Asian Pacific Association for the Study of the Liver (APASL) to diagnose HBV infection, establish the indication for therapy, and to monitor antiviral treatment responses and emergence of drug resistance.[46-48] HBV-DNA quantification also provides valuable prognostic information. Recently, the impact of viral load on the risk of HCC was assessed in a population-based prospective cohort of untreated CHB Taiwanese patients (REVEAL-HBV study). Among them, 85% were HBeAg negative and were followed for a mean duration of 11 years. The cumulative incidence of HCC increased with serum HBV-DNA level. It ranged from 1.3% to 14.9% for patients with an HBV-DNA level of less than 300 copies/mL (∼60 IU/mL) and106 copies/mL (∼200 000 IU/mL) or more, respectively (P < 0.001).

Methods: The medical records of 214 cases in 205 patients who were treated with ESD and diagnosed

with early gastric cancer (EGC) were reviewed retrospectively with a focused on endoscopic findings Results: Seven were an undifferentiated type EGC that initially had been diagnosed as differentiated adenocarcinoma (U group). The other 207 cases were diagnosed as differentiated type EGC (D group). Flat lesion was significantly more dominant in the U group than the D group (43% vs. 10%, p = 0.032). A moderate EPZ-6438 mw differentiated type at initial biopsy and submucosal invasion were more significantly diagnosed in the U group than the D group (p = 0.009 and p = 0.029, respectively). Conclusion: Of the EGC cases initially diagnosed as differentiated adenocarcinoma by forceps biopsy, check details the rate of cases of undifferentiated adenocarcinoma finally diagnosed after ESD was approximately 5%. Moderate differentiation

and submucosal invasion were significant factors of undifferentiated EGC with a histological discrepancy between the initial forceps biopsy and ESD specimens. Also, this study suggests that the flat lesion is the dominant endoscopic finding of unintentionally undifferentiated adenocarcinoma. Key Word(s): 1. early gastric cancer; 2. endoscopic finding; 3. endoscopic

submucosal dissection; 4. undifferentiated type Presenting Author: KYOUNGWON JUNG Additional Authors: DO HOON KIM, EUN JEONG GONG, JI YONG AHN, KWI SOOK CHOI, JEONG HOON LEE, KEE WOOK JUNG, KEE DON CHOI, HO JUNE SONG, GIN HYUG LEE, HWOON YONG JUNG, JIN HO KIM Corresponding Author: KYOUNGWON JUNG Affiliations: Asan Medical Center, Asan Medical Center, Asan Medical Center, Asan Medical Center, Asan Medical Center, Asan Medical Center, Asan Medical Center, Asan Medical MCE公司 Center, Asan Medical Center, Asan Medical Center, Asan Medical Center Objective: Gastrointestinal stromal tumors (GIST) are the most common mesenchymal tumors of the gastrointestinal tract. With the recent advances in endoscopic technology, endoscopic resection (ER) has been attempted for the curative treatment of gastric GIST. Here we aim to investigate the feasibility and safety of ER of gastric GIST. Methods: Subjects who underwent ER for gastric GIST at the Asan Medical Center from May 2005 to April 2014 were eligible. Patient factors, tumor factors, procedure factors, and clinical outcomes were evaluated using medical record. Results: A total of 25 patients underwent ER for GIST.

Serum HBsAg and HBV DNA levels were measured with the Abbott Architect HBsAg QT assay and the Cobas Amplicor HBV Monitor Test throughout treatment, respectively. Results: The baseline features were: median age: 49 years, 75.3% men, 37.9% HBeAg-positive (N = 137), 59.2% genotype B infection, median ALT: Daporinad concentration 87 IU/L, HBV DNA: 6.56 log1 0copies/mL, and qHBsAg: 3.3 log10IU/mL. Among them, 249, 1 86 and 94 patients had received ETV therapy for ≧3, 4 and 5 years, respectively (mean duration: 46.5±14.6 months (M)). At 3 and 12M of therapy,

25.6% (HBeAg-positive: 38.4% vs -negative: 17.7%) and 30.8% (HBeAg-posi-tive:40.8% vs -negative: 24.9%) of patients had qHBsAg decline from baseline of ≧50%, respectively. For HBeAg-positive patients, there were significant declines in qHBsAg level between baseline and 3M, 12 and 24M (P=0.0281), and 36 and 48M (P=0.01 1 6). For HBeAg-negative patients, there were significant declines in qHBsAg level between baseline and 3M, 6 and 12M,12 and 24M, 24 and 36M, and 36 and 48M (all P<0.05). Patients were categorized in three subgroups according to the pattern

of qHBsAg decline from baseline:≧50% at 3M, ≧50% at 12M, and <50% at 12M. For HBeAg-positive patients, the subgroup with qHBsAg decline from baseline of ≧50% at 3M of therapy had significantly lower qHBsAg levels than the other two subgroups up to 3 years of treatment. Multi-variate logistic regression analyses identified genotype B (OR=2.572, P=0.0460), ALT ≧120 IU/L (OR=9.295, P<0.0001) and baseline qHBsAg ≧5000 IU/mL (OR=3.795, P=0.0045) as predictors Pritelivir supplier of qHBsAg decline from baseline of ≧50% at 3M of therapy. For HBeAg-negative patients, the

qHB-sAg levels between the subgroups with qHBsAg decline from baseline of ≧50% at 3 or 12M of therapy were similar but was significantly lower than the subgroup with qHBsAg decline from baseline of <50% at 12M of therapy. Multivariate logistic regression analyses identified ALT ≧120 IU/L (OR=8.255, P<0.0001) and baseline qHBsAg ≧5000 log10 IU/mL (OR=6.31 1, P<0.0001) as predictors of qHBsAg 上海皓元医药股份有限公司 decline from baseline of ≧50% at 12M of therapy. Conclusion: Higher base-line serum qHBsAg and ALT levels are predictors of qHBsAg decline from baseline of ≧50% for both HBeAg-positive and -negative patients undergoing ETV therapy. Disclosures: The following people have nothing to disclose: Hsueh-Chou Lai, Cheng-Yuan Peng, Wen-Pang Su, Chia-Hsin Lin, Po-Heng Chuang, Jon-Ta Kao, Sheng-Hung Chen BACKGROUND The goal of HBV treatment is to reduce disease progression to (decompensated) cirrhosis, HCC and death. Entecavir (ETV) inhibits HBV replication and reduces HCC. Recently, CU-HCC, GAG-HCC, and REACH-B HCC-risk scores showed to predict HCC in Asian ETV treated patients. The aim of this study was to investigate risk factors for development of HCC under ETV treatment. METHODS We studied all HBV monoinfected patients treated with ETV monotherapy from 1 1 European referral centers within the Virgil Network.

For patients with MELD

scores above 30, MELD score was the only independent predictor. this website Patients with MELD scores over 30 were at the late stage of ACLF, and factors other than viral replication had a great impact on the prognosis. The livers of these patients had already undergone massive or sub-massive hepatic necrosis. Suppressing viral replication with lamivudine at this late stage was unlikely to be effective, as the main determinants for recovery were liver regeneration and the rapid cessation of ongoing necroinflammation. This could be the reason why some patients’ conditions deteriorated even though the replication of HBV had been suppressed by lamivudine. Our study has suggested that the prognosis of patients with ACLF may be related to the pretreatment HBV DNA load and the JQ1 decline of HBV DNA load during therapy. We found that the mortality of the patients with high HBV DNA load was higher than that

of patients with low HBV DNA load, which may be due to high HBV DNA load patients failing to eradicate HBV at an early stage of liver failure, and a continuously stimulated immune system clearing HBV causes progressive liver damage. Liver failure in patients with low HBV DNA level may be due to the excess of immune reaction. Our study also suggested that for patients with a MELD of score 20–30 (at the early and middle stage of liver failure), by week 4, the mortality with a HBV DNA load decline of more than 2 log10 上海皓元医药股份有限公司 was lower than that of a less than 2 log10 decline. The decreased mortality may be related to the marked reduction of HBV DNA level by lamivudine relieving inflammatory reaction and improving liver function. Therefore, for the patients with a MELD score of 20–30, an early and effective antiviral therapy based on the combination therapy (including artificial liver support system and liver transplantation) could achieve a better therapeutic outcome. More potent antiviral drugs such as entecavir and tenofovir are now available. It is conceivable that these drugs might be even better, especially in reaching a rapid decrease in viral load and a faster

recovery, for the patients with a MELD score of 20–30 who can not achieve a 2 log10 HBV DNA decline. This study has proved that there is no significant difference in mortality between HBeAg-positive and -negative patients treated with lamivudine. HBeAg status before treatment has little effect on mortality in the lamivudine treatment group. HBV DNA load is more valuable than HBeAg status in predicting the prognosis of patients. In this study, we have confirmed that pretreatment HBV DNA load and the decline of HBV DNA load during therapy are not associated with the mortality of HBeAg-negative patients. It may be related to the late stage of chronic hepatitis, severe necrosis and fibrosis of liver, mutation of pre-core and basic core promoter, low HBV DNA load and cases limitation.

, MD, PhD Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Vargas, Hugo E., MD (AASLD Postgraduate Course) Advisory Committees

or Review Panels: Eisai Grant/Research Support: Merck, Gilead, Idenix, Novartis, Z-VAD-FMK manufacturer Vertex, Janssen, Bristol Myers, Ikaria, Abbott Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Vargo, John, MD (AASLD/ASGE Endoscopy Course) Advisory Committees or Review Panels: Olympus America, Inc, Boston Scientific, Inc, Cook Medical, Inc Consulting: Ethicon EndoSurgery Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Volk, Michael, MD (Early Morning Workshops) Nothing to disclose Content of the presentation does not include discussion www.selleckchem.com/products/H-89-dihydrochloride.html of off-label/investigative use of medicine(s), medical

devices or procedure(s) Vos, Miriam B., MD (SIG Program) Nothing to disclose

Content of the presentation does not include medchemexpress discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Ward, John W., MD (Early Morning Workshops, SIG Program) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Warren, Kenneth R., PhD (Federal Focus) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Watkins, Paul B., MD (Early Morning Workshops, General Hepatology Update) Consulting: Abbott, Actelion, Boerringer-Ingelheim, Cempra, Genzyme, Roche, Merck, Medicine COmpany, Momenta, Janssen, Novartis, Otsuka, Pfizer, Sanolfi, Takeda, UCB, Bristol-Myers Squibb, GSK Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Watt, Kymberly D.

Results: POEM was successfully performed and effectively released the dysphagia symptom in all patients. Both the patient symptom scores of achalasia, and the manometric pressure were significantly reduced after POEM. The median Eckardt score was 6.3 ± 1.9 and 0.8 ± 1.6 before and 6 months after POEM, respectively (P < 0.01). Manometric pressure studies (mean lower esophageal sphincter pressure) showed substantial improvement following POEM (preoperative 47.3 mmHg vs. postoperative 20.6 mmHg, P < 0.01). There was one case of intraoperative Gefitinib molecular weight complications: full-thickness esophagotomy, which was repaired endoscopically with no sequelae. Conclusion: POEM appears

to be a safe, effective and less invasive treatment against achalasia. However, further studies on technical method amendments and long-term follow-up examinations are still required. Key Word(s): 1. Esophageal; 2. Achalasia; 3. HRM; 4. POEM;

Presenting Author: UMITBILGE DOGAN Additional Authors: MUSTAFASALIH AKIN, SERKAN YALAKI, NEVINAKCAER OZTURK, AGAHBAHADIR OZTURK Corresponding Author: UMITBILGE DOGAN Affiliations: Objective: Superior mesenteric artery (SMA) syndrome is an unusual cause of proximal intestinal obstruction. The selleckchem syndrome is characterized by compression of the third portion of the duodenum due to narrowing of the space between the superior mesenteric artery and aorta and is primarily attributed to loss of the intervening mesenteric fat pad. We present the case of a 19-year old female who presented with epigastric pain, weight loss, and vomiting. Methods: A 19-year-old thin girl (BMI 13.8) presented with an 18-month history of severe

postprandial epigastric pain, nausea, anorexia, and weight loss. Upper gastrointestinal examination revealed a distended stomach and proximal duodenum to the level of the SMA. Upper endoscopy demonstrated a large, fluid-filled stomach. The duodenum was dilated down to the third part, at which point a tight, pulsating extrinsic stricture was noted. The endoscope could not be advanced past this narrowing. A CT scan of her abdomen confirmed a dilated stomach and proximal duodenum to the level of the SMA medchemexpress in the absence of any external masses (Figure). The patient was successfully treated with open duodenojejunostomy. One month later, she remains asymptomatic with a total weight gain of 1.2 kg. Results: SMAS can be difficult to diagnose and diagnosis is often made on clinical suspicion and radiologic evidence of obstruction. Features of SMA syndrome on upper gastrointestinal series are a dilated proximal duodenum and vertical or oblique compression of the third portion of the duodenum. In our case, abdominal CT with intravenous contrast and upper gastrointestinal series were the only studies required for diagnosis. Although endoscopy is of minor positive diagnostic value, we feel it is mandatory in all patients to rule out intraluminal pathology.

We monitored their aminotransferase levels, Child-Pugh score, MELD score, HBeAg, HBV DNA level and change of ascites at 3 months, 6

months, 9 months, and 12 months after antiviral treatment. We defined clinical responder as patients with a minimum of 1 point of reduction of Child-Pugh score and decreased ascites or patients with more than 2 points of reduction of Child-Pugh score and virological responder as patients with more than reduction of 2 log10 copies of HBV DNA. Results: Eighty (65%) patients were defined as responder after 12 months of antiviral treatment. Baseline ALT, AZD2281 purchase HBV DNA and positive rate of HBeAg of responder are higher than that of non-responder. Patients in response group had the significant improvement of Child-Pugh score

(−1.41 ± 1.90, P < 0.001), the remarkable reduction in HBV DNA level (−3.30 ± 1.68 log10 copies/mL, P < 0.001), the decrease of ascites (36.3%, P < 0.001) compared to the findings before treatment. Serum HBV DNA level at 3 months after treatment showed significant difference between response group (−2.74 ± 1.5 log10 copies/mL) and non-response group (−0.31 ± 1.0 log10 copies/mL) (P < 0.001), whereas serum HBV DNA undetectable rate, seroconversion rate and ALT normalization did not. Conclusion: It is possible to predict the clinical and virological response in patients with hepatitis B virus-related liver cirrhosis by checking the reduction in serum HBV DNA level at 3 months after treatment. Key Word(s): 1. Hepatitis B virus; 2. Liver 上海皓元医药股份有限公司 click here cirrhosis; 3. Antiviral

treatment; 4. Treatment predictor; Presenting Author: MANEESHA BHULLAR Additional Authors: JOHN YAMBA Corresponding Author: MANEESHA BHULLAR Affiliations: Royal Melbourne Hospital; Ballarat Base Hospital Objective: Peginterferon (PEG-IFN) alpha in combination with ribavirin (RBV) represents the most optimal therapy for chronic hepatitis C. Despite its great efficacy, interferon therapy is associated with a spectrum of side effects. Pulmonary toxicities are a rare side effect which may include interstitial pneumonitis, sarcoidosis, pleuritis, bronchiolitis obliterans organizing pneumonia (BOOP), and exacerbation of asthma. Interstitial pneumonitis is a rare but rapidly progressing and potentially fatal adverse event that has been described. This review describes the classification, epidemiology, natural history, diagnostic criteria and management of Interferon-related interstitial pneumonitis and includes an illustrative patient. Methods: A systematic review of the literature using relevant databases was performed to ascertain patients with chronic hepatitis C who developed interstitial pneumonitis on interferon-based therapy, either as a standalone therapy or in combination with ribavirin.

In vitro molecular and cell biology experiments were performed to elucidate the mechanism of SULF1 action. Gene expression microarray was used to identify SULF1-regulated pathways in both transgenic

mice and human HCC. Results Transgenic (Tg) mice overexpressing Sulf1 (Sulf1-Tg) show a higher incidence of large and multifocal tumors with DEN induced learn more carcinogenesis compared to wild type (WT) mice. Lung metastases were found in 75% of Sulf1 transgenic mice but not in WT mice. Significant induction of the TGFβ pathway in Sulf1-Tg mice was demonstrated by microarray gene expression, immunohistochemistry (IHC) and immunoblotting. In vitro studies using immunoblotting, immunocytochemistry and lucif-erase reporter assays confirmed the role of SULF1 in the regulation of TGFβ pathway activation. Further, overexpression of SULF1 promotes TGFβ-induced epithelial-mesenchymal-transi-tion (EMT) both in vivo and in vitro. In cell lines, SULF1 overex-pression augmented TGFβ mediated increase in cell migration and invasiveness. SULF1 expression was also shown to release TGFβ1 into the conditioned

supernatant medium by ELISA assay. Anti heparan sulfate antibodies were used to demonstrate decreased 6-O- sulfation of HCC cell surface after trans-fection with SULF1 by flow cytometry and immunofluorescence. Mutating the catalytic site of SULF1 aborted the desulfating actions of SULF1 and thus abrogated TGFβ pathway activation and the release of selleck screening library TGFβ into the supernatant. This confirms that release of TGFβ medchemexpress from the cell surface by desulfation of HSPGs is the mechanism for SULF1-mediated TGFβ pathway activation. Human HCC overexpressing SULF1 were associated with poorer overall survival (p=0.03; HR 3.1 (1.8-5.4)) and recurrence free survival (p=0.002; HR 4.1 (1.9-8.3)) compared to HCC with low SULF1 expression. We also found strong correlations of SULF1 expression with TGFβ expression and with more than 30 TGFβ related epithelial mesenchymal transition genes in human

HCC. Conclusions In summary, our study proposes a novel role of SULF1 in HCC tumor progression through augmentation of the TGFβ pathway. These findings define SULF1 as a potential biomarker for tumor progression and as a novel target for drug development for HCC. Disclosures: Lewis R. Roberts – Grant/Research Support: Bristol Myers Squibb, ARIAD Pharmaceuticals, BTG, Wako Diagnostics, Inova Diagnostics, Gilead Sciences The following people have nothing to disclose: Renumathy Dhanasekaran, Chun-ling Hu, Gang Chen, Abdul M. Oseini, Catherine D. Moser, Toin H. van Kuppe-velt, Wei Zhou, Jan van Deursen, Taofic Mounajjed, Martin E. Fernandez-Zapico BACKGROUND: Hepatocellular carcinoma (HCC) is a common complication of chronic viral hepatitis.