Prophylaxis with nucleoside analogs is essential for preventing HBV reactivation in HBsAg positive patients. In contrast,

HBsAg negative with HBcAb and/or HBsAb positive patients should be monitored monthly for an increase in serum HBV DNA during and 12 months after completion of chemotherapy. Nucleoside analogs should be administrated immediately when HBV DNA becomes positive during this period. This strategy facilitates PD0325901 mouse commencement of nucleoside analogs at an early stage of HBV reactivation and results in prevention of severe hepatitis. “
“Proton pump inhibitors (PPI) and H2-receptor antagonists (H2RA) are frequently prescribed in hospitalized patients with cirrhosis. There are conflicting reports regarding the role of acid-suppressive therapy in predisposing hospitalized patients with cirrhosis to spontaneous bacterial

peritonitis (SBP). The aim of this meta-analysis was to evaluate the association between acid-suppressive therapy and the risk of SBP in hospitalized patients with cirrhosis. We searched MEDLINE and four other databases for selleck products subject headings and text words related to SBP and acid-suppressive therapy. All observational studies that investigated the risk of SBP associated with PPI/H2RA therapy and utilized SBP as an endpoint were considered eligible. Data from the identified studies were combined by means of a random-effects model and odds ratios (ORs) were calculated. Eight studies (n = 3815 patients) selleck compound met inclusion criteria.

The risk of hospitalized cirrhotic patients developing SBP increased when using acid-suppressive therapy. The risk was greater with PPI therapy (n = 3815; OR 3.15, 95% confidence interval 2.09–4.74) as compared to those on H2RA therapy (n = 562; OR 1.71, 95% confidence interval 0.97–3.01). Pharmacologic acid suppression was associated with a greater risk of SBP in hospitalized patients with cirrhosis. Cirrhotic patients receiving a PPI have approximately three times the risk of developing SBP compared with those not receiving this medication. Prospective studies may help clarify this relationship and shed light on the mechanism(s) by which acid-suppressive therapy increases the risk of SBP in hospitalized patients with cirrhosis. “
“Background and Aim:  According to the Rome III definition, irritable bowel syndrome (IBS) has been a biopsychosocial dysfunction. We tried to know whether the IBS clinical manifestations were comparable to other countries. Method:  We have reviewed the IBS publications in Taiwan, thus its clinical significances are summarized and compared to others. Results:  Among a selected population of paid physical checkup, the Rome I & II criteria defined prevalences were 17.5% and 22.1%, respectively without an observed female predominance. However, female was a factor leading to constipation predominant IBS (C-IBS).

15 The SNP rs12979860 is located 3 kb upstream

of the IL28B gene, which codes for IFN-λ3 and strongly predicts response to HCV treatment in patients of European and African American origin infected with HCV genotype 1.9, 13 The rs8099917 SNP is located 8 kb downstream of the IL28B gene and 6 kb upstream of the IL28A gene, which codes for IFN-λ2. For this SNP, association to viral response to PEG-IFN/ribavirin treatment has been demonstrated in Australians of North European descent and in Japanese patients.10, 11 There also seems to be a relationship between SNPs near the IL28B gene and viral load9, 13 Selleck Dabrafenib and also biomarkers associated with stage and activity of liver disease, namely patient alanine aminotransferase (ALT) and gamma glutamyltransferase levels.16, 17 The effect of these SNPs on regulation of the IFN-λ family, if any, is yet to be elucidated because the exact causal variant has not been

determined. Interestingly, the distribution of these SNPs in different ethnicities can also explain part of the lower treatment success rate of African Americans in PEG-IFN/ribavirin therapy compared to Europeans and Asians, and the relatively high success rates in East Asians.9 The importance of SNPs near IL28B has been studied for treatment response to some extent in HCV genotype 2–infected patients in mixed cohorts.15 Data Wnt mutation is scarce on HCV genotype 3–infected patients. The primary aim of the current study this website was therefore to assess the relationship between the IL28B genotype and viral response to PEG-IFN/ribavirin

therapy in patients infected with HCV genotype 3. Secondary aims were to assess the relationship between the IL28B genotype and natural history of infection including immunity, activity, and development of liver fibrosis. ALT, alanine aminotransferase; APRI, aspartate aminotransferase platelet ratio index; HCV, hepatitis C virus; IFN, interferon; IU, international units; NR, nonresponse; PEG-IFN, pegylated interferon-α alpha; RVR, rapid viral response; SVR, sustained viral response. Data and clinical samples from two clinical trials were pooled for the present study, a Scandinavian randomized controlled trial18 (RCT, n = 428) and a nonrandomized trial19 (n = 122). In both trials patients were included if they were HCV RNA–positive, treatment naive, and had HCV genotype 2 or 3 and raised ALT levels. Patients were excluded if they were known to have injected drugs or abused alcohol within the last 6 months, had poorly controlled psychiatric illness, decompensated cirrhosis, or were hepatitis B surface antigen (HBsAg) or anti-human immunodeficiency virus–positive.

Clinical data was obtained at endoscopic follow up and also by structured phone interview at 30 days post CER and at the end of follow up. A validated dysphagia score was used. Endoscopic dilatation was performed for dysphagia. Results: Between January

2006 and February 2014, 98 of the 126 patients that were referred for endoscopic management HGD or EOA met inclusion criteria (78.4% male, mean age 66 years). CER was technically successful in 94.5% of patients and was established after a median of 2 sessions. Table 1: Patient, lesion and technical outcome data based on use of VBS.   VBS (n = 23) No VBS (n = 75) p value Median follow up (months, (IQR)) 12 (6–15) 39 (24–45) 0.03 Male 75.0% 80.9% 0.32 Age at AZD1152-HQPA in vivo first EMR 66.2 68.1 0.44 Median C / M length 1 / 3 1 / 3 0.25 CER achieved 91.3% 96.0% 0.53 Oesophageal stricture 26.1% 40.0% 0.06 Need for dilatation 21.7% 33.2% 0.07 Median dilatations (IQR) 2 (1–3) 3 (1–3) 0.13 Median dysphagia score during CER (IQR) 1 (0–2) 2 (1–3) 0.04 Median dysphagia score at follow up (IQR) 0 (0–1) 0 (0–1) 0.60 Conclusions: In this small

pilot study VBS appears to hold promise as a treatment in the prevention of PEROS from CER. Larger prospective randomised see more studies are required to definitively evaluate the role of VBS in the prevention of PEROS. 1. Chung A et al. Complete Barrett’s excision by stepwise endoscopic resection in short-segment disease: long term click here outcomes and predictors of stricture. Endoscopy 2011; 43:1025. FF BAHIN,1,5 NG BURGESS,1,5 S KABIR,2 R PEREZ-DYE,3 V SUBRAMANIAN,4 D MCLEOD,4 H MAHAJAN,4 M PELLISE,1 R SONSON,1 MJ BOURKE1,5 1Department of Gastroenterology and Hepatology, Westmead Hospital, Sydney, NSW, 2Department of Surgery, Westmead Hospital, 3Department of Animal Care, Westmead Hospital, 4Department of Anatomical Pathology, Westmead Hospital, 5University of Sydney, Sydney, NSW Background: Multiband mucosectomy (MBM) is a safe and effective treatment for dysplastic Barrett’s

oesophagus and early oesophageal adenocarcinoma. MBM is associated with infrequent procedural complications, with an incidence of major bleeding, perforation and chest pain requiring hospitalization of <1%. The major limitation of MBM is oesophageal stricture development, which is related to the circumferential and vertical resection extent. Occurrence of strictures may also be influenced by depth, extent and severity of tissue injury. The two main electrosurgical currents (ESC) used for endoscopic resection of oesophageal lesions are microprocessor controlled current (MCC) and low power forced coagulation current (LPFC). Unlike LPFC, MCC limits voltage by on sensing tissue resistance and has a theoretical advantage of limiting the depth of tissue injury. An ESC that effectively excises neoplastic tissue without causing deep injury may limit the occurrence of post MBM strictures.

Clinical data was obtained at endoscopic follow up and also by structured phone interview at 30 days post CER and at the end of follow up. A validated dysphagia score was used. Endoscopic dilatation was performed for dysphagia. Results: Between January

2006 and February 2014, 98 of the 126 patients that were referred for endoscopic management HGD or EOA met inclusion criteria (78.4% male, mean age 66 years). CER was technically successful in 94.5% of patients and was established after a median of 2 sessions. Table 1: Patient, lesion and technical outcome data based on use of VBS.   VBS (n = 23) No VBS (n = 75) p value Median follow up (months, (IQR)) 12 (6–15) 39 (24–45) 0.03 Male 75.0% 80.9% 0.32 Age at Selleckchem Carfilzomib first EMR 66.2 68.1 0.44 Median C / M length 1 / 3 1 / 3 0.25 CER achieved 91.3% 96.0% 0.53 Oesophageal stricture 26.1% 40.0% 0.06 Need for dilatation 21.7% 33.2% 0.07 Median dilatations (IQR) 2 (1–3) 3 (1–3) 0.13 Median dysphagia score during CER (IQR) 1 (0–2) 2 (1–3) 0.04 Median dysphagia score at follow up (IQR) 0 (0–1) 0 (0–1) 0.60 Conclusions: In this small

pilot study VBS appears to hold promise as a treatment in the prevention of PEROS from CER. Larger prospective randomised NVP-LDE225 supplier studies are required to definitively evaluate the role of VBS in the prevention of PEROS. 1. Chung A et al. Complete Barrett’s excision by stepwise endoscopic resection in short-segment disease: long term selleck products outcomes and predictors of stricture. Endoscopy 2011; 43:1025. FF BAHIN,1,5 NG BURGESS,1,5 S KABIR,2 R PEREZ-DYE,3 V SUBRAMANIAN,4 D MCLEOD,4 H MAHAJAN,4 M PELLISE,1 R SONSON,1 MJ BOURKE1,5 1Department of Gastroenterology and Hepatology, Westmead Hospital, Sydney, NSW, 2Department of Surgery, Westmead Hospital, 3Department of Animal Care, Westmead Hospital, 4Department of Anatomical Pathology, Westmead Hospital, 5University of Sydney, Sydney, NSW Background: Multiband mucosectomy (MBM) is a safe and effective treatment for dysplastic Barrett’s

oesophagus and early oesophageal adenocarcinoma. MBM is associated with infrequent procedural complications, with an incidence of major bleeding, perforation and chest pain requiring hospitalization of <1%. The major limitation of MBM is oesophageal stricture development, which is related to the circumferential and vertical resection extent. Occurrence of strictures may also be influenced by depth, extent and severity of tissue injury. The two main electrosurgical currents (ESC) used for endoscopic resection of oesophageal lesions are microprocessor controlled current (MCC) and low power forced coagulation current (LPFC). Unlike LPFC, MCC limits voltage by on sensing tissue resistance and has a theoretical advantage of limiting the depth of tissue injury. An ESC that effectively excises neoplastic tissue without causing deep injury may limit the occurrence of post MBM strictures.

Phenothiazines, the group to which

promethazine belongs, exert their influences through blockage of D2 receptors in the basal ganglia and limbic system.[38] The mechanism by which phenothiazines act in migraine is still indefinite. It is probably associated with the cumulative effect of its antagonistic activity at several receptors (adrenergic, muscarinic cholinergic, Pritelivir order histaminic, and serotonergic receptors), as well as at chemoreceptor trigger zone of brain medulla.[39, 40] The clinical pharmacology and practical applications of promethazine hydrochloride have been described by Bain et al.[41] Since its introduction, promethazine has been used as an antiemetic drug for prevention and treatment of nausea and vomiting induced

by narcotic therapy,[42] migraine episodes,[43] cancer chemotherapy,[44] motion sickness,[45] and during labor.[46] The clinical effects appear within average 20 minutes after oral administration with duration of 4-6 hours lasting effect.[47] Promethazine is one of the most important element of antihistaminic drugs providing substantial level of sedation and headache relief.[48] It possesses more sedative effect than some of the other conventional antiemetic medications.[49] In the current trial, according to outpatient basis, the rate of patient selleck compound population reporting a baseline moderate intensity of migraine (65.7% of moderate and 34.3% of severe migraine) corresponds with that frequently included in triptan studies (65% of moderate and 35% of severe migraine).[33, 50] Outpatient selleck kinase inhibitor management is the preferred method for treating acute migraine headache, and consists of nonsteroidal anti-inflammatory drugs, D2 antagonists, serotonin agonists, opioids, local anesthetics, and steroids.[51] In this

study, we decided to study combination of sumatriptan from triptan group and promethazine because sumatriptan as a specific and selective serotonin agonist has extensive efficacy, tolerability, and safety record in acute migraine therapy. The optimum oral dose of sumatriptan has been determined at 50 mg,[52] which is the lowest dose with maximum therapeutic benefit and the highest effective dose with placebo-level AEs.[53] This dosage provides efficacy similar to the 100-mg dose of sumatriptan.[14] Previous studies have demonstrated that oral sumatriptan (50 mg) is an efficient therapy for the variety of headaches reported by the general population of migraine sufferers.[54] Moreover, a meta-analysis of 53 randomized controlled trials of oral triptans showed that the efficacy of sumatriptan 50 mg was widely expressive of the triptan class.[1] Consequently, sumatriptan 50 mg was selected as the active comparator for this trial. Considering the total percentage of patients taking the second dose of study drug, a statistically significant difference was obtained in favor of SP treatment compared with SPr (49.0% vs 22.6%).

Hence, in patients with NAFLD, circulating miRNAs can be explored for improving diagnosis of liver injury and population screening Apitolisib concentration of CVD. “
“Background and Aim:  A significant proportion with inflammatory bowel disease (IBD) exhibit an adverse clinical phenotype reflected in endpoints like surgery and hospitalizations. We sought to identify clinico-demographic factors associated with these adverse consequences that may be amenable to change. Methods: 

Over 6 months IBD patients visiting a metropolitan center were prospectively identified and given a comprehensive survey addressing patient knowledge, mental health and satisfaction with medical care along with other clinical data. Logistic regression analyses assessed for associations between clinico-demographic variables and adverse clinical endpoints (previous surgery [ever] and/or recent inpatient admission over a 16 month observation period). Results:  Of 256 IBD patients,

162 responded (response rate 63%); 95 (59%) had Crohn’s disease (CD), 63 (40%) ulcerative colitis (UC), four indeterminate colitis; 53% were female. Factors associated with a greater likelihood of hospitalization included moderate/severe disease activity, psychological co-morbidity, numbers of medications and outpatient visits selleck (odds ratio [OR] 7.09 [2.83–17.76], 4.13 [1.25–13.61], 1.26 [1.03–1.54], 1.17 [1.00–1.37] respectively; all P < 0.05). Post-surgical patients were more likely to have CD, more currently active disease and longer disease duration (OR 8.55 [2.43–29.4], 3.52 [1.26, 9.87], 1.14 [1.08, 1.21] respectively; all P < 0.02), yet were less likely to have previously seen a gastroenterologist, OR 0.25 [0.08–0.76] (P = 0.01). Conclusions:  ‘At risk’ patients (those previously operated, with ongoing disease activity,

see more dissatisfaction and/or psychological comorbidities) may benefit from early identification and more intensive management. Specialist gastroenterology care appears to be under-utilized in operated patients yet may reduce future IBD morbidity. “
“B cells are present within chronically inflamed liver tissue and recent evidence implicates them in the progression of liver disease. In addition, a large proportion of hepatic lymphomas are of B-cell origin. The molecular signals that regulate normal and malignant B-cell recruitment into peripheral tissue from blood are poorly understood, leading us to study human B-cell migration through hepatic sinusoidal endothelial cells in flow-based adhesion assays. In such assays, human blood-derived B cells were captured from shear flow without a previous rolling phase and underwent firm adhesion mediated by vascular cell adhesion molecule-1 (VCAM-1).

TDF was well tolerated overall; 3 patients (1.1%) discontinued the study early for an AE (2-MRI and 1-NRF). No patients had a confirmed increase in serum creatinine of ≥0.5 mg/dL, and 1% (2-NRF) had transient PO4 <2 mg/dL. Nine MRI patients had CLCr <50 mL/min (pre-treatment range: 49–61 mL/min) that stabilized with dose adjustment. No differences were observed in % change in spine or hip BMD over 96 weeks, and no clinically relevant bone loss was noted in either group. At Week 96 there was no significant difference (missing = failure) in % with HBV DNA < 400 copies/mL, or rates of ALT normalization or HBeAg loss/seroconversion. Conclusions: The

safety, PK, and efficacy of patients with MRI receiving TDF were similar to NRF patients; in MRI patients there was no evidence of increased

risk for renal- or bone-related complications. W SIEVERT,1 S STRASSER,2 E GANE,3 J GEORGE,4 F WEILERT,5 www.selleckchem.com/products/Everolimus(RAD001).html JF FLAHERTY,6 P DINH,6 KM KITRINOS,6 JG MCHUTCHISON,6 P MARCELLIN7 1Monash University and Monash Medical Centre, Melbourne, VIC; 2Royal Prince Alfred Hospital, Pirfenidone solubility dmso Sydney, NSW; 3Auckland City Hospital, Auckland, New Zealand; 4Storr Liver Unit, University of Sydney at Westmead Hospital, Sydney, NSW; 5Waikato Hospital, Hamilton, New Zealand; 6Gilead Sciences, Foster City, CA, USA; 7Hôpital Beaujon, Clichy, France. Background: We previously reported that 5 years of tenofovir DF (TDF) therapy in mostly treatment naïve patients results in sustained virological suppression with no development

of resistance and was associated with either the halting or regression of fibrosis in 96% of patients. Here we present 6 year results from these two ongoing 8 year studies (Studies 102 and 103). Methods: After 48 weeks of double-blind comparison of TDF to adefovir dipivoxil, find more all patients undergoing liver biopsy were eligible to continue open-label TDF. Patients were assessed every 3 months for safety and efficacy with annual resistance surveillance; annual assessments of bone mineral density (BMD) of the spine and hip by DXA were added starting at year 4. Results: In a total 641 patients who were initially randomized and treated, 585 (93%) entered the TDF extension phase, and at Year 6, 466 (73%) remain on study. Efficacy results at Year 6 are shown in the table. TDF was well tolerated over the 6 year evaluation period. Less than 2% of patients discontinued TDF due to an adverse event, and ≤1.5% experienced a confirmed renal event (≥0.5 mg/dL increase in serum creatinine from baseline, phosphorus <2 mg/dL, or CrCL <50 mL/min). BMD (T scores) was stable over 2 years of evaluation. No resistance to TDF has been detected through Year 6. Conclusions: In these two trials, TDF remains safe and effective over a 6 year treatment period, with no detectable resistance to TDF; a relatively low rate of renal events and no evidence of clinically relevant bone loss were also observed.

Figure 3B for the same patient with K19 staining highlights CoH loss around a portal tract. K7 staining highlighted the same biliary structures as did K19 staining, but also, in some specimens (Table 1), showed very focal periportal hepatocyte click here positivity which is common (although usually more widespread) in typical PBC biopsy specimens. EpCAM showed identical patterns of staining to

K19, differing in subcellular localization as expected (EpCAM is membranous, K19 is cytoplasmic), whereas no EpCAM-positive hepatocytes were seen in any normal, minimal change PBC, or CHC specimens (data not shown). In current American Association for the Study of Liver Diseases; (AASLD) Practice Guidelines3 diagnosis of PBC can be made with compatible biochemical tests (esp. elevated AP), positive AMA (found in ∼95% of patients), and/or a compatible histological liver biopsy specimen. However, no standard case definition has been universally accepted.10 We have previously suggested that marked CoH loss (recognized selleck screening library by immunostaining for K19 or other cholangiocyte marker) is an earliest

change in PBC,4 a finding confirmed by others,11 although no studies have assessed clinical outcomes of patients with suspected PBC, who have minimally injured liver biopsies by routine stain, but marked CoH loss with immunostaining, a finding we term “minimal change PBC. We prospectively identified patients suspected to have PBC, but who did not meet definitive, nonbiopsy criteria for diagnosis. Five of six study patients had detectable serum autoantibodies, two of whom were AMA-positive prior see more to treatment (becoming AMA-negative with treatment) and four of six had either antismooth muscle antibody (ASMA) or ANA, serologic findings typical for AMA-negative PBC.12 The four AMA-negative patients (67%) is a higher rate than has been previously reported, which was 1/10 (10%) in our control group, in keeping with other published reports.13, 14 The difference may relate to our small cohort size and not have meaning; however, it could indicate that PBC identifiable only by CoH loss is such

an early disease stage that perhaps AMA have not yet become detectable by standard assays. To exclude the possibility that CoH loss is a nonspecific finding, unrelated to PBC, we compared the study group to two disease control specimen sets, both of which had preserved CoH. Compared to CHC, we confirm that CoH loss is not a nonspecific reaction to a chronic, portal, and peri-portal inflammation. In order to exclude the possibility that the study patients were simply recovering from an acute injury that would have spontaneously improved even without treatment, we assessed biopsy specimens from patients with chronic elevated serum liver tests for greater than 6 months, but without clinical data to indicate inciting infections or toxins. Biopsy specimens showed clustered macrophages indicating recent hepatic activity, but ongoing hepatitis was absent.

Figure 3B for the same patient with K19 staining highlights CoH loss around a portal tract. K7 staining highlighted the same biliary structures as did K19 staining, but also, in some specimens (Table 1), showed very focal periportal hepatocyte Pexidartinib supplier positivity which is common (although usually more widespread) in typical PBC biopsy specimens. EpCAM showed identical patterns of staining to

K19, differing in subcellular localization as expected (EpCAM is membranous, K19 is cytoplasmic), whereas no EpCAM-positive hepatocytes were seen in any normal, minimal change PBC, or CHC specimens (data not shown). In current American Association for the Study of Liver Diseases; (AASLD) Practice Guidelines3 diagnosis of PBC can be made with compatible biochemical tests (esp. elevated AP), positive AMA (found in ∼95% of patients), and/or a compatible histological liver biopsy specimen. However, no standard case definition has been universally accepted.10 We have previously suggested that marked CoH loss (recognized GS-1101 price by immunostaining for K19 or other cholangiocyte marker) is an earliest

change in PBC,4 a finding confirmed by others,11 although no studies have assessed clinical outcomes of patients with suspected PBC, who have minimally injured liver biopsies by routine stain, but marked CoH loss with immunostaining, a finding we term “minimal change PBC. We prospectively identified patients suspected to have PBC, but who did not meet definitive, nonbiopsy criteria for diagnosis. Five of six study patients had detectable serum autoantibodies, two of whom were AMA-positive prior selleck chemicals llc to treatment (becoming AMA-negative with treatment) and four of six had either antismooth muscle antibody (ASMA) or ANA, serologic findings typical for AMA-negative PBC.12 The four AMA-negative patients (67%) is a higher rate than has been previously reported, which was 1/10 (10%) in our control group, in keeping with other published reports.13, 14 The difference may relate to our small cohort size and not have meaning; however, it could indicate that PBC identifiable only by CoH loss is such

an early disease stage that perhaps AMA have not yet become detectable by standard assays. To exclude the possibility that CoH loss is a nonspecific finding, unrelated to PBC, we compared the study group to two disease control specimen sets, both of which had preserved CoH. Compared to CHC, we confirm that CoH loss is not a nonspecific reaction to a chronic, portal, and peri-portal inflammation. In order to exclude the possibility that the study patients were simply recovering from an acute injury that would have spontaneously improved even without treatment, we assessed biopsy specimens from patients with chronic elevated serum liver tests for greater than 6 months, but without clinical data to indicate inciting infections or toxins. Biopsy specimens showed clustered macrophages indicating recent hepatic activity, but ongoing hepatitis was absent.

In this respect, serum is CP-690550 supplier a difficult target to develop high-specificity diagnosis markers. In this context, CA19-9 and CEA can also be expected to be useful for bile diagnosis. Unfortunately, the sensitivity of CA19-9 is not high enough, and that of CEA is still lower.4, 6, 8, 9 At present, however, CA19-9 is regarded as a “high-sensitivity” marker for the bile diagnosis of CC, although the reported diagnostic scores are not satisfactory; i.e., 65.0% (sensitivity), 69.0% (specificity), and 0.69 (area under the curve [AUC]).7 On the other hand, imaging techniques such as ultrasonography, computed tomography, and magnetic resonance

cholangiography are also performed as well as pathological diagnosis for confirmation of CC. However, this diagnosis of CC is difficult because of its location, size, and desmoplastic characteristics.4-6 Regarding the diagnosis of LY2109761 order CC, biliary cytology and brush cytology are performed routinely, although the sensitivity of exfoliative biliary cytology is generally low (40%-69%).10-12

Thus, a novel biological diagnostic marker for CC is needed to provide a fully workable method to identify the lesion at as early a stage as possible. Aberrant glycosylation is often associated with individual steps of carcinogenesis and progression.13, 14 For example, CA19-9 is a representative carbohydrate antigen, sialyl-Lea, whose expression is associated closely with cancers originating from digestive tissues. Critically, however, core proteins that carry this classic epitope have not been characterized fully. By contrast, α-fetoprotein (AFP) has been shown to function as a good diagnostic marker of hepatocellular carcinoma (HCC), and

its sensitivity and specificity have been improved significantly by combining measurement of AFP find more level with Lens culinaris agglutinin reactivity (AFP-L3).15, 16 AFP-L3 is defined as a glycoprotein carrying biantennary N-glycan(s) having a α1,6 core fucose, whose expression is relatively low in liver cirrhosis. This difference in expression emphasizes the importance of glycosylation change (glyco-alteration) occurring on the same protein.17 Thus, glyco-alteration of particular glycoproteins has attracted increasing attention among biomarker investigators. We recently developed a simple and ultrasensitive procedure for differential glycan profiling based on a lectin microarray.18-20 This novel array technology enables a straightforward, high-throughput glycan analysis with multiplex lectins that can target even formalin-embedded small tissue sections (<1.5 mm in diameter, 5 μm in thickness).21 Using this advanced technology, we identified Wisteria floribunda agglutinin (WFA) as the best probe to detect glyco-alteration in ICC and to distinguish the expression in ICC lesions from that in normal specimens. We further identified mucin 1 (MUC1) as a potential ICC-specific glycoprotein marker that carries WFA-positive glycans.