8 There is also evidence demonstrating that dysregulated LPCs possess tumor-initiating ability in vivo, which suggests that LPCs may participate in hepatocarcinogenesis.9, 10 Our most current study showed that LPCs in HBx knockin mice could be transformed and develop bilineage liver cancer in the presence of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC).11 Therefore, whether malignant transformation of LPCs in the persistent cirrhotic microenvironment this website could initiate HCC deserves exploration. Transforming growth

factor β (TGF-β) is the most potent hepatic profibrogenic cytokine predominantly produced by activated mesenchymal cells upon chronic liver damage.12 Moreover, Talazoparib price TGF-β has also been reported as a multifunctional cytokine that exerts its biological effects on tissue and organ development, cellular proliferation, differentiation, survival, and apoptosis.13 In the liver, TGF-β is hypothesized to serve as the important link among chronic injury, cirrhosis, and HCC.14 Accumulating evidence has demonstrated that TGF-β modulates the expression of numerous genes relevant to tumor development.15 It has been assigned a central role in the epithelial-mesenchymal transition, which is a critical cellular

event during tumor metastasis.16 It has been well established that HCCs usually occur in those cirrhotic livers where TGF-β is highly expressed compared with healthy controls, which suggests a possible pro-oncogenic role of TGF-β in HCC initiation.17 Although the mechanism remains to be defined, TGF-β seems to be very important in HCC occurrence in patients with

cirrhosis. In this study we investigated the influence of hepatic TGF-β on the transition of LPCs to T-ICs and the underlying molecular mechanism. medchemexpress The results provide new insight into hepatic T-ICs-targeted HCC prevention and therapy. AFP, alpha fetal protein; AKT, v-akt murine thymoma viral oncogene homolog; α-SMA, alpha smooth muscle actin; CSC, cancer stem cell; DEN, diethylnitrosamine; FOXO3a, forkhead family of transcriptional regulators subfamily O, 3a; HCC, hepatocellular carcinoma; LPC, liver progenitor cell; PTEN, phosphatase and tensin homolog deleted on chromosome 10; TGF-β, transforming growth factor beta; T-IC, tumor initiating cell. Thirty male Wistar rats and 20 male C57BL/6 mice were purchased from Shanghai Experimental Center of Chinese Academy of Science and maintained under pathogen-free conditions. The hepatocarcinogenesis model in rats was induced by intraperitoneal injections of diethylinitrosamine (DEN; Sigma-Aldrich, St. Louis, MO) once a week at 70 mg/kg for 10 weeks. Two rats were sacrificed biweekly thereafter to monitor HCC development. All of the remaining rats were sacrificed 22 weeks after the first DEN administration.

4) and then used to treat cells at the indicated doses. Sorafenib (kindly provided by Bayer HealthCare, Germany) and lapatinib (purchased from GlaxoSmithKline plc) were prepared in dimethyl sulfoxide. Solvent alone was added to the untreated cells as the control

in each experiment. Cell viability was assayed at 24 hours OTX015 and 48 hours after treatment; for UV treatment, the assays were performed 24 hours after exposure to 30, 65, or 100 mJ/cm2 of UV-B. Cell viability/survival was determined using WST1 assays (Roche Applied Science, Mannheim, Germany), while cell apoptosis was measured by detection of caspase-3 activation (Caspase 3/7 Assay, Promega) as described.7 The experiments were conducted at least twice in triplicate, and the mean of each dose was used to calculate the half maximal inhibitory concentration. Details regarding antibodies, immunoblotting, and immunohistochemistry, immunofluorescence, and confocal microscopy are provided in the Supporting Information.22 Anti-NPM mouse monoclonal

antibody and anti-BAX rabbit polyclonal antibody were used as primary antibodies and anti-mouse and anti-rabbit antibodies coupled with short complementing DNA strands were used as secondary antibodies. Ligation of the DNA strands to a circularized PD0332991 price oligomer in case of direct contact between NPM and BAX and the subsequent rolling circle amplification incorporating labeled nucleotides was performed using the Duolink II kit (Olink Bioscience, Uppsala, Sweden) according to the manufacturer’s instructions. After being washed and counterstained with 4′,6-diamidino-2-phenylindole, the slides were mounted and inspected under a fluorescence microscope. Details regarding subcellular fractionation and co-immunoprecipitation are provided in the Supporting Information. The

tumors and their paratumor liver tissues and related clinical data (all anonymous) from 110 patients with HCC were requested from the Taiwan Liver Cancer Network. Normal liver tissue was obtained from a patient with focal nodule hyperplasia who had undergone tumor resection. The Internal Review Board for Medical Ethics of Chang Gung Memorial Hospital approved the specimen collection procedures, and informed consent was obtained from each subject or subject’s family. All HCC tissues 上海皓元 were reviewed, and the most representative areas of embedded tissue samples were carefully selected and sampled for the tissue microarray blocks. Two core samples were selected from different areas of each HCC tissue. The immunohistochemistry (IHC) scores are defined as follows: 0, negative; 1, weakly positive or in <20% of HCC cells; 2, moderately positive or in 20% to 60% of HCC cells; 3, strongly positive or in >60% HCC cells. The IHC scores were determined by two independent observers (S. J. L. and T. C. C.), where there was disagreement, the slides were re-examined and a consensus was reached by the observers. A Fisher’s exact test was used for comparison between variables.

After determination of total protein by the Lowry assay, 10% polyacrylamide gels were equiloaded with samples, electrophoresed at 90 V, electrotransferred to PVDF membranes, and probed with primary mouse monoclonal antibodies for HMGB-1 or glutathione (Abcam, Cambridge, UK). Secondary goat antimouse horseradish peroxidase (HRP) was used (1:4,000). Blots were developed by ECL (Thermo Scientific, Asheville, NC). Total GSH from whole liver homogenates was measured using the Glutathione Assay Kit

(Cayman Chemicals, Ann Arbor, MI) according to the manufacturer’s protocol. For PCR assays, RNA was isolated from pancreas using a Qiagen RNEasy isolation kit (Qiagen, Germantown, MD). check details qPCR was performed using a standardized preconfigured PCR array (SA Biosciences, Frederick, MD) on the Stratagene MX3000P

(Promega, Madison, WI) according to the respective manufacturers’ protocols. (See Additional Supporting Methods.) To evaluate a possible role for DC in either exacerbating or protecting against APAP toxicity, we employed CD11c.DTR mice in which transient DC depletion can be effected (Supporting Fig. 1). Mice were depleted of DC or mock-depleted and then challenged with APAP. At 12 hours mice were sacrificed and the extent of liver injury determined by histopathology. Mice treated with APAP and depleted of DC (APAP-DC) had markedly more extensive Talazoparib in vivo centrilobular necrosis compared with controls (Fig. 1A,B). Consistent with these findings, serum liver enzymes were highly elevated in APAP-DC mice (Fig. 1C). Similarly, NPC production of inflammatory mediators after APAP challenge, including MCP-1 and IL-6, were higher in mice depleted of DC (Fig. 1D). DC depletion alone, in the absence of APAP challenge, had no effect (Fig. 1A-D). Similarly, effects of APAP were similar in both CD11c.DTR and WT mice, in the absence of 上海皓元医药股份有限公司 DC depletion (not shown). Notably, APAP metabolism appeared unchanged in APAP-DC mice compared with APAP treatment

alone based on tissue glutathione assay and glutathione adduct formation (Supporting Fig. 2A,B). To determine if there was higher systemic toxicity in APAP-challenged mice after DC depletion, we measured serum levels of inflammatory mediators. We found that serum MCP-1, IL-6, and TNF-α were elevated in APAP-DC mice (Fig. 1E,F). However, as expected, organ damage was limited to the liver, as the lungs, kidneys, pancreas, and intestine were histologically normal (Supporting Fig. 3). To determine whether DC depletion resulted in higher APAP-mediated mortality, mice were treated with APAP and depleted of DC or mock-depleted and then observed for up to 2 weeks. Remarkably, approximately half of APAP-DC mice died within 48 hours of challenge, whereas death was rare in control animals (Fig. 2). There was no further mortality observed in APAP-DC mice after 48 hours from the time of APAP challenge.

2; Weishampel, 1997). We divide these into four general (and not mutually exclusive) classes: defense, communication, thermoregulation and sensory

function. These features can be attributed to repulsion of predators and to conspecifics of the same sex in agonistic behaviors (non-exclusively). Notable examples are the horns and frills of ceratopsians, the plates and spikes of stegosaurs, the scutes and tail club of ankylosaurs and the domes of pachycephalosaurs. Weishampel (1981) tested the possibility of a defensive function of lambeosaurine crests and concluded that the bone was too thin to have been of any use in this regard. Ankylosaurs would seem to pose the least controversial example of a defensive function for bizarre structures, in this case the dermal scutes (traditionally and tellingly called ‘armor’) and tail ‘club’ (in ankylosaurids only: Carpenter, 1997, 2001; Vickaryous, Maryanska EPZ-6438 molecular weight & Weishampel, 2004). Scutes cover the skull, the neck, the back, and much of the tail, but there is great variety in their size, form and extent among ankylosaurs

(Carpenter, 1997). This suggests that there was no ‘optimal’ pattern of scute form and distribution, and therefore it is difficult to propose that a defensive function was successively ‘improved’ in ankylosaurs. However, consideration of their outgroups shows that ankylosaurs had more extensive dermal ossifications than the basal thyreophorans Scutellosaurus and Scelidosaurus (the latter often considered an ankylosaur), not to mention the stegosaurs, which lost all but the parasagittal rows (Main et al., Alvelestat ic50 2005). This pattern points to defense as a plausible

basal function of ankylosaur scutes, and suggests that whatever the variations in scute form and distribution, they were ‘good enough’ to serve an adequate defensive function. Yet, as Carpenter (1997: p. 315, fig. 22.6) notes, the variation in scute form, and notably in the more conspicuous long neck spikes, suggests no obvious defensive strategy (see also Scheyer & Sander, 2004), and may instead medchemexpress be primarily related to display. Sexual dimorphism has not been established, so sexual selection has no support, but social selection (Hieronymus et al., 2009) could be investigated further. Several evolutionary strategies may have been involved here. The enlarged and fused scutes at the end of the ankylosaurid tail, preceded by a series of fused caudal vertebrae, have often been invoked as a weapon, and this seems to be supported by the enlarged areas of muscle attachment on the pelvis, hindlimbs and transverse processes of the anterior caudal vertebrae, despite some limits in vertical mobility (Vickaryous et al., 2004). Most attributions of defense to the frills of neoceratopsians have focused on Triceratops (Fig. 3).

2; Weishampel, 1997). We divide these into four general (and not mutually exclusive) classes: defense, communication, thermoregulation and sensory

function. These features can be attributed to repulsion of predators and to conspecifics of the same sex in agonistic behaviors (non-exclusively). Notable examples are the horns and frills of ceratopsians, the plates and spikes of stegosaurs, the scutes and tail club of ankylosaurs and the domes of pachycephalosaurs. Weishampel (1981) tested the possibility of a defensive function of lambeosaurine crests and concluded that the bone was too thin to have been of any use in this regard. Ankylosaurs would seem to pose the least controversial example of a defensive function for bizarre structures, in this case the dermal scutes (traditionally and tellingly called ‘armor’) and tail ‘club’ (in ankylosaurids only: Carpenter, 1997, 2001; Vickaryous, Maryanska Palbociclib price & Weishampel, 2004). Scutes cover the skull, the neck, the back, and much of the tail, but there is great variety in their size, form and extent among ankylosaurs

(Carpenter, 1997). This suggests that there was no ‘optimal’ pattern of scute form and distribution, and therefore it is difficult to propose that a defensive function was successively ‘improved’ in ankylosaurs. However, consideration of their outgroups shows that ankylosaurs had more extensive dermal ossifications than the basal thyreophorans Scutellosaurus and Scelidosaurus (the latter often considered an ankylosaur), not to mention the stegosaurs, which lost all but the parasagittal rows (Main et al., PF-01367338 datasheet 2005). This pattern points to defense as a plausible

basal function of ankylosaur scutes, and suggests that whatever the variations in scute form and distribution, they were ‘good enough’ to serve an adequate defensive function. Yet, as Carpenter (1997: p. 315, fig. 22.6) notes, the variation in scute form, and notably in the more conspicuous long neck spikes, suggests no obvious defensive strategy (see also Scheyer & Sander, 2004), and may instead medchemexpress be primarily related to display. Sexual dimorphism has not been established, so sexual selection has no support, but social selection (Hieronymus et al., 2009) could be investigated further. Several evolutionary strategies may have been involved here. The enlarged and fused scutes at the end of the ankylosaurid tail, preceded by a series of fused caudal vertebrae, have often been invoked as a weapon, and this seems to be supported by the enlarged areas of muscle attachment on the pelvis, hindlimbs and transverse processes of the anterior caudal vertebrae, despite some limits in vertical mobility (Vickaryous et al., 2004). Most attributions of defense to the frills of neoceratopsians have focused on Triceratops (Fig. 3).

Methods: All EUS-P performed at our institution from August 2005 to March 2014 were retrospectively retrieved. Corresponding EUS findings, cytology, and follow-up information were reviewed. EUS-P was performed with the curvilinear

echoendoscope and a 22- CHIR-99021 nmr (n = 41) or 25-guage (n = 1) fine needle. EUS-P was performed via transgastric (n = 24), transduodenal (n = 1), or transrectal (n = 17) approach. Patients undergoing EUS-P via transrectal approach received intravenous prophylactic antibiotics during the procedure. Results: Forty-two consecutive patients (30 men, 12 women; mean age 73.5 years, range, 49–92 years) were identified. Before EUS-P, previous and/or present diagnosis of malignancy had been made in 38 of 42 (90.5%) patients. Ascites confirmed by EUS-P was visible in 14 of 42 (33.3%) CT before EUS. The mean volume of ascites obtained was 12.0 ml (range 1–50 ml). Thirty-one percent (13 of 42) had a proven malignancy. There were two false-negative cytology results. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of EUS-P for diagnosing malignant ascites was 86.7%, 100%, 100%, 93.1%, and 95.2%, respectively. There were no procedure-related complications. Conclusion: EUS-P

is Smoothened antagonist a safe and effective procedure for diagnosing malignant ascites. Nevertheless, negative ascitic fluid cytology from EUS-P does not rule out the presence of peritoneal carcinomatosis. Key Word(s): 1. EUS; 2. EUS-guided paracentesis; 3. ascites; 4. malignant ascites Presenting Author: SU JIN HONG Additional Authors: SHIN HEE KIM, JAE PIL HAN, HEE YOON JANG, MOON HAN CHOI, YUN NAH LEE, BONG MIN KO Corresponding Author: SU JIN HONG Affiliations: Soonchunhyang University School of Medicine, Soonchunhyang University School of Medicine, Soonchunhyang University School of Medicine, Soonchunhyang University School of Medicine, Soonchunhyang University School of Medicine, Soonchunhyang University School of Medicine Objective: A dual focus two-stage optical lens technology was recently introduced. In the near focus mode, endoscopists can perform a close examination of mucosal tissue and capillary networks. The

aim of this study was to investigate the magnifying images on the near 上海皓元 focus method (NFM) compared to those on the conventional magnification method (CMM) under narrow band imaging (NBI) in the patients with gastric epithelial tumors. Methods: An experienced endoscopist performed endoscopies by using NFM and CMM in the 20 enrolled patients with gastric epithelial tumors, respectively. We selected 40 images of 40 sessions of endoscopies in the patients. Ten endoscopists asynchronously reviewed for image quality. The image quality was rated on a 5-point Likert scale (from poor, 1, to excellent, 5) for mucosal microsurface structure, subepithelial microvascular architecture, and demarcation line. All of the enrolled patients received endoscopic submucosal dissection (ESD).

However, deficiency of both ERK and JNK markedly reduced the basal expression of the Cyp7a1 and Cyp8b1 genes, adding another layer of Alvelestat mw complexity in regulating bile-acid synthesis after

MAPK activation. Our study suggests that activating Fxr in the intestine may result in a stronger suppression of bile-acid synthesis, which may be used as a strategy to inhibit bile-acid synthesis to treat diseases with overt bile-acid production. In contrast, inhibiting Fxr in the intestine may lead to enhanced cholesterol conversion to bile acids, which may be used as a useful strategy to reduce cholesterol levels. The authors thank Dr. Silvia Giordano (University of Torino, Torino, Italy) for the cJun-shRNA vector. Additional Supporting Information may be found in the online version of this article. “
“Along with twin and family studies, recent genome-wide association studies suggest that genetic factors contribute to the susceptibility and severity of primary biliary cirrhosis (PBC). Although several reports have demonstrated that the human leukocyte antigen

(HLA) DRB1*08:03 allele is B-Raf inhibitor drug associated with disease susceptibility in Japan, the precise analysis of HLA haplotypes and the role of amino acid alignment have not been fully clarified. We investigated HLA class I A, B, and C and HLA class II DRB1 and DQB1 alleles and haplotypes in 229 Japanese patients with PBC and compared them with the published data of 523 healthy subjects. Significant associations were found with PBC susceptibility for the DRB1*08:03-DQB1*06:01 (13% versus 6%; MCE P = 0.000025; odds ratio [OR] = 2.22) and DRB1*04:05-DQB1*04:01 haplotypes (17% versus 13%; P = 0.044; OR = 1.38). Conversely, there were significant

protective associations with the DRB1*13:02-DQB1*06:04 (2% versus 5%; P = 0.00093; OR = 0.27) and DRB1*11:01-DQB1*03:01 haplotypes (1% versus 4%; P = 0.03; OR = 0.37). The frequency of the DRB1*09:01-DQB1*03:03 haplotype was significantly higher in patients who had received orthotopic liver transplantation (33% versus 11%; P = 0.0012; OR = 3.96). Furthermore, the frequency of serine at position 57 (P = 0.0000015; OR = 1.83) of the DRβchain differed the most in patients with PBC, compared with healthy subjects. Conclusion: This study established the role of HLA haplotypes in determining PBC susceptibility and progression in the Japanese population. Further resequencing of the HLA region is required to more precisely identify the genetic components of PBC.

The gold standards for the final diagnosis were

histologic findings of surgically resected specimen. Additionally, immunophenotyping of specimens obtained by EUS-FNA and surgical resection specimens were compared. Results: Postoperative histological diagnosis were 109 GISTs (85.8%), 7 neurinomas (5.5%), 5 SMT like cancers (3 primary gastric cancers and 2 metastatic cancers) (3.9%), 2 leiomyomas (1.6%), 2 Glomus tumors (1.6%), 1 accessory spleen (0.8%), Vorinostat supplier and 1 gauzeoma (0.8%). In 4 cases puncture was not performed because of anatomical problems. The diagnostic rate of the gastric hypoechoic solid SMT by EUS-FNA was 93.7% (119/127). In 119 surgically resected cases who were conclusively diagnosed by preoperative EUS-FNA, the diagnostic accuracy of EUS-FNA using immunohistochemical analysis of gastric hypoechoic solid SMT was 95.7% (114/119). No major complications were encountered. Conclusion: EUS-FNA with immunohistochemical analysis is an selleck chemicals accurate and safe preoperative histologic test of differential diagnosis of Gastric SMT. Key Word(s): 1. EUS-FNA; 2. GIST; 3. SMT;

4. stomach; 5. immunohistochemical analysis; 6. histology Presenting Author: TEPPEI AKIMOTO Additional Authors: KAZUMASA MIYAKE, YUTA MARUKI, HIROSHI YAMAWAKI, YASUHIRO KODAKA, HIROYUKI NAGOYA, NOBUE UEKI, TETSURO KAWAGOE, SEIJI FUTAGAMI, CHOITSU SAKAMOTO Corresponding Author: TEPPEI AKIMOTO Affiliations: Nippon Medical School, Nippon Medical School, Nippon Medical School, Nippon Medical School, Nippon Medical Schoo, Nippon Medical School, Nippon Medical School, Nippon Medical School, Nippon Medical School Objective: It has been recommended, if antithrombotic treatment is

at least a single use, to perform endoscopic biopsy without cessation of antithrombotic agents, also in the guideline of Japan since 2012. Past reports supporting the guidelines, have indicated the safety of biopsy 上海皓元医药股份有限公司 for these patients by evaluating the development of severe gastrointestinal bleeding complication. However, since such patients are basically elderly, and have comorbidity of cerebro-cardiovascular disease, even if there is no severe bleeding complication after biopsy, anemia due to asymptomatic potential bleeding could lead to serious condition. Therefore, we investigated the development of bleeding complication after biopsy, containing asymptomatic potential bleeding. Methods: This prospective cohort study entered consecutive outpatients who needed esophagogastroduodenoscopy without cessation of antithrombotic agents in our institution, and hemoglobin levels were checked just before endoscopy. Patient performed biopsies among these patients were re-checked hemoglobin levels 1 to 2 weeks later, and were asked about episodes of bleedig and thrombosis.

Portal vein thrombosis is observed in 10–20% of patients with cirrhosis,[16] and increased with cirrhosis severity.[17] These data support our report that Child–Pugh class B was a common point of portal vein thrombosis. Zocco et al.[18] showed an association between portal vein thrombosis and high MELD score. Kim et al.[12] recently reported that MELD-Na score is more useful than MELD score alone. Guha et al.[19] recommended that the MELD-Na score should be measured when toxicity after radiation therapy to the liver is

evaluated. The MELD-Na score of Tyrosine Kinase Inhibitor Library solubility dmso the patients experienced portal vein thrombosis was 11 of higher in our report. Vascular injury is another risk factor for portal vein thrombosis.[20] Irradiation can cause vascular injury.[21, 22] D2 of the portal vein of 40 Gy or more was a common point of portal vein thrombosis in our report. High doses to the portal vein also may be a risk factor for portal vein thrombosis through vascular injury. Bile duct toxicity after SBRT for liver tumors was evaluated with dose–volume metrics in one study.[11] Two cases of bile duct stenosis were reported. One patient was treated twice with SBRT and the high-dose area of more than 80 Gy MG-132 order corresponded to the biliary

stenosis region. In another patient, the biliary tract was exposed to more than 20 Gy but did not correspond to the bile duct stenosis region. They concluded that SBRT with 40 Gy or less in five fractions for liver tumors was feasible with regard to biliary toxicity. In our report, bile duct of the patient who experienced bile duct stenosis was also irradiated with more than 20 Gy. Barney et al.[23] reported one case of grade 3 biliary stenosis after SBRT for cholangiocarcinoma. The patient was treated to a dose of 50 Gy in five fractions for positive resection margins after surgery for intrahepatic cholangiocarcinoma. In our report, the patient who experienced bile duct stenosis also had a history of cholangiocarcinoma and left hepatic lobectomy, although there was no evidence of recurrence of cholangiocarcinoma. In conclusion, portal vein thrombosis may be necessary

to be considered when SBRT for HCC is administrated to patients in higher Child–Pugh class 上海皓元医药股份有限公司 with higher D2 of the portal vein. “
“Background and Aims:  To evaluate and compare laparoscopic splenectomy and partial splenic embolization as supportive intervention for cirrhotic patients with hypersplenism to overcome peripheral cytopenia before the initiation of and during interferon therapy or anticancer therapy for hepatocellular carcinoma. Methods:  Between December 2000 and April 2008, 43 Japanese cirrhotic patients with hypersplenism underwent either laparoscopic splenectomy or partial splenic embolization as a supportive intervention to facilitate the initiation and completion of either interferon therapy or anticancer therapy for hepatocellular carcinoma. We reviewed the peri- and post-intervention outcomes and details of the subsequent planned main therapies.

Portal vein thrombosis is observed in 10–20% of patients with cirrhosis,[16] and increased with cirrhosis severity.[17] These data support our report that Child–Pugh class B was a common point of portal vein thrombosis. Zocco et al.[18] showed an association between portal vein thrombosis and high MELD score. Kim et al.[12] recently reported that MELD-Na score is more useful than MELD score alone. Guha et al.[19] recommended that the MELD-Na score should be measured when toxicity after radiation therapy to the liver is

evaluated. The MELD-Na score of CH5424802 mw the patients experienced portal vein thrombosis was 11 of higher in our report. Vascular injury is another risk factor for portal vein thrombosis.[20] Irradiation can cause vascular injury.[21, 22] D2 of the portal vein of 40 Gy or more was a common point of portal vein thrombosis in our report. High doses to the portal vein also may be a risk factor for portal vein thrombosis through vascular injury. Bile duct toxicity after SBRT for liver tumors was evaluated with dose–volume metrics in one study.[11] Two cases of bile duct stenosis were reported. One patient was treated twice with SBRT and the high-dose area of more than 80 Gy R428 clinical trial corresponded to the biliary

stenosis region. In another patient, the biliary tract was exposed to more than 20 Gy but did not correspond to the bile duct stenosis region. They concluded that SBRT with 40 Gy or less in five fractions for liver tumors was feasible with regard to biliary toxicity. In our report, bile duct of the patient who experienced bile duct stenosis was also irradiated with more than 20 Gy. Barney et al.[23] reported one case of grade 3 biliary stenosis after SBRT for cholangiocarcinoma. The patient was treated to a dose of 50 Gy in five fractions for positive resection margins after surgery for intrahepatic cholangiocarcinoma. In our report, the patient who experienced bile duct stenosis also had a history of cholangiocarcinoma and left hepatic lobectomy, although there was no evidence of recurrence of cholangiocarcinoma. In conclusion, portal vein thrombosis may be necessary

to be considered when SBRT for HCC is administrated to patients in higher Child–Pugh class MCE with higher D2 of the portal vein. “
“Background and Aims:  To evaluate and compare laparoscopic splenectomy and partial splenic embolization as supportive intervention for cirrhotic patients with hypersplenism to overcome peripheral cytopenia before the initiation of and during interferon therapy or anticancer therapy for hepatocellular carcinoma. Methods:  Between December 2000 and April 2008, 43 Japanese cirrhotic patients with hypersplenism underwent either laparoscopic splenectomy or partial splenic embolization as a supportive intervention to facilitate the initiation and completion of either interferon therapy or anticancer therapy for hepatocellular carcinoma. We reviewed the peri- and post-intervention outcomes and details of the subsequent planned main therapies.