These results indicate that deletion of GNMT is associated with an increased expression of genes inducing steatosis

(CD36, ADFP, PPARγ, CYP4A10, CYP4A14, UCP2) and also with a reduction in the expression of PPARα, a major activator of fatty acid oxidation, and that these changes are prevented by NAM administration. Moreover, these findings indicate that the hepatic reduction in total transmethylation flux caused by deletion of GNMT and the concomitant accumulation of SAM can be compensated by NNMT if exogenous NAM is provided. Additionally, our results indicate that NAM administration to GNMT-KO mice prevents global DNA buy CP-868596 hypermethylation as well as the abnormal expression of numerous genes involved in fatty acid metabolism, oxidative stress, fibrosis, apoptosis, and proliferation observed in untreated animals. More significantly, NAM treatment not only normalized the expression of all these genes and proteins in GNMT-KO mice, it also prevented the development of fatty liver and fibrosis. The mechanism by which GNMT deletion leads to fibrosis is not known; it is possible that increased lipid

accumulation and apoptosis in GNMT-KO hepatocytes activate hepatic stellate cells,37, 38 the central mediators of liver fibrogenesis. Accordingly, NAM may attenuate fibrogenesis by preventing hepatic fat accumulation and apoptosis by lowering SAM content. At present, however, alternative Selleck Erlotinib direct effects of NAM on stellate cell activation cannot be excluded. In conclusion, these results rule out the possibility that the interaction of GNMT with other

target proteins, such as arrestin-3 and β-arrestin-111 may play a critical role in the initiation of liver disease in GNMT-KO mice. Because GNMT expression is down-regulated in patients with cirrhosis and HCC, and because some medchemexpress individuals with GNMT mutations have spontaneous liver disease,3, 4, 9, 10 the clinical implications of the present findings are obvious, at least with respect to the latter group. NAM has been used for many years to treat a broad spectrum of diseases without significant side effects.39, 40 Our findings suggest that individuals with GNMT mutations are likely to benefit from NAM treatment. We thank Begoña Rodríguez for technical assistance. Additional Supporting Information may be found in the online version of this article. “
“Crohn’s disease pathogenesis involves alterations in the gut microbiota. We characterised the mucosa associated microbiota at the time of surgical resection and 6 months later to identify bacterial profiles associated with recurrence and remission. Tissue samples were collected from surgical resection specimens in 12 Crohn’s disease patients, and at 6 months post-operative colonoscopy from the neo-terminal ileum and anastomosis. Endoscopic recurrence was assessed using the Rutgeerts score. Microbiota was characterized using microarray and 454 pyrosequencing.

6B).

Notably, cluster C2 that encompassed subtype MAPK inhibitor A HCC and CK19+ neoplastic lesions in the rat also included human HCC defined by the progenitor-type HB signature and the worst clinical prognosis.19 An optimized gene classifier from the CK19-associated genes contained 110 genes that demonstrated a highly significant prognostic power with a probability of correct class prediction of 0.98 (P < 0.001) (Fig. 6C; Supporting Table 3). The overall performance of the classifier in seven different prediction models ranged from 89%-98% (Supporting Table 4A,B). Accordingly, the gene signature efficiently predicted both survival of patients (P < 0.009) and time to recurrence (P < 0.006) (Fig. 6D,E). A Cox proportional hazard model applied to test the prognostic utility of the gene classifier discriminated the patients according to the clinical prognosis (Fig. 7). Using Wald statistics, 29 significant genes were then identified (P < 0.01) with at least a twofold difference in expression ratio. This signature successfully differentiated the patients according to survival, thus

strengthening the prognostic power of the CK19-associated gene signature. In this study, we report a comprehensive characterization of the neoplastic development induced in the rat liver by the RH protocol. To investigate evolution of the early preneoplastic p38 MAPK inhibitor lesions, the persistent GSTP+ lesions (Fig. 1) ranging from foci to fully developed HCC were examined for the expression of the HPC marker CK19 and subjected to global gene expression analysis (Fig. 4). A subset of the early focal lesions (9/19) as well as adenomas (8/20), eHCC (12/13), and all HCC (8/8) were CK19+ (Figs. 2 and

3; Supporting Fig. 3). Significantly, unsupervised clustering of hepatic lesions without prior knowledge of CK19 staining clearly differentiated the CK19+ from CK19-negative lesions (Fig. 4). Assessment of the translational value of animal models of human cancer that are generated under conditions far different from those seen in humans poses a major challenge. As an attempt to meet 上海皓元医药股份有限公司 this challenge, we earlier established a comparative functional genomics approach to evaluate the usefulness of mouse models for human liver cancer.34, 35 This approach has been successfully used for other cancers as well.33, 36 Here we applied this approach to show a co-segregation of the CK19+ rat lesions with human HCC of the subclass A and HB subtypes (Fig. 6). Recently, we determined that the gene expression profiles of HB subtype and fetal rat hepatoblasts are closely related,19 suggesting that the CK19+ foci may be of HPC origin. Furthermore, the CK19+ foci clustered together with the more advanced HCCs, indicating that they might progress to full-blown HCC.

Bands for claudin-4, which is not expressed in the liver, and claudin-5, which is expressed only in endothelial junctions,16 were not detected (Fig. 3A and data not shown). RTPCR analysis showed that expression of the claudin-2 gene was 10-fold lower in KO

mice, suggesting its regulation at the transcriptional level by β-catenin (Fig. 3B). Immunostaining for claudin-2 showed prominent zone 3 staining in WT but not in KO livers (Supporting Fig. 2). Hepatic tight junctions form the blood–bile barrier that keeps sinusoidal blood spatially separated from canalicular bile. We asked whether disruption of hepatic tight junction integrity from loss of claudin-2 could account for the bile secretory defect in KO mice. We tested the functional integrity of hepatic tight junctions in KO mice by assaying for biliary FD-40 excretion after intravenous injection (Fig. 3C). Disruption of tight junctions Antifection chemical causes an early peak in bile fluorescence.13 RXDX-106 mw No such early peak in fluorescence was detected in KO mice to suggest defective tight junction integrity. Instead, KO mice had a significant delay in FD-40 excretion in bile, likely resulting from their lower bile flow rate. Evaluation by transmission electron microscopy showed normal appearing tight junctions in KO mice (Fig. 3D). To further evaluate the cholestatic phenotype in KO mice, we stained liver sections with TRITC-phalloidin for F-actin, which exhibits pericanalicular localization

in hepatocytes. WT livers exhibited interconnected, evenly spaced “train-track” bile canaliculi (Fig. 4A,B). In contrast, KO livers showed distorted bile canaliculi

(Fig. 4C,D) with occasional grossly misshapen “corkscrew” shaped canaliculi (Fig. 4D-F). We confirmed that these abnormal structures seen in KO livers on F-actin staining were bile canaliculi by double-labeling liver sections with TRITC-phalloidin and anti–zona occludens 1 antibody (Supporting Fig. 2). Bile canalicular morphology was also evaluated by scanning electron microscopy (Fig. 5A-D). Canaliculi in KO livers were dilated, with an average diameter of approximately 1 μM, which was 25%-40% greater than in WT mice. Canaliculi in KO livers were tortuous and showed frequent blind loops. Strikingly, there was a marked medchemexpress paucity of microvilli within canaliculi in KO mice with corresponding bare areas within the canalicular lumina (Fig. 5C,D). The subsinusoidal surface of KO hepatocytes also showed a relative decrease in microvilli by both scanning (Fig. 5D) and transmission electron microscopy (Fig. 5F). The ultrastructure of bile ducts within portal triads appeared normal in KO mice (data not shown). Cholic acid feeding has been used to study bile acid-mediated liver toxicity.17 To determine the effect of cholic acid feeding, mice were fed either chow or chow supplemented with 0.5% cholic acid for 2 weeks. Both strains of mice had body weight loss on the cholic acid diet (Fig. 6A) but increase in liver weight and liver-to-body weight ratio (Fig. 6B).

To further elucidate the mechanism for inhibiting Notch1 signaling Y-27632 concentration activity by HBx expression,

we first performed qRT-PCR to investigate the effect of HBx expression on the transcriptional level of Notch 1. We were not able to show differences of Notch1 mRNA levels between control and HBx-transfected Huh7 cells using qRT-PCR (Fig. 2A). qRT-PCR and flow cytometry analyses were used to determine the effect of HBx on the expression levels of the five ligands of Notch1. Neither mRNA nor protein levels of Jagged-1, Jagged-2, DLL-1, DLL-3, and DLL-4 were affected by HBx expression (Fig. 2B,C). It was postulated that expression of HBx might suppress Notch1 signaling through the inhibition of Notch1 cleavage. Western blotting of the protein levels of full-length Notch1 (Notch1-FL) and extracellular truncated Notch1 (NEXT1) revealed that in contrast to decreased ICN1 protein level,

NEXT1 protein level was increased, whereas Notch1-FL protein level was unaffected by HBx transfection in Huh7 cells (Fig. 2D). Because Notch1 signaling activation requires two consecutive proteolytic cleavages mediated by TACE and γ-secretase, respectively, which means TACE-mediated extramembranous cleavage releases NEXT1 from Notch1-FL, and the consecutive γ-secretase–mediated intramembranous cleavage releases ICN1 from NEXT1,15 decreased ICN1 protein level and increased NEXT1 protein level in the presence of unaffected Notch1-FL protein level might be due to reduced ICN1 releasing from NEXT1 through inhibited γ-secretase–mediated proteolytic cleavage by HBx expression. BMS-777607 These results 上海皓元医药股份有限公司 suggest that HBx decreases ICN1 protein level through reduction of Notch1 cleavage rather than affecting Notch1 transcription or its ligand expression. Two consecutive Notch1 cleavages after ligand binding are mediated by TACE and γ-secretase.18 γ-Secretase is a large protease complex composed of catalytic

subunits (Psen1 and Psen2) and accessory subunits (PEN2, APH1, and Nct).27 To further characterize whether TACE or γ-secretase, and which component of γ-secretase was involved in the process of reduced Notch1 cleavage by HBx, qRT-PCR for TACE, Psen1, Psen2, PEN2, APH1, and Nct were performed on HBx-transfected Huh7 cells. Compared with control cells, HBx-overexpressing cells displayed no significant differences of TACE, Psen2, PEN2, APH1, or Nct mRNA levels, but reduction of Psen1 mRNA levels was observed (Fig. 3A). Consistent with the reduction of Pesn1 mRNA levels, western blotting revealed that Pesn1 protein level was also decreased after HBx transfection in Huh7 cells (Fig. 3B). To examine the effect of HBx expression on Psen1 promoter activity, luciferase reporter assay with pGL3-Psen1-Pro plasmid and pGL3-Basic control vector were employed in transfected Huh7 cells. The relative luciferase activity of Psen1 promoter was reduced in the HBx-overexpressing cells compared with that of control cells (Fig. 3C).

001). The causes of death were multiorgan failure (n = 14), septic shock (n = 6), liver failure (n = 5), acute respiratory distress syndrome (n = 1), and unknown (n = 2). This study confirms that terlipressin and albumin is an effective therapy for the management of type 1 HRS in patients with cirrhosis.1–5, 11, 12, 21 Forty-six percent of patients included responded to treatment with a marked improvement of renal function. This efficacy rate is similar to that reported in a recent meta-analyses.13

Moreover, the results of the current study confirm the previous observations of studies including lower numbers of patients, Palbociclib indicating that response to treatment is associated with an improvement of circulatory function that is markedly impaired in patients with HRS.16, 17, 21–24 In fact, patients who responded to therapy selleck chemical showed a significant increase in arterial pressure and a suppression of the markedly increased activity of the renin-angiotensin-aldosterone system and sympathetic nervous system at the end of treatment; these findings

are consistent with an improvement of the low effective arterial blood volume characteristic of HRS.1–5, 11, 12 By contrast, no increase in arterial pressure was observed in patients who did not show an improvement in renal function. These findings strongly suggest that the beneficial effect of terlipressin in the management of HRS is related to its capacity of improving systemic hemodynamics. Reasons for the lack of improvement of systemic hemodynamics in some patients with type 1 HRS treated with terlipressin are unknown but may include, 上海皓元医药股份有限公司 among others,

increased levels of vasodilator cytokines, increased bacterial products or latent infections, and presence of concomitant adrenal insufficiency. These possible causes deserve investigation in order to improve the efficacy of treatment. The current study was intended to assess predictive factors of response to terlipressin and albumin in a consecutive series of patients with type 1 HRS treated with the same standardized protocol. Independent predictive factors of response to treatment were baseline serum bilirubin levels and an increase in MAP of 5 mm Hg at day 3 of treatment. Seven of the 7 patients (100%) with baseline serum bilirubin <10 mg/dL who showed an increase in MAP ≥5 mm Hg at day 3 responded to treatment with terlipressin and albumin. By contrast, only one of the 11 (9%) patients with baseline serum bilirubin ≥10 mg/dL and a change in MAP <5 mm Hg had response to treatment. Predictive factors of response reported in previous studies in patients with HRS included baseline Child-Pugh and MELD scores, serum creatinine, and arterial pressure.

Results: Thirty-eight patients were included in this analysis. The majority of the included patients were white (90%) males (100%) with median age at initial cancer diagnosis of 70 years. Eight patients developed recurrent CRC. Six of these eight patients underwent a total proctocolectomy at the time of diagnosis of recurrent cancer. There was no evidence of metastasis at the time of the completion colectomy. Recurrence free survival after partial colectomy was 97%, 80% and 67% at 1, 5, and 10 years after partial colectomy Conclusion: Current guidelines recommend total protocolectomy in patients with UC who develop CRC. Our study suggests that partial colectomy

may be a viable option, especially in older patients with close endoscopic surveillance, as about one-fifth of the cohort developed recurrent lesions and all of these were detected prior to any metastasis. Key Word(s): 1. Palbociclib mTOR inhibitor Colorectal cancer; 2. partial colectomy; 3. ulcerative colitis; Presenting Author: BONG OH MA Additional Authors: DAE HYEON CHO, HAEJIN YANG, KWANG MIN KIM, SANG GOON SHIM Corresponding Author: DAE HYEON CHO Affiliations: Sungkyunkwan University Samsung Changwon Hospital

Objective: Crohn’s disease (CD) is a chronic relapsing inflammatory disorder of the gastrointestinal tract. It may have a number of extra-intestinal manifestations including psoriasis. However, few have evaluated the association between psoriatic arthritis (PsA) and CD. Herein, we present a case of 52-year-old woman with concurrent PsA and CD. Methods: A 52-year-old woman was referred to our hospital for experiencing abdominal pain and watery diarrhea for 2 weeks. She had been diagnosed with

psoriatic arthritis for 1 year in our rheumatology department and managed well. Results: The abdomen was distended and there were no gross bloody diarrhea. Abdominopelvic computed tomography revealed edematous wall thickening of the entire colon with large amounts 上海皓元医药股份有限公司 of ascites. Fluid analysis from paracentesis was consistent with transudate. After fluid administration and antibiotic therapy, the patient became stable and colonoscopy was carried at 2 weeks. Ulcers with scars were noted at the terminal ileum and ileocecal valve. Large longitudinal ulcers and inflammatory polyps were also noted from entire colon with a segmental pattern. Colonic histopathology of biopsies demonstrated the inflammation involved the mucosa and submucosa with granulomas supporting the diagnosis of CD. Following consultation with a rheumatologist, treatment with prednisone 30 mg/day, mesalazine 3 g/day and azathioprine 50 mg/day was introduced. After 3 weeks of intensive immunosuppressive therapy, there were marked improvements in clinical presentation of Crohn’s disease. And the patient’s manifestation with psoriatic arthritis is also stabilized with immunosuppressive therapy.

According to the Canadian escalating model, the dose and frequency of administration can be adapted to individual demands. More recent publications describe the prevention of inhibitors attributed to early prophylaxis. These reports have led to the clinical practice AG-014699 datasheet to start prophylaxis very early. The German model, in particular, recommends low dose and low frequency prophylaxis to be started before the first bleed in order to avoid factor VIII (FVIII)

administration in an acute bleeding situation with an upregulated immune system in the context with so called “danger signals”. This strategy, however, is yet to be proven. In addition, the high costs of prophylaxis, difficult venous access in young children and the knowledge that more than 10% of severe haemophilia patients possess

a milder phenotype have been barriers for the initiation of early prophylaxis. The development of an inhibitor against FVIII/FIX represents the most serious complication in the treatment of a click here haemophilic patient. An incidence of around 30% in previously untreated patients (PUPs) with severe haemophilia has been described. The development of neutralizing antibodies directed against FVIII, which usually occurs during the initial phase of FVIII exposure (first 50 exposure days [EDs]), is carried out by a complex immune response in which both genetic (FVIII gene mutation, ethnicity, HLA type, immunogenotype) and environmental factors (age of start of treatment, intensity of the treatment and administration mode, type of factor concentrate) are involved. Since the introduction of recombinant FVIII (rFVIII) concentrates, the influence of the type of factor on inhibitor development has been intensely debated. Two possible explanations have been considered in order to explain the rather low inhibitor formation with the use of plasma-derived concentrates (pdFVIII): an immunomodulatory effect by cytokines and the presence of von Willebrand factor. However, systematic reviews and meta-analyses of numerous studies on development of inhibitors in PUPs could not show convincing evidence medchemexpress in favour of any of the product

types. The results of randomized, prospective trials are necessary to resolve the debate. The identification of the factors with an impact on inhibitor development, particularly treatment related ones, can offer clues to design prevention strategies. In 2003, a North American and European consensus meeting about haemophilia stipulated that primary prophylaxis should be started before age 2 years, before any clinically evident joint bleeding, and before the onset of joint damage [1]. However, precisely when joint damage begins is unclear, and the following factors complicate the clinical picture: not all patients with haemophilia develop arthropathy [2], only a few joint bleeds may cause damage [3], and the number of clinical haemarthroses correlates only weakly with magnetic resonance imaging (MRI) outcomes [4].

It is well known that medium surrounding

tumor is acidic and cytosolic pH is alkaline. Acid pump antagonist is the reversible inhibitor of gastric H+/K+-ATPase by competing with K+ on the surface of the enzyme so that is independent of secretory status and results rapid onset. Recent studies suggested that proton pump inhibitors induced selective apoptosis of cancer Selleckchem Erlotinib cells due to changes of intracellular and extracellular acidity in tumor cells. However, effect of acid pump antagonist to tumor cells has not been studied. The aim of this study is to evaluate the effect of acid pump antagonist Ceritinib (YH-1885) on apoptosis of human colorectal adenocarcinoma cell lines (CaCO2). Methods: For MTT assay, human CaCO2 cell lines were incubated with each concentrations of YH 1885 for 24 hours in 37°C incubator and concentrations showed 25% and 50% of cell viability were selected. Apoptosis of human CaCO2 cell lines was measured by performing TUNEL assay with the concentrations decided by MTT assay. We measured apoptosis related signals such as Bax, Bcl-2,

cleaved PARP, caspase-3, caspase-8 using western blot analysis. Results: TUNEL assay showed that YH-1885 induced the apoptosis of human CaCO2 cells. The expression of major signals related apoptosis such as Bax, cleaved PARP, caspase-3, caspase-8 were significantly increased and anti-apoptosis signal, Bcl-2 was decreased. Conclusion: Acid pump antagonist may have an effect to microenvironment of tumor cells and induces apoptosis of human CaCO2 cell

medchemexpress lines. Further studies are needed to evaluate the apoptotic effect of acid pump antagonist for tumor cells. Key Word(s): 1. CaCO2 cell lines; 2. acid pump antagonist; 3. MTT assay; 4. Apoptosis; Presenting Author: LING ZHANG Additional Authors: HAN LIN, ZHAOSHEN LI, DUOWU ZOU Corresponding Author: LING ZHANG Affiliations: Changhai hospital Objective: Functional constipation is a common and well-recognized public health problem, which influences patient quality of life and consumes many healthcare resources. Anorectal manometry plays an important role in the diagnostic procedure. We aimed to investigate the anorectal motility of patients with functional constipation using 3-dimensional high resolution manometry (3-D HRM). Methods: The study included 65 constipation patients visited between June 2011 and March 2013. Patients with constipation and healthy control subjects underwent anorectal manometry by 3-D HRM.

We examined the role of heme-sensing nuclear receptor Rev-erbα, a transcriptional repressor involved in metabolic and circadian regulation

known to promote adipogenesis in preadipocytes, in HSC transdifferentiation. We discovered that Rev-erbα protein was up-regulated in activated HSCs and injured livers; however, transcriptional repressor activity was not affected by fibrogenic treatments. Surprisingly, increased protein expression was accompanied with increased cytoplasmic accumulation of Rev-erbα, which demonstrated distributions similar to myosin, the major cellular motor protein. Cells overexpressing a cytoplasm-localized Rev-erbα exhibited enhanced contractility. Ectopically expressed ZD1839 concentration Rev-erbα responded to both adipogenic ligand and fibrogenic transforming growth factor beta treatment. Rev-erb ligand SR6452 down-regulated cytoplasmic expression of Rev-erbα, decreased expression of fibrogenic markers and the activated phenotype in HSCs, and ameliorated

fibrosis and PH in rodent models. Conclusions: Up-regulation of Rev-erbα is an intrinsic fibrogenic response characterized by cytoplasmic accumulation of the protein in activated HSCs. Cytoplasmic expression of Rev-erbα promotes BGJ398 in vitro a contractile phenotype. Rev-erbα acts as a bifunctional regulator promoting either anti- or profibrogenic response, depending on milieu. Rev-erb ligand SR6452 functions by a previously undescribed mechanism, targeting both nuclear activity and cytoplasmic expression of Rev-erbα. Our studies identify Rev-erbα as a novel regulator of HSC transdifferentiation and offers exciting new insights on the therapeutic potential of Rev-erb ligands. (Hepatology 2014;59:2383–2396) “
“Sorafenib is the standard systemic therapy for patients with advanced hepatocellular carcinoma (HCC). We aimed to assess the efficacy 上海皓元医药股份有限公司 and safety of sorafenib therapy in very elderly patients aged 80 years and older with advanced HCC. In a retrospective multicenter study in Japan, we reviewed 185 patients (median age, 71 years; 82% male;

95% Child–Pugh class A) with advanced HCC who received sorafenib therapy. Data were compared between 24 (13%) patients aged 80 years and older and 161 (87%) patients aged less than 80 years. We used propensity score matching to adjust for differences between the two groups. Median overall survival was 10.6 months in all patients: 11.7 months in patients aged 80 years and older and 10.5 months in those aged less than 80 years. There were no significant differences in overall survival, tumor response, and frequency and severity of drug-related adverse events between patients aged 80 years and older and those aged less than 80 years in both the entire study cohort and the propensity-matched cohort. Sorafenib may be effective and well tolerated, even in patients with advanced HCC who are aged 80 years and older, as well as those aged less than 80 years.

We examined the role of heme-sensing nuclear receptor Rev-erbα, a transcriptional repressor involved in metabolic and circadian regulation

known to promote adipogenesis in preadipocytes, in HSC transdifferentiation. We discovered that Rev-erbα protein was up-regulated in activated HSCs and injured livers; however, transcriptional repressor activity was not affected by fibrogenic treatments. Surprisingly, increased protein expression was accompanied with increased cytoplasmic accumulation of Rev-erbα, which demonstrated distributions similar to myosin, the major cellular motor protein. Cells overexpressing a cytoplasm-localized Rev-erbα exhibited enhanced contractility. Ectopically expressed Pembrolizumab Rev-erbα responded to both adipogenic ligand and fibrogenic transforming growth factor beta treatment. Rev-erb ligand SR6452 down-regulated cytoplasmic expression of Rev-erbα, decreased expression of fibrogenic markers and the activated phenotype in HSCs, and ameliorated

fibrosis and PH in rodent models. Conclusions: Up-regulation of Rev-erbα is an intrinsic fibrogenic response characterized by cytoplasmic accumulation of the protein in activated HSCs. Cytoplasmic expression of Rev-erbα promotes CP-690550 purchase a contractile phenotype. Rev-erbα acts as a bifunctional regulator promoting either anti- or profibrogenic response, depending on milieu. Rev-erb ligand SR6452 functions by a previously undescribed mechanism, targeting both nuclear activity and cytoplasmic expression of Rev-erbα. Our studies identify Rev-erbα as a novel regulator of HSC transdifferentiation and offers exciting new insights on the therapeutic potential of Rev-erb ligands. (Hepatology 2014;59:2383–2396) “
“Sorafenib is the standard systemic therapy for patients with advanced hepatocellular carcinoma (HCC). We aimed to assess the efficacy 上海皓元 and safety of sorafenib therapy in very elderly patients aged 80 years and older with advanced HCC. In a retrospective multicenter study in Japan, we reviewed 185 patients (median age, 71 years; 82% male;

95% Child–Pugh class A) with advanced HCC who received sorafenib therapy. Data were compared between 24 (13%) patients aged 80 years and older and 161 (87%) patients aged less than 80 years. We used propensity score matching to adjust for differences between the two groups. Median overall survival was 10.6 months in all patients: 11.7 months in patients aged 80 years and older and 10.5 months in those aged less than 80 years. There were no significant differences in overall survival, tumor response, and frequency and severity of drug-related adverse events between patients aged 80 years and older and those aged less than 80 years in both the entire study cohort and the propensity-matched cohort. Sorafenib may be effective and well tolerated, even in patients with advanced HCC who are aged 80 years and older, as well as those aged less than 80 years.