One early post- procedure-related complication occurred with cyst wall-separation MK-8669 resulting in intra-peritoneal air leak, which was endoscopically sealed using a “bear-claw” clip and patient had unremarkable

recovery with antibiotic therapy alone. Conclusion: EUS-guided therapy for peri-pancreatic fluid collections is clinically successful in the majority of patients by endoscopic means alone, while adjunctive “conventional” therapy can be reserved for those with incomplete clinical response. Using large diameter stents with or without nasocystic drainage is most helpful for patients with complex collections. J BROOKER, G DICKSON Waikato Hospital Background: Early oesophageal neoplasia is seen in patients with Barrett’s oesophagus as well as squamous lesion. Cap-assisted ligation EMR provides tissue staging to assist in treatment decisions and may achieve curative treatment. Methods: Retrospective review of prospective database of patients referred of early oesophageal neoplastic lesions between April 2010–May 2014. Results: The 14 patients (mean age 68.5 yrs, range 53–81 yrs) with early stage disease (11 males, 78.6%) underwent EMR. Underlying Barrett’s oesophagus was present in 11/14 (78.6%) with 8 having a visible nodule. Prior biopsy showed high grade dysplasia (HGD) in 10 (91%)

and 1 (9%) suspected adenocarcinoma. Three patients had suspected squamous neoplasia. Resected pathology confirmed adenocarcinoma in 4 patients (1 T1a, 2 T1sm and 1 early T2), HGD in one and LGD in 6 patients. EMR of squamous lesions Abiraterone nmr showed 2 LGD and 1 papilloma. Adenocarcinoma patients underwent chemoradiation alone in 2, chemoradiation and surgery 1 and surgery 1 alone, respectively. Six patients with prior HGD underwent HALO ablation therapy to treat residual Barrett’s oesophagus. No adverse events were recorded related to EMR. Conclusion: Cap-assisted ligation EMR is safe to perform in patients with early oesophageal neoplasia. This allows better tissue

staging of neoplastic lesions to determine appropriate adjunctive therapy with curative intent. AYS TING,1 D CROAGH,1,2 S ALEXANDER,3,4 D DEVONSHIRE,1 MP SWAN1 1Department of Gastroenterology, Monash Health, Melbourne, VIC, Australia, 2Monash University, Melbourne, VIC, Australia, MCE公司 3Department of Gastroenterology, Barwon Health, Geelong, VIC, Australia, 4School of Medicine, Deakin University, Geelong, VIC, Australia Introduction: In the last two decades, there have been numerous advancements in technology and innovations that have impacted ERCP practice. Varying recommendations exist to guide this practice but adherence to these guidelines is currently unknown. This survey was conducted to assess how ERCP is currently performed in Australia and to guide future research into this area of interventional endoscopy.

(HEPATOLOGY 2011;) Hepatitis B virus (HBV) and hepatitis C virus (HCV) are the two most common causes of chronic liver disease globally. Worldwide, approximately 350 million and 170 million people are infected with HBV and HCV, respectively.1, 2 Dual infection with HBV

and HCV is possible because of common routes of infection and is frequently found in several high-risk populations, such as injection drug users, hemodialysis patients, organ transplant recipients, and human buy NVP-AUY922 immunodeficiency virus–positive individuals.3 Thus, dual infection with both viruses is not uncommon, with a review of prevalence data suggesting that 2%-10% of hepatitis C antibody (anti-HCV)–positive patients are hepatitis B surface antigen (HBsAg)-positive and that anti-HCV is found in 5%-20% of patients with chronic hepatitis B.3 The prevalence of HBV and HCV dual infection is likely to vary depending on different geographic areas and may depend on the ethnic makeup of a given population. Investigators in Eastern Europe found a dual infection rate of nearly 1% in a healthy cohort.4 A European

study of 59 dual-infected patients found that geographic region, age >42 years, prior history of blood transfusion, and injection drug users were independently associated with HBV/HCV dual infection compared with a control group of HBV-monoinfected patients.5 The HBV/HCV dual infection Ulixertinib mouse rate in medchemexpress the United States may be both underreported and potentially on the rise. In recent years, the number of immigrants from Asia and the Pacific region,

an area where HBV is endemic, has increased substantially to approximately 14 million individuals.6, 7 Patients infected with both HBV and HCV are generally more likely to develop fulminant hepatitis in the acute phase or more advanced disease such as cirrhosis and hepatocellular carcinoma (HCC) with chronic dual infection and are also at a greater risk to fail interferon-based antiviral treatment.8-14 Although HBV/HCV dual infection has been shown to lead to more severe forms of liver disease, the interaction between the hepatitis B and C viruses appears to be one of reciprocal inhibition, each preventing or greatly decreasing the ability of the other virus to replicate.11, 15-22 In general, the most common pattern of viral interaction is for HCV to be dominant with detectable HCV RNA in combination with very low or undetectable levels of HBV DNA and negative hepatitis B e antigen (HBeAg) with detectable HBeAg antibody.3 However, this pattern of HCV dominance is not uniform, and some studies have reported that HBV may be dominant.23-25 Additionally, the reciprocal inhibition of each virus on the other virus may prevent identification of dual-infected patients because of negative serum HBV DNA and/or HCV RNA by polymerase chain reaction (PCR) tests.

Two possible mechanisms have been proposed to explain how ductular

reactions promote liver fibrosis33: (1) by secreting profibrogenic factors, and (2) by promoting epithelial mesenchymal transition.34 In this study, we have selleck compound shown that conditioned media from cells overexpressing HAIs, and recombinant HAI-2, stimulated fibroblasts to express collagens, so HAI-1 and -2 might serve as profibrogenic factors in ductular reactions. Such profibrogenic effects, however, may be direct or indirect, because conditioned media might contain not only HAI-1 or HAI-2, but also other factors that are possibly processed by both HAIs. The possible role of both HAIs in epithelial mesenchymal transition remains to be determined. Ductular reactions have been demonstrated to recapitulate some of the differentiation processes involved LY2157299 chemical structure in normal liver development,15 and so to better understand the role of HAI-1 and -2 in BA or other cholangiopathies, we sought to examine their functions in liver development. We found that both HAIs were highly expressed

in mouse hepatoblast-derived bipotential cells and probably expressed in human HSCs in BA livers, whereas in human fetal liver, HAI-1 and -2 were differentially expressed in HSCs and hepatoblasts, respectively, according to the definition and staging of HSCs and hepatoblasts proposed by Dr. Lola M. medchemexpress Reid and colleagues.24 Thus, both HAIs might function as regulators keeping hepatic precursor cells in a less-differentiated status prior to undergoing differentiation. To link the roles of the HAIs in hepatic differentiation and fibrosis, two seemingly unrelated phenomena, we propose that the key discriminative factor may be the action

dose and duration of HAI expression. At higher expression levels and longer durations, the HAIs may shift from being favorable physiological regulators to demons with pathological roles in BA or other cholangiopathies. For example, an initial moderate increase in HAI expression in BA livers may indicate the role of HAIs in participating in a compensatory activation of HSCs for bidirectional differentiation, which is accompanied by down-regulation of HAI expression after this process (right panels, Fig. 6C,D). However, the persistent and extremely high levels of HAI-1 and -2, as seen in advanced BA, might block differentiation of hepatic cells, induce fibrogenic activity in adjacent fibroblasts, and contribute to fibrosis. This hypothesis may be supported by our observations showing that fibrosis frequently accompanies persistent ductular reactions rich in HAI-positive cells in other cholangiopathies. It is possible, therefore, that an intervention to down-regulate the extremely high levels of HAI-1 and/or HAI-2 in BA livers may slow disease progression by generating more differentiated cells with less fibrosis.

Two possible mechanisms have been proposed to explain how ductular

reactions promote liver fibrosis33: (1) by secreting profibrogenic factors, and (2) by promoting epithelial mesenchymal transition.34 In this study, we have Depsipeptide shown that conditioned media from cells overexpressing HAIs, and recombinant HAI-2, stimulated fibroblasts to express collagens, so HAI-1 and -2 might serve as profibrogenic factors in ductular reactions. Such profibrogenic effects, however, may be direct or indirect, because conditioned media might contain not only HAI-1 or HAI-2, but also other factors that are possibly processed by both HAIs. The possible role of both HAIs in epithelial mesenchymal transition remains to be determined. Ductular reactions have been demonstrated to recapitulate some of the differentiation processes involved NVP-BEZ235 mw in normal liver development,15 and so to better understand the role of HAI-1 and -2 in BA or other cholangiopathies, we sought to examine their functions in liver development. We found that both HAIs were highly expressed

in mouse hepatoblast-derived bipotential cells and probably expressed in human HSCs in BA livers, whereas in human fetal liver, HAI-1 and -2 were differentially expressed in HSCs and hepatoblasts, respectively, according to the definition and staging of HSCs and hepatoblasts proposed by Dr. Lola M. medchemexpress Reid and colleagues.24 Thus, both HAIs might function as regulators keeping hepatic precursor cells in a less-differentiated status prior to undergoing differentiation. To link the roles of the HAIs in hepatic differentiation and fibrosis, two seemingly unrelated phenomena, we propose that the key discriminative factor may be the action

dose and duration of HAI expression. At higher expression levels and longer durations, the HAIs may shift from being favorable physiological regulators to demons with pathological roles in BA or other cholangiopathies. For example, an initial moderate increase in HAI expression in BA livers may indicate the role of HAIs in participating in a compensatory activation of HSCs for bidirectional differentiation, which is accompanied by down-regulation of HAI expression after this process (right panels, Fig. 6C,D). However, the persistent and extremely high levels of HAI-1 and -2, as seen in advanced BA, might block differentiation of hepatic cells, induce fibrogenic activity in adjacent fibroblasts, and contribute to fibrosis. This hypothesis may be supported by our observations showing that fibrosis frequently accompanies persistent ductular reactions rich in HAI-positive cells in other cholangiopathies. It is possible, therefore, that an intervention to down-regulate the extremely high levels of HAI-1 and/or HAI-2 in BA livers may slow disease progression by generating more differentiated cells with less fibrosis.

[97] With 1H NMR, the investigators characterized the metabolic differences in four different intestinal sections (distal jejunum, distal ileum, proximal colon, and distal colon) between inflamed and healthy mice, and employed a highly specific LC-MS methodology called selected reaction monitoring to quantify a panel of 63 inflammatory markers of interest in healthy and inflamed distal ileum tissue, finding wide-ranging alterations in metabolism of cholesterols, triglycerides, and phospholipids between disease and health.[97] Almost simultaneously, independent researchers in USA and Canada performed

targeted metabolite profiling using 1H NMR on urine collected from IBD patients, and on IBD serum, plasma, and urine, respectively.[98, Ganetespib order 99] Both groups reported only nominally differentiated metabolic profiles

in CD and UC.[98, 99] Proteomics and metabolomics are fledging bioanalytical fields and many investigators have been inspired to quickly demonstrate the prodigious resolving power that these technologies are capable of. As bioanalytical methods advanced, biomarkers were developed that significantly affected IBD management; the monitoring of thiopurine metabolites to predict hepatotoxicity in thiopurine analogue therapy,[100] fecal calprotectin as a noninvasive measure of intestinal inflammation,[72] and ASCA and pANCA as complimentary tools in differentiating CD and UC,[85] among others[14] (Fig. 1). Nevertheless, the grievance seems to be that such tools, http://www.selleckchem.com/products/BI6727-Volasertib.html and novel definitive tools, have not come as a result of high-throughput, hypothesis-free “omics” methodologies.[12-14, 101] Determining the domains of proteomics and metabolomics may seem trivial to physicians

facing practical situations on a day-to-day basis. Yet the question of how the omics can progress clinical medicine lies in this crux. In defining proteomics and metabolomics, we ask ourselves—how do we understand biological process? What is the difference between systems biology and traditional physiology?[12, 102] As a starting point, the suffix of -omics refers 上海皓元医药股份有限公司 to the totality of a given system, and the effort to profile it.[103] Differentiating and defining proteomics and metabolomics, therefore, is grounded in what we constitute as the total protein content, and total metabolite content, in a given cell. The proteome, first described as “the total protein complement able to be encoded by a given genome,”[104] has undergone stark revision to include “the set of all protein isoforms and modifications, the interactions between them, (and) the structural description of proteins and their higher order complexes.”[16, 105, 106] Because the human genome project accounted the number of unique human genes to be in the vicinity of 35 000, scientists have been able to deduce that there are possibly 10 million unique protein species that are the result of, and subject to, approximately 200 different PTMs.

Thus, PG and histamine, by increasing VP create a perivascular edema that dilutes and delays toxic agents reaching the subepithelial capillaries. Otherwise, damaging chemicals may induce severe early vascular injury resulting in blood flow stasis, hypoxia, and necrosis of surrounding epithelial and mesenchymal cells. In this complex response, increased mucus and/or bicarbonate secretion

seem to cause luminal dilution of gastrotoxic chemicals that is further reinforced by a perivascular, histodilutional component. This mechanistic explanation would encompass the protective actions of diverse agents as PG, small doses of histamine, motility stimulants, and dilute irritants (i.e. “adaptive cytoprotection”). Thus, although markedly increased VP is pathologic, slight increase in VP seems to be protective,

that is, a key element in the complex pathophysiologic response during selleck chemicals acute gastroprotection. Over the years, “gastroprotection” was also applied to accelerated healing of chronic gastroduodenal ulcers without reduction of acid secretion. The likely main mechanism here is the binding of angiogenic growth Tamoxifen price factors (e.g. basic fibroblast growth factor, vascular endothelial growth factor) to the heparin-like structures of sucralfate and sofalcone. Thus, despite intensive research of the last 30 years, gastroprotection is incompletely understood, and we are still far away from effectively treating Helicobacter pylori-negative ulcers and preventing nonsteroidal anti-inflammatory drugs-caused erosions and ulcers in the upper and lower gastrointestinal tract; hence “gastric cytoprotection” research is still relevant. It’s not widely known that gastroprotective drugs (e.g. sofalcone, sucralfate) which prevent and/or accelerate healing of gastric ulcers, without inhibiting acid secretion, were first introduced in Japan, before or around Andre Robert’s historic article on “gastric cytoprotection” in 1979.[1, 2] Furthermore,

some poorly defined and locally acting “protective” drugs (e.g. carbenoxolone and bismuth salts) were empirically used in Europe and North America, but their mechanisms of action were not widely investigated.[3] Since medchemexpress Robert’s studies were solely focused on prostaglandins (PG), they became the center of gastrointestinal (GI) research for more than 30 years, preceding the popularity of Helicobacter pylori investigations. As endogenous products, PG were implicated in mediating the gastroprotective effect of other drugs such as sofalcone and sucralfate[4, 5] despite that the cyclooxygenase inhibitor indomethacin diminished but never abolished gastroprotection by other drugs. Another group of endogenous substances, that is, sulfhydryls (SH), investigated in parallel with PG, also seem to play a mechanistic role in gastroprotection, especially since SH alkylators like N-ethylmaleimide (NEM) counteract virtually any form of gastroprotection.

Regarding the health utility values, the Netherlands had the highest health utility value with a mean of 0.915 followed by Canada (0.791), Ireland (0.786), UK (0.768), France (0.687) and Poland (0.629) (Table 2). The majority of the French respondents are currently

on-demand treatment 62% compared to Canada 13%, Ireland 20%, the Netherlands 8% and the UK 8%. This may explain why the health utility value in the French cohort is closer to Poland where 79% are on-demand. A total of 13 respondents (mean age 27.5 ± 4.6 years) had a previous history Selleck LDK378 of an inhibitor, with 10 on primary prophylaxis, two with on-demand and one with secondary prophylaxis. All patients have had access to immune tolerance induction (ITI). The calculated factor consumption per year was 326 000 IU. The group reported a large number of target joints, serious bleeding episodes, reduced joint mobility, recurrent bleeding and requirement for surgical procedures. The mean utility value of the inhibitor cohort was 0.798. The aim of this study was to further examine the differences in selleck compound medical outcomes and health utility values in respondents who had full access to prophylaxis from birth and those who received prophylaxis for varying periods through their lives and those who continued entirely with varying levels of on-demand therapy. The results show, that long-term prophylaxis

results in less bleeding, less damage to joints, less serious bleeding episodes, lower number of recurrent bleeding episodes, lower haemophilia-related work absence and higher utility value. Our findings support the view that prophylaxis started at a young age and continued into adulthood is an extremely effective treatment for patients with severe haemophilia, similar to other studies [3, 5-7, 10]. The differences in the number of bleeding episodes, requirement for surgical procedures, reduced mobility, absence from work and overall health utility demonstrate

the clear benefits of long-term prophylaxis over on-demand therapy. It is not surprising that the highest utility values were found in the patients from the Netherlands as prophylaxis has been 上海皓元医药股份有限公司 available continuously since early childhood. When comparing the Always On-demand group with the Always on Prophylaxis group, the most significant differences in EQ-5D dimensions were found in mobility problems and higher pain/discomfort. A number of studies on cost effectiveness [11-13] have reported the difference in utility values between prophylaxis and on-demand of 0.03 and 0.08. Our results and previous study [7] suggest that the benefit of prophylaxis continued into adulthood increased the utility value more significantly, dependent on the level of on-demand treatment available, and could range from 0.16 to 0.247.

Further, the gut flora show marked inter-individual

variability, and the relationship of gut flora with obesity is far from perfect. Thus, although the current human data do show an association between profile of gut microflora and obesity, these do not prove causation. Data from animals are much more convincing; however, these may be species specific and may not apply to humans. Insulin resistance plays a central role in the development of hepatic steatosis and also contributes to hepatic inflammation. Several lines of evidence strongly suggest a role for gut microflora in the induction of insulin resistance. Obese individuals have a higher prevalence of intestinal bacterial overgrowth.[26] Cell walls of gram-negative bacteria contain lipopolysaccharide (LPS) NVP-AUY922 manufacturer or endotoxin, which can activate an inflammatory cascade through both toll-like receptor (TLR) 4-dependent and TLR4-independent pathways, resulting in upregulation of genes for several cytokines (tumor necrosis factor-α [TNF-α] and interleukin [IL]-6), inducible nitric oxide synthase, nuclear factor-κB (NF-κb), inhibitor of NF-κB,

etc. These inflammatory mediators are known to induce a state of insulin resistance.[27] Persons with NAFLD have an increased intestinal permeability than controls.[28] Y-27632 ic50 Serum endotoxin levels are higher in patients with type II diabetes mellitus, a classical state of insulin resistance.[29] Modification of gut microbes in mice using probiotics or anti-TNF-α antibodies has been shown to reduce serum inflammatory cytokines levels, improve insulin resistance, and reduce hepatic steatosis at histology.[30] However, extrapolation of these MCE公司 data to humans may be difficult because of differences in diet, genetics,

metabolism, environmental factors, and presence of associated disease conditions. The classical two-hit hypothesis for NASH considers hepatic steatosis as the first hit that sensitizes hepatocytes to a variety of other insults; one of these insults (the second hit) then induces progression of some cases from NAFLD to NASH (Fig. 1).[31] The proposed second hits have included genetic factors, oxidative stress, TLR-mediated signaling in Kupffer cells, and adipose tissue-derived inflammatory cytokines. Gut microbiota may provide another second hit, either through innate immune mechanisms or through excessive endogenous production of alcohol. Liver is rich in cells of the innate immune system.

(Wilhelminenspital Medizinische Abteilung, Wien, Austria); Markus Heim, M.D. (Universitätsspital Basel-Medizinische Klinik, Basel, Switzerland); Ming-Yang Lai, M.D. (National Taiwan University Hospital, Taipei, Taiwan); Eric Lawitz, M.D. (Alamo Medical Research, San Antonio, TX); Yoav Lurie, M.D. (Gastrointestinal and Liver Disease Unit, Sourasky Medical Center, Tel Aviv, Israel); Darius Moradpour,

M.D. (Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland); Beat Müllhaupt, M.D. Sorafenib concentration (Universitätsspital Zürich, Zürich, Switzerland); Francesco Negro, M.D. (Hôpitaux Universitaires, Genéve, Switzerland); Court Pedersen, M.D. (Odense Universitets Hospital, Odense, Denmark); Ramón Planas Vila, M.D. (H. de Badalona Germans Trias I Pujol, Barcelona, Spain); Mark Russo, M.D. (Carolinas Medical Center, Charlotte, NC); Rifaat Safadi, M.D. (Liver Unit, Italian [Holy Family] Hospital, Nazareth, Israel); Alejandro Soza, M.D. (Hospital de la Pontificia Universidad

Catolica, Hepatologia, Santiago, Chile); Ulrich Spengler, M.D. (Rheinische Friedrich-Wilhelms-Universitaet Bonn, Bonn, Germany); Rudolf Stauber, M.D. (MedUni Graz, Klinische Abteilung für Gastroenterologie und Hepatologie, Graz, Austria); Petr Urbanek, M.D. (Hepato-gastro-enterologie, Hradec Kralove, Selleckchem BGB324 Czech Republic); Elena Volchkova, M.D. (Clinical Hospital of Infectious Diseases #2, Moscow, Russian Federation); Miroslava Volfova, M.D. (Klin Med s.r.o., Praha, Czech Republic); Stefan Zeuzem, M.D. (Klinikum der Johann-Wolfgang-Goethe-Universitaet, Frankfurt,

Germany). Additional Supporting Information may be found in the online version of this article. “
“It is unclear how proliferating cells elicit suppression 上海皓元医药股份有限公司 on cell proliferation and how cancer cells evade this growth suppression. Using a loss-of-function screening of the human kinome and phosphatome to identify genes suppressing tumor initiation in human hepatocellular carcinoma (HCC), we identified 19 genes and characterized one of the top-scoring tumor suppressor candidates, protein tyrosine phosphatase receptor type F (PTPRF). We found that PTPRF was induced during cell proliferation by cell-cell contact. Ectopic expression of wild-type PTPRF, but not the phosphatase-inactive mutant, suppressed cell proliferation and colony formation in soft-agar assays. In contrast, PTPRF silencing led to cell hyperproliferation, enhanced tumor colony formation in soft agar, and increased xenograft tumor growth in nude mice. Mechanistically, PTPRF silencing showed aberrant ERK-dependent signaling including the phosphorylation/stabilization of v-myc avian myelocytomatosis viral oncogene homolog (MYC) through the direct activation of v-src avian sarcoma viral oncogene homolog (SRC) and suppression of PP2A. This PTPRF-mediated growth suppression during cell proliferation functioned independently of the Hippo-Yap pathway. Clinically, PTPRF was down-regulated in 42% HCC (37/89), 67% gastric cancer (27/40), and 100% colorectal cancer (40/40).

(Wilhelminenspital Medizinische Abteilung, Wien, Austria); Markus Heim, M.D. (Universitätsspital Basel-Medizinische Klinik, Basel, Switzerland); Ming-Yang Lai, M.D. (National Taiwan University Hospital, Taipei, Taiwan); Eric Lawitz, M.D. (Alamo Medical Research, San Antonio, TX); Yoav Lurie, M.D. (Gastrointestinal and Liver Disease Unit, Sourasky Medical Center, Tel Aviv, Israel); Darius Moradpour,

M.D. (Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland); Beat Müllhaupt, M.D. selleck inhibitor (Universitätsspital Zürich, Zürich, Switzerland); Francesco Negro, M.D. (Hôpitaux Universitaires, Genéve, Switzerland); Court Pedersen, M.D. (Odense Universitets Hospital, Odense, Denmark); Ramón Planas Vila, M.D. (H. de Badalona Germans Trias I Pujol, Barcelona, Spain); Mark Russo, M.D. (Carolinas Medical Center, Charlotte, NC); Rifaat Safadi, M.D. (Liver Unit, Italian [Holy Family] Hospital, Nazareth, Israel); Alejandro Soza, M.D. (Hospital de la Pontificia Universidad

Catolica, Hepatologia, Santiago, Chile); Ulrich Spengler, M.D. (Rheinische Friedrich-Wilhelms-Universitaet Bonn, Bonn, Germany); Rudolf Stauber, M.D. (MedUni Graz, Klinische Abteilung für Gastroenterologie und Hepatologie, Graz, Austria); Petr Urbanek, M.D. (Hepato-gastro-enterologie, Hradec Kralove, Gefitinib mouse Czech Republic); Elena Volchkova, M.D. (Clinical Hospital of Infectious Diseases #2, Moscow, Russian Federation); Miroslava Volfova, M.D. (Klin Med s.r.o., Praha, Czech Republic); Stefan Zeuzem, M.D. (Klinikum der Johann-Wolfgang-Goethe-Universitaet, Frankfurt,

Germany). Additional Supporting Information may be found in the online version of this article. “
“It is unclear how proliferating cells elicit suppression 上海皓元医药股份有限公司 on cell proliferation and how cancer cells evade this growth suppression. Using a loss-of-function screening of the human kinome and phosphatome to identify genes suppressing tumor initiation in human hepatocellular carcinoma (HCC), we identified 19 genes and characterized one of the top-scoring tumor suppressor candidates, protein tyrosine phosphatase receptor type F (PTPRF). We found that PTPRF was induced during cell proliferation by cell-cell contact. Ectopic expression of wild-type PTPRF, but not the phosphatase-inactive mutant, suppressed cell proliferation and colony formation in soft-agar assays. In contrast, PTPRF silencing led to cell hyperproliferation, enhanced tumor colony formation in soft agar, and increased xenograft tumor growth in nude mice. Mechanistically, PTPRF silencing showed aberrant ERK-dependent signaling including the phosphorylation/stabilization of v-myc avian myelocytomatosis viral oncogene homolog (MYC) through the direct activation of v-src avian sarcoma viral oncogene homolog (SRC) and suppression of PP2A. This PTPRF-mediated growth suppression during cell proliferation functioned independently of the Hippo-Yap pathway. Clinically, PTPRF was down-regulated in 42% HCC (37/89), 67% gastric cancer (27/40), and 100% colorectal cancer (40/40).