“
“Dysphagia, difficulty or delay in preparation and/or passage of a liquid or solid bolus is a common problem in our population. The optimal evaluation of the patient with dysphagia requires an understanding of the pathogenesis, the ability to use the history to differentiate between oropharyngeal and esophageal dysphagia and appropriate use of diagnostic testing. This chapter reviews the key components of the history and reviews in detail the optimal use of imaging studies, upper GI endoscopy, and esophageal function testing in the evaluation of these

complex cases. An algorithm for evaluation and treatment is presented. “
“Focusing on TNFSF15 instead of NOD2, we set out to evaluate whether combining serologic and genetic markers could distinguish between Crohn’s disease (CD) and ulcerative colitis (UC), and whether they could be used Lapatinib molecular weight to stratify the disease behavior of Taiwanese CD patients. Clinical information, serum isolation, and DNA were collected after obtaining informed consent. The serological

markers were analyzed by ELISA kits and the genetic analysis for TNFSF15 single-nucleotide polymorphisms (SNPs) by Sequenom. Statistic analyses were conducted by SAS 9.2 (Cary, NC, USA). This study included 108 patients (55 CD, 53 UC) and 60 healthy controls. An initial low positive rate and low sensitivity for the serological markers led Antiinfection Compound Library solubility dmso us to reset the cut-off values. This reset cut-off for ASCA IgA yielded a sensitivity of 0.291 and specificity of 0.925 for differentiating CD from UC patients. The reset cut-off value for p-ANCA (anti-MPO) had a sensitivity of 0.461 and a specificity of 0.817 for differentiating inflammatory bowel disease patients from healthy controls. Among the TNFSF15 SNPs, rs4263839 associated 上海皓元医药股份有限公司 with CD in Taiwan (P = 0.005), haplotype analysis did not increase the association. Combining the genetic marker TNFSF15 (rs4263839) and serological marker ASCA IgA increased the area under the curve from 0.61 to 0.70 for predicting stenosis/perforating phenotype, compared to ASCA IgA alone. Serological markers need to be tested and tailored to different countries/ethnicities. Combining the genetic

marker TNFSF15 with ASCA IgA increased the power of predicting stenosis/perforating phenotype in CD patients with TNFSF15 but not with a NOD2 genetic background. “
“Background and Aim:  We aimed to prospectively determine patient burden and patient preference for magnetic resonance enteroclysis, capsule endoscopy and balloon-assisted enteroscopy in patients with suspected or known Crohn’s disease (CD) or occult gastrointestinal bleeding (OGIB). Methods:  Consecutive consenting patients with CD or OGIB underwent magnetic resonance enteroclysis, capsule endoscopy and balloon-assisted enteroscopy. Capsule endoscopy was only performed if magnetic resonance enteroclysis showed no high-grade small bowel stenosis. Patient preference and burden was evaluated by means of standardized questionnaires at five moments in time.

S7). Our data suggest that SH-J1 cells infected with Lcn2-expression adenovirus expressed Lcn2 as a 25 kDa protein, after which it was secreted into the

medium where it formed homo- and heterodimeric complexes (Supporting Fig. S8). Immunohistochemical staining in our cohort of patients demonstrated that Lcn2 immunoreactivity was localized at the front of tumor tissue adjacent to the connective matrix (Fig. 1E, upper panels). Lcn2 expression increased in various tumor stages (Fig. 1E, middle panels). However, analysis of tissue microarray (TMA) data from an independent cohort of patients revealed various staining intensities according to the grade of differentiation of HCCs; very little staining was observed in dedifferentiated HCCs (GIII/IV) (Fig. 1E, lower panels). In addition, cells that had undergone Vemurafenib ic50 EMT (SH-J1 and SCK) and EMT-relevant HCCs (GIV) appeared to express less Lcn2 than cells and tissues with an epithelial check details phenotype. Thus, we investigated the correlation between Lcn2 expression and EMT marker expression in HCC samples using TMA analysis (Supporting Fig. S9). The staining intensity of Lcn2 was positively correlated with the expression of epithelial markers such as E-cadherin (P < 0.001), desmoplakin I/II (P < 0.001), and CK18 (P = 0.03), and inversely correlated

with the expression of fibronectin (P = 0.016) and vimentin (P = 0.002), implying that Lcn2 上海皓元医药股份有限公司 expression

is positively correlated with epithelial marker expression and inversely related to EMT marker expression (Supporting Table S6). In our cohort of patients, statistical analysis revealed that Lcn2 immunoreactivity was positively correlated with stage, but not Edmondson differentiation grade or recurrence, in patients without a distant metastasis who underwent surgical resection (Table 1). Immunofluorescence assays revealed that GFP-tagged Lcn2 overlapped with Lcn2 immunoreactivity and that GFP-tagged Lcn2 was localized in both the nucleus and cytoplasm of Hep3B and THLE2 cells (Supporting Fig. S10), whereas endogenous Lcn2 was localized mainly in the cytoplasm. To determine whether human Lcn2 is involved in tumor cell proliferation or tumorigenicity in HCC cells with an EMT phenotype, we established SH-J1 cells stably expressing Lcn2. The transfectants showed a more adherent morphology than vector control cells (Fig. 2A). Furthermore, the tetrazolium salt 3-(4,5-dimethylthiazol-2-yl)−2,5-diphenyl tetrazoliumbromide (MTT) assay revealed that the proliferation rate of SH-J1 cells stably expressing Lcn2 was lower than that of vector control cells (Fig. 2B). Next, Lcn2-expressing SH-J1 cells were inoculated subcutaneously into nude mice to determine whether Lcn2 affects tumorigenicity.

Jiang, Kenneth Mukamal, Elliot B. Tapper, Yusuke Tsugawa Background: A number of cross-sectional studies have demonstrated an inverse association between light to moderate alcohol consumption and presence of fatty liver; we have also reported an inverse correlation between drinking frequency and the prevalence Selinexor purchase of fatty liver in men. However, the influence of alcohol consumption on the development or remission of fatty liver is still controversial. Methods: We obtained clinical and laboratory data from 10,054 Japanese subjects who voluntarily underwent a baseline health checkup and once or more

of follow-up studies from 2006 to 2011. The development or remission of fatty liver was assessed by ultrasonography. The time of fatty liver development or remission

was assumed to be the midpoint between the checkup at which the change of fatty liver status was observed for the first time and that of the one before it. Using Cox proportional hazard model, we performed multivariable analyses to evaluate the XAV-939 purchase influence of alcohol consumption on the development or remission of fatty liver with following factors: overweight or obesity (BMI > 25 kg/m2), dyslipidemia, hypertension, glucose intolerance, hyperuricemia, smoking, exercise, and age. Results: After excluding cases with concurrent liver disease and/or missing component of data, we analyzed 8,879 cases (median age, 47 years old). The total follow-up period was 17,999.8 person-years. At baseline, 2,309 of 5,488 men (42.1%) and 461 of 3,391 women (13.6%) had fatty liver. BMI (mean ± SD) in cases with and without fatty liver was 25.9 ± 3.1 kg/m2 and MCE公司 22.4 ± 2.4 kg/m2 in men, and 25.9 ± 3.4 kg/m2 and 20.9 ± 2.5 kg/m2 in women. In men, the amount of alcohol consumed

(mean ± SD) in each drinking frequency category (drinking 1-3 days/week, drinking 4-6 days/week, and daily drinking) was 62 ± 60 g/week (n =1,347),189 ± 112 g/week (n = 976), and 272 ± 132 g/week (n =1,764), respectively. During the follow-up, 491 cases of development and 418 cases of remission of fatty liver were observed. The remission of fatty liver was directly associated with drinking on 4-6 days/week (hazard ratio [HR], 1.50; 95% confidence intervals [CI], 1.12-2.01) and daily drinking (HR, 1.38; 95% CI, 1.05-1.81) after adjustment for other confounders. The association between alcohol consumption and the development of fatty liver was not significant. In women, 245 cases of development and 99 cases of remission of fatty liver were observed. The change of fatty liver status was not associated with alcohol consumption. Conclusions: In the longitudinal study, the protective effect of frequent alcohol consumption against fatty liver appeared to be mainly therapeutic rather than preventive in men.

30 We have also documented an increase in apoptotic cell death in HCV-infected, autophagy-impaired IHHs, and this reflects that autophagy promotes cell survival. It is possible

that HCV-mediated autophagy may sustain cell viability during virus-induced stress in order to prevent apoptosis. IFN-α can induce cell death by modulating the Janus kinase/signal transducer and activator of transcription (STAT) or phosphoinositide 3-kinase/protein kinase B signaling pathway, STAT3 activation, or cytokine induction.38 Y-27632 clinical trial Therefore, IFN induction in HCV-infected, autophagy-impaired cells may mediate apoptotic cell death. Autophagy has been suggested to extend the survival time of human parvovirus B19–infected erythroid cells during viral expansion.39 Hepatitis B virus–encoded transcriptional transactivator

protein X up-regulates BCN1 expression and stimulates autophagy.40 We have shown previously that HCV infection enhances BCN1.12 Therefore, it is plausible that HCV induces autophagy to prolong cell survival. This process may help to initiate the development of liver disease progression, including hepatocellular carcinoma, through an as yet uncharacterized mechanism. In conclusion, the results from this study reveal that Ceritinib nmr HCV infection in autophagy-knockdown cells induces the IFN signaling pathway and enhances hepatocyte death. Therefore, autophagy serves as a pivotal entity that may help HCV in establishing persistent infection, reducing antiviral innate immunity, and promoting cell survival. The interaction of the virus with the autophagy machinery involves multiple pathways that have only just begun to be characterized. However, other mechanisms, either simultaneously or subsequently, may also be involved in the establishment 上海皓元医药股份有限公司 of chronic HCV infection in humans. The authors thank Charlie Rice, Takaji Wakita, and Chen Liu for providing the HCV clones and HCV NS5A antibody and Leonard Grosso for helping to measure the genome copy number of HCV (IU/mL). “
“Single nucleotide polymorphisms (SNPs) located in lncRNA CASC8 gene may influence the process of splicing and stability of mRNA conformation,

resulting in the modification of its interacting partners. Genome-wide association studies (GWAS) have identified the SNP rs10505477 and SNP rs1562430 in CASC8 were associated with risk of the colorectal cancer (CRC) and breast cancer, respectively. In the present study, we genotyped the 940 surgically resected gastric cancer patients to explore the association between these two SNPs (e.g., rs10505477 and rs1562430) and survival of gastric cancer in a Chinese population. We found that the patients carrying rs10505477 GG genotype survived for a longer time than those with the GA and AA genotypes (log-rank P = 0.030). The similar result was also found in the dominant model (GA/AA versus GG, HR = 1.32, 95% CI = 1.08–1.63, log-rank P = 0.008).

21, 33, 34 In our study, coimmunoprecipitation with anti-STAT1 antibody followed by immunoblotting with HEV anti-ORF3 or ORF2 antibody, showed that

ORF3 protein, but not ORF2 protein, could bind to STAT1 in HEV-A549 cells. HEV ORF3 protein has the ability to optimize the Ku-0059436 mw cellular environment for viral infection and replication by interacting with multiple cellular proteins involved in signal transduction, such as mitogen-activated protein kinase (MAPK) phosphatase, CIN85, α-1-microglobulin, and bikunin precursor protein.7, 11, 35-37 In this study, our transfection experiments with HEV ORF3 showed that the STAT1 phosphorylation and IFN-α–stimulated genes PKR, 2′,5′-OAS, and MxA were inhibited in the IFN-α–treated A549 cells. It is thus reasonable to conclude that the binding of HEV ORF3 protein to STAT1 inhibits STAT1 phosphorylation and then suppresses the expression of IFN-α–stimulated GSI-IX supplier genes. Furthermore, we observed some differences in the inhibition

pattern of IFN-α–stimulated genes when HEV ORF3 alone was used compared with the whole virus infection of A549 cells. The expression of target gene MxA was inhibited in HEV ORF3-transfected cells but not in HEV-infected A549 cells and the increased levels of STAT1 were observed in HEV-infected A549 cells but not in HEV ORF3-transfected cells. Further studies are needed to determine more definitively the precise mechanism of IFN signaling inhibition in HEV infection. An intriguing finding was the increased levels of STAT1 during HEV infection. Such increased levels of STAT proteins during viral infection have recently been shown by other RNA viruses, such as human metapneumovirus (hMPV) and respiratory syncytial virus (RSV).38, 39 It is unclear what mechanisms caused these increased levels and what biological relevance, if any, the increased STAT levels may have in viral infections. One potential explanation

could be that expression of the STATs is up-regulated in response to HEV infection in an IFN-independent manner. Viruses have been shown to up-regulate ISGs in such a manner by activation of IRF3.40 A component of the HEV virion could be recognized by a pathogen-associated molecular MCE公司 pattern receptor, which then causes STAT protein levels to be increased without dependence on IFN, as previously demonstrated in hantavirus infection.41 Alternatively, the increased levels of STAT1 could be due to the reduction of normal degradation of STAT1. Because the STAT proteins have a relatively long biological half-life of 2 or 3 days,42 the increased levels shown here may be attributed to a gradual build-up of STAT1 during the course of our experiments. In conclusion, the data from our study show that IFN-α signal pathway plays an important role in HEV replication in host cells, and point to the role of type I IFN and STAT1 in protecting the host cells from HEV infection.

A polymorphism of the interleukin 23 receptor (IL23R) gene on chromosome 1p31 confers significant protection against the development of CD in Caucasians6 but not in the Japanese population.7 Further, the latter study did not demonstrate an association between the genetic variants of the autophagy-related 16-like 1 (ATG16L1) gene or the chromosome 5p13.1 locus and the development of CD in the Japanese population.7 The tumor necrosis factor superfamily member 15 (TNFSF15) gene of chromosome 9q32 contributes towards the risk of developing Crohn’s disease in both Japanese and European

IWR1 populations.8,9 In summary most genetic variants linked to IBD discovered so far through fine-mapping in regions of genetic linkage, the candidate gene approach, and in genome-wide association studies, vary according to ethnicity. While there is a lower rate of familial clustering of both CD and UC in Asia in comparison with

Caucasians,3,10 this is most likely related to the overall low disease prevalence rates, and is expected to increase as the IBD prevalence rises. The overall attributable risk of a positive family history in Asians is likely to be similar to that of Caucasians.11 Within individual Asian countries, ethnic-racial differences influence the rates of IBD. In Malaysia and Singapore, two multi-ethnic countries, the incidence of UC is consistently higher in Indians than in the Chinese and Malays, whereas Malays are relatively protected against the development of CD.12–14 Not only do Indians have a higher prevalence of UC, but severity of disease, prevalence of extra-intestinal manifestations and trend towards more extensive

FK228 disease are also higher.14 Ethnicity combines genetic, social, socioeconomic, cultural and dietary factors so the exact reasons for these differences remain, as yet, undefined. However, geographical, climatic and infective etiologies are less likely to be important determinants given that these incidence rates differ within the same limited areas. Migration studies have also demonstrated the interaction between genes and the environment. The background prevalence and incidence of UC is high in the Punjab region of north 上海皓元医药股份有限公司 India.15 Second generation South Asian immigrants to the United Kingdom, however, have demonstrated even higher incidence and prevalence rates than local Caucasians, indicating that under certain changing environmental conditions the emergence of IBD is favoured.16 Alternatively, certain environmental factors in Asia, no longer active after migration to the West, may be suppressing the clinical development of IBD. In this issue of the Journal of Gastroenterology and Hepatology, the Asia Pacific Inflammatory Bowel Disease Working Group publishes consensus statements in UC.17 These statements cover the epidemiology, diagnosis, and medical and surgical management of UC, but with emphasis on several points of interest to Asian countries.

Again, the observed differences in δ13C values likely result from differences in the amino acid composition of blood serum vs. vibrissae keratins. It has been long recognized that another commonly analyzed tissue, bone collagen, has a distinctive amino acid composition that produces larger than normal diet-tissue δ13C fractionation. While “soft” tissues such as muscle, liver, and skin are 13C-enriched by only 1‰–2‰ relative to diet, bone collagen typically has δ13C

values that are 4‰–5‰ higher than diet (Koch 2007). Accurate interpretation of intertissue isotopic differences requires careful consideration of such tissue-dependent discrimination patterns. Many marine mammals experience seasonal cycles in food intake anti-CTLA-4 antibody and energy demands that may impact the physiological processes that govern isotopic fractionation during metabolism and tissue synthesis. For example, many pinniped and mysticetes are capital breeders, storing vast amounts of fat to provide energy during reproduction and nursing. Some of these animals also undertake long migrations during which food intake may be limited. Because blubber is primarily composed of 13C-depleted lipids, it has a significantly lower δ13C value than a piscivorous (pinniped) or planktonic (mysticete) diet. An animal

that relies selleck screening library on blubber stores to maintain metabolism will be “consuming” a food source with a lower δ13C value than its regular diet and have a Δ13Ctissue-diet value that is lower than when it is not relying on fat. Such factors may influence Δ15Ntissue-diet values as well. Catabolism of protein from lean tissues (e.g., muscle) during periods of nutritional stress may cause δ15N values to rise as the animal continues

to shed waste that is 14N-enriched relative to the body. Furthermore, the nitrogen source for any additional protein deposition is body tissue, which is already 15N-enriched relative to dietary sources. A number of laboratory and a few field experiments have explored the utility of stable isotopes as proxies of nutritional stress (e.g., Hobson et 上海皓元 al. 1993, Polischuck et al. 2001, Cherel et al. 2005). For experiments in which no exogenous protein was supplied to subjects, significant bulk tissue or whole body 15N-enrichments of 0.5‰–2.5‰ were observed. In a wild population, Cherel et al. (2005) found significant 15N-enrichments in the plasma, red blood cells, and feathers of fasting penguins, which rely exclusively on endogenous protein when breeding and molting. Finally, in a longitudinal study tracking pregnant women, in those with severe morning sickness who entered negative nitrogen balance, hair δ15N values rose by 0.4‰–1.2‰ (Fuller et al. 2004, 2005). Overall, such effects would lead to increased Δ15Ntissue-diet values for animals in nutritional stress. Isotopic consequences of growth, pregnancy, and lactation have received little study.

Again, the observed differences in δ13C values likely result from differences in the amino acid composition of blood serum vs. vibrissae keratins. It has been long recognized that another commonly analyzed tissue, bone collagen, has a distinctive amino acid composition that produces larger than normal diet-tissue δ13C fractionation. While “soft” tissues such as muscle, liver, and skin are 13C-enriched by only 1‰–2‰ relative to diet, bone collagen typically has δ13C

values that are 4‰–5‰ higher than diet (Koch 2007). Accurate interpretation of intertissue isotopic differences requires careful consideration of such tissue-dependent discrimination patterns. Many marine mammals experience seasonal cycles in food intake selleck chemicals llc and energy demands that may impact the physiological processes that govern isotopic fractionation during metabolism and tissue synthesis. For example, many pinniped and mysticetes are capital breeders, storing vast amounts of fat to provide energy during reproduction and nursing. Some of these animals also undertake long migrations during which food intake may be limited. Because blubber is primarily composed of 13C-depleted lipids, it has a significantly lower δ13C value than a piscivorous (pinniped) or planktonic (mysticete) diet. An animal

that relies this website on blubber stores to maintain metabolism will be “consuming” a food source with a lower δ13C value than its regular diet and have a Δ13Ctissue-diet value that is lower than when it is not relying on fat. Such factors may influence Δ15Ntissue-diet values as well. Catabolism of protein from lean tissues (e.g., muscle) during periods of nutritional stress may cause δ15N values to rise as the animal continues

to shed waste that is 14N-enriched relative to the body. Furthermore, the nitrogen source for any additional protein deposition is body tissue, which is already 15N-enriched relative to dietary sources. A number of laboratory and a few field experiments have explored the utility of stable isotopes as proxies of nutritional stress (e.g., Hobson et 上海皓元 al. 1993, Polischuck et al. 2001, Cherel et al. 2005). For experiments in which no exogenous protein was supplied to subjects, significant bulk tissue or whole body 15N-enrichments of 0.5‰–2.5‰ were observed. In a wild population, Cherel et al. (2005) found significant 15N-enrichments in the plasma, red blood cells, and feathers of fasting penguins, which rely exclusively on endogenous protein when breeding and molting. Finally, in a longitudinal study tracking pregnant women, in those with severe morning sickness who entered negative nitrogen balance, hair δ15N values rose by 0.4‰–1.2‰ (Fuller et al. 2004, 2005). Overall, such effects would lead to increased Δ15Ntissue-diet values for animals in nutritional stress. Isotopic consequences of growth, pregnancy, and lactation have received little study.

Furthermore, the disappearance of extravasations indicates the resolution of hemorrhaging because of the high sensitivity of CEUS for detecting hemorrhaging.

Taken together, CEUS enables real-time and repeated assessment of hemorrhaging and its resolution without radiation exposure, unlike CT. CEUS has some limitations. First, CEUS has some blind areas, such as the subphrenic area or areas surrounding intestinal gas. However, most hemorrhages after US-guided RFA occur in the visual area. Second, adequate images of deep regions cannot be obtained.3 Third, CEUS depends on the selleck chemicals llc skill of the operator. In conclusion, when hemorrhaging is suspected, CEUS is a useful tool for detecting extravasation and confirming its resolution. “
“With recipients living longer after undergoing liver transplant (LT), significant causes of their morbidity and mortality post-transplant are not related to recurrent liver disease. The lifelong use of immunosuppressive therapy places

these recipients at risk for a variety of general medical conditions. These medical conditions include renal disease, hypertension, diabetes mellitus, dyslipidemia, obesity and osteoporosis. Up to one-third of long-term buy Doxorubicin LT survivors will develop significant renal dysfunction or cardiovascular mortality. More than half of all LT recipients will develop some aspect of the metabolic syndrome. Prevention of general medical conditions after LT relies on screening appropriately (cancer screening per national guidelines, and regular dermatology assessment for skin cancer) and controlling risk factors for cardiovascular disease. In addition, regular health maintenance should

include bone densitometry and adhering to vaccination guidelines. “
“We read with interest the recent article by Lehmann et al. in Hepatology,1 showing that biliverdin decreased expression of hepatitis C virus (HCV) genes in cell lines expressing HCV replicons. Heme oxygenase-1 (HMOX1), which catalyzes the rate-controlling step of heme catabolism, with formation of equimolar amounts of biliverdin, carbon monoxide, and iron, is recognized to be a key cytoprotective and MCE antioxidant enzyme.2, 3 Although the HMOX1 gene is up-regulated by many stressful stimuli, including increased oxidative stress,2, 3 its activity has been reported to be low in livers of subjects with chronic hepatitis C,4 even though this is a condition characterized by increased hepatic oxidative stress.5 Genetic variations in the promoter region of the HMOX1 genes, including the A/T polymorphism at position −413 and the length of (GT)n repeats closer to the transcription starting point, have been reported to influence HMOX1 gene expression.

siRNA targeting FGF18 also impaired the cells’ potential to form clones at a low cell density or in soft agar. With respect to the tumor microenvironment, FGF17 and FGF18 stimulated the growth of HCC-derived myofibroblasts, and FGF8, FGF17, and FGF18 induced the proliferation and tube formation of hepatic endothelial cells. Conclusion: FGF8, FGF17, and FGF18 are involved in autocrine and paracrine signaling in HCC and enhance the survival of tumor selleck cells under stress conditions, malignant behavior, and neoangiogenesis. Thus, the FGF8 subfamily supports the development and progression of hepatocellular malignancy. (HEPATOLOGY

2011) Hepatocellular carcinoma (HCC) is the third-leading cause of cancer deaths worldwide.1 Important risk factors for this disease are persistent infections with hepatitis viruses and chronic steatohepatitis due to ethanol abuse and obesity,

which contribute to the increasing incidence of HCC in industrialized countries. Most HCC cases have a very PLX3397 mw poor prognosis. This dramatic situation stems in part from the rare detection of tumors at early stages and from the high inherent resistance of HCC to chemotherapeutic agents. Much hope, therefore, is focused on obtaining a better understanding of the disturbed signaling pathways relevant to this disease in order to develop new preventive, diagnostic, and therapeutic options.2 HCC often emerges with a background of persistent liver injury, inflammation, and hepatocellular proliferation, which are characteristic of chronic hepatitis and cirrhosis.3 It is assumed that these liver diseases induce increasing aberrations in cellular signaling networks, which lead to the appearance of early precursor lesions of cancer.4, 5 These lesions overrespond to growth stimulatory cytokines and show enhanced proliferation and insufficient elimination of cells by apoptosis.4, 6, 7 This appears to select for premalignant and malignant cell populations with increasingly dysregulated

downstream signaling medchemexpress pathways, such as the Ras, phosphoinositide 3-kinase, and wnt pathways.8-10 Hepatocarcinogenesis is dependent on the development of a tumor-specific microenvironment of inflammatory cells, small vessels, myofibroblast (MFs), and extracellular matrix components.11, 12 These epithelial-mesenchymal interactions in early and advanced stages of hepatocarcinogenesis are driven by various growth factor systems. In particular, the signaling pathways induced by erythroblastic leukemia viral oncogene homolog receptors, hepatocyte growth factor, and insulin-like growth factor have been determined to contribute to the development of liver tumors and their stroma.3, 7, 13 However, our current understanding of the complex tumor-stroma interactions is far from complete. The fibroblast growth factor (FGF) system is known to be widely involved in nonliver carcinogenesis.