Data was subjected to a two-tailed Student t test and a P value of ≤0.05 was considered statistically significant. Student t Epacadostat mouse test with Welch correction was applied to serum bilirubin measurements due to unequal variance among experimental groups. HNF-6 is expressed within the liver and extrahepatic biliary system throughout embryonic development.22, 23 To investigate the consequence of HNF-6 deletion on BEC specification and IHBD development,

we limited genetic alterations to the liver. We accomplished this through the use of Albumin-Cre (Alb-Cre) recombinase transgene. Alb-Cre activity is detected within the BHPC population prior to differentiation into hepatocytes and BECs.11 Hepatoblast-specific inactivation of HNF-6 by Alb-Cre

was assessed by real-time RT-PCR of HNF-6 mRNA expression. With Alb-Cre–directed recombination, HNF-6 mRNA was decreased compared to control at embryonic day 16.5 (E16.5) and this reached significance in the postnatal period (Fig. 1A,B). To determine timing of HNF-6 protein loss directed by Alb-Cre recombination, immunostain analysis was performed at E16.5, E18.5, GPCR Compound Library cell line and P0. At E16.5, HNF-6 protein was seen in a similar pattern in both control and HNF-6 KO mice, limited to periportal BECs (Fig. 1C,D). At E18.5, HNF-6 protein expression was visible in nearly all BECs and hepatocytes in control mice (Fig. 1E). However, by E18.5, HNF-6 protein expression was limited in HNF-6 KO mice to a few isolated hepatocytes and a Glycogen branching enzyme few isolated BECs surrounding larger hilar portal veins (Fig. 1F, arrows). This pattern was consistent postnatally at P0 (Fig. 1G,H). These data indicate that Alb-Cre expression leads to inactivation of HNF-6 in both BHPC lineages by E18.5. The observed loss of HNF-6 protein in both hepatocytes and BECs is in agreement with previous ROSA26 reporter analysis, which has also demonstrated Alb-Cre directed recombination in cells contributing to both BHPC lineage derivatives.8, 11 Following this characterization, we then investigated the consequence of conditional loss of HNF-6 alone and in the setting of chronic cholestasis induced by the conditional loss of Notch signaling. To study

the effect of HNF-6 loss in a genetic model of chronic cholestasis, we used a described model of Notch signaling loss through Alb-Cre–mediated deletion of RBP-J.11, 24 Because RBP-J is the DNA-binding partner required by all four Notch receptors to effect canonical target gene expression, this approach circumvents possible functional redundancy through different receptors. Liver-specific inactivation of both HNF-6 and RBP-J (hereafter referred to as DKO) results in elevation of both total bilirubin and alkaline phosphatase (Table 1) versus control, HNF-6 loss alone, and RBP-J loss alone (P < 0.01). The fraction of conjugated bilirubin was similar between DKO and control genotypes (DKO: 56.4% ± 12.8%; Control: 31.4% ± 13.4%, P = 0.22).

Both groups showed comparable initiation of DNA synthesis 30 hours after PH, while Casp8ΔhepaNemoΔhepa livers had reduced number of hepatocytes in S-phase exclusively 40 hours after surgery (Fig. 7A,B). This correlated with slightly impaired cyclin A2 mRNA and protein expression (Fig. 7C,D). However, cyclin D1 expression in Casp8ΔhepaNemoΔhepa mice and control livers

was identical within the first 48 hours after PH (Fig. 7E), indicating that accelerated G1/S-phase transition and onset of DNA synthesis in regenerating Casp8Δhepa livers Regorafenib datasheet depends on aberrant NF-κB induction. Remarkably, the slightly delayed DNA synthesis in Casp8ΔhepaNemoΔhepa mice did not impair liver mass restoration during the first 14 days after PH (Fig. 7F). However, untreated Casp8ΔhepaNemoΔhepa mice exhibited hepatomegaly at baseline and 6 weeks after PH Casp8ΔhepaNemoΔhepa mice again revealed significantly increased liver mass (Fig. 7F) which was associated with slightly increased cyclin A and D levels after completion of liver mass restoration (336 hours post-PH, Fig. 7C,E). Accordingly, Selleck Vemurafenib proper liver regeneration

requires balanced expression of Casp8 and NEMO. Casp8 is the most apical caspase during extrinsic apoptosis mediated by death-receptors. In addition, Casp8 may have nonapoptotic functions, e.g., by regulating NF-κB transcriptional activity.[19] In the present study we characterized the consequences of hepatocyte-specific Liothyronine Sodium Casp8 deletion for liver regeneration in mice. We tested the hypothesis that loss of Casp8 would either prevent proper termination of liver growth or affect the early events of TNF-dependent signaling after PH. The present study revealed that termination of liver regeneration

is independent of Casp8. However, loss of Casp8 resulted in deregulation of all interphase cyclins and in accelerated onset of DNA synthesis after PH. These unexpected effects could be linked to premature RIP1 kinase activation affecting the downstream NF-κB and JNK/cJun pathways, respectively. Concomitant NEMO deletion restored normal onset of hepatocyte proliferation in Casp8-deficient livers but eventually induced hepatomegaly. Previous work from Ben Moshe et al.[20] revealed completely opposite results compared to our own study, including high mortality postsurgery, impaired early liver regeneration, and delayed expression of interphase cyclins. However, that study used a different experimental setting (33% hepatectomy) and a different Casp8 knockout allele (ΔExon 1-2). We thus conclude that the effects of Casp8 depletion on liver regeneration could be allele-specific and may depend on the strength of the regeneration stimulus. Casp8Δhepa mice showed normal liver regeneration after PH despite excessive DNA synthesis. This was unexpected, as aberrant DNA replication could result in enhanced cell division and in augmented liver growth.

In xenograft animal experiments, we found that overexpressed miR-7 effectively repressed tumor growth (3.5-fold decrease in mean tumor volume; n = 5) and abolished extrahepatic migration from liver to lung

in a nude mouse model of metastasis (n = 5). The number of visible nodules on the lung surface was reduced by 32-fold. A correlation between miR-7 and PIK3CD expression was also confirmed in clinical samples of HCC. Conclusion: These findings indicate that miR-7 functions as a tumor suppressor and plays Small molecule library manufacturer a substantial role in inhibiting the tumorigenesis and reversing the metastasis of HCC through the PI3K/Akt/mTOR-signaling pathway in vitro and in vivo. By targeting PIK3CD, mTOR, and p70S6K, miR-7 efficiently regulates the PI3K/Akt

pathway. Given these results, miR-7 may be a potential therapeutic or diagnostic/prognostic target for treating HCC. (HEPATOLOGY 2012;55:1852–1862) Hepatocellular carcinoma (HCC) is one of the most common malignant tumors worldwide.1 Despite the clinical implementation of numerous therapeutic strategies, HCC has a global mortality rate of 94%.2 Given this statistic, there is an urgent need to develop novel strategies for the diagnosis, treatment, and prognosis of HCC. Recent studies indicate that microRNAs (miRNAs) function to regulate tumor growth and metastasis and are considered AG-014699 in vivo promising targets for the diagnosis and prognosis of a number of cancers.3 miRNA-expression profiling has been characterized in a variety of cancers,

including breast cancer, lung cancer, ovarian cancer, and HCC.3-5 Previous studies have demonstrated that certain miRNAs are correlated with the proliferation and survival of HCC, including miR-1995 and miR-26a.6 Webster et al.7 recently found that miRNA-7 (miR-7) can regulate epidermal growth factor receptor (EGFR) expression, which is usually overexpressed in epithelial tumors, such as HCC.8 microRNA-7 (miR-7) was first reported to inhibit glioblastoma growth by regulating insulin receptor substrate 2 (IRS2) through the EGFR/IRS2/Akt pathway.9 Reddy et al.10 also discovered an upstream activator of miR-7 and a novel miR-7 target, p21-activated kinase 1 (Pak1), which is involved in the metastasis of breast cancer. These findings Vitamin B12 suggest that miR-7 may be associated with HCC progression through the regulation of EGFR expression and other key components of the EGFR pathway. Additionally, the phosphoinositide 3-kinase (PI3K)/AKT/mTOR (mammalian target of rapamycin) pathway, an important pathway downstream of EGFR, is known to be associated with cell proliferation, survival, and motility/metastasis. Based on previous studies indicating that the overexpression of miR-7 inhibits the Akt pathway in glioblastoma,9 we tested whether miR-7 could regulate HCC tumor growth and metastasis through interactions with the PI3K/AKT/mTOR pathway.

Overall, the US-22 genotype isolates from potato were more aggressive than those from tomato. The local isolate Pi97-5 (US-8) was the most aggressive Selleckchem Ixazomib isolate in most of the of potato cultivars. The infection of periderm was evaluated in terms of the number of eyes and lenticels infected using isolates representing genotypes US-8 and US-22 of P. infestans to determine whether the new introduced genotype in Michigan was likely to infect tubers through the periderm without wounding. The

isolates Pi97-5 (US-8) and Pi10-012 (US-22) (Table 1) previously identified as aggressive strains on tuber tissue were selected to infect three potato cultivars with different levels of resistance. In general, moderate lenticel infection was observed, but infected tubers had mycelial growth on the surface 10 days after inoculation

[DAI (Fig. 3)]. The anova of the main effects resulted in a significant difference between the genotypes US-8 and US-22 but not for cultivars. Also the interaction of genotype and cultivar for lenticel infection rated as AUDPC was not significant (Table 5). Mean values for AUDPC for genotype US-22 were lower in all cultivars, but the lowest were from cvs. Atlantic and Stirling. In contrast, the US-8 isolates FDA-approved Drug Library datasheet were more aggressive on Atlantic and less aggressive on Stirling (Fig. 4). The impact of tuber blight on epidemics caused by Phytophthora infestans emphasizes the importance of characterizing the interaction of different genotypes against different cultivars and the effect that new genotypes could have on the existing host-plant material. Tuber blight importance has been identified previously as a critical factor in storage and season-to-season transmission (Johnson and Cummings 2009; Kirk et al. 2009, 2010; Nyankanga et al. 2010). The resistance of six different cultivars against twelve isolates representing five different genotypes of P. infestans was assessed in this study. The newly identified genotype US-22 was compared with other genotypes

ROCK inhibitor already identified and collected from the field. We focused on the resistance responses in medullar tissue and periderm, to determine the risk of the new genotype US-22 to potato growers. Large differences in susceptibility measured as medullar tissue darkening were observed among the different isolates of P. infestans on the potato cultivars. The evaluation of tuber blight on medullar tissue revealed that isolates of genotype US-8 were the most aggressive in medullar tuber tissue in comparison with the other genotypes tested. Colombian isolates of P. infestans were less aggressive, probably due to a lack of pathogenic fitness to infect tubers, a phenomenon that has been observed previously in other lineages found in South America (Oyarzún et al. 2005). The UK isolates designated as genotype Blue-13 were highly aggressive and similar in aggressiveness in medullar tuber tissue to US-8 genotypes of P. infestans.

53 We were not able to assess population substructure in our analysis, because ancestry-informative markers are not yet available for NHANES III. There is little clinical or epidemiological evidence that some individuals or populations may be biologically more resistant or susceptible to HAV infections. It is possible that the three SNPs

identified in our study may simply be markers of population subgroups who have higher exposure to HAV or who migrated to the United States from a region where HAV is highly endemic. Additionally, the statistical power to detect significant associations with uncommon genetic variants was limited. Selleckchem PR 171 This study had 80% power to detect associations in odds ratio ≥1.3 among variants with a minor allele frequency ≥12% in non-Hispanic whites, ≥16% in non-Hispanic blacks, beta-catenin tumor and ≥24% in Mexican Americans (Supporting Table 5). It did appear that this study was adequately powered to detect in each racial/ethnic group the three associations that were significant in the Mexican American population (Supporting Table 6). The implicated markers are suggested to be functional by epidemiological, in vitro, or in

vivo studies,35, 36, 42, 45-47 but it is possible that they may be proxies for the true causal variants. If this is the case, then differences in linkage disequilibrium (Supporting Fig. 1) may hamper our ability to detect associations across all three racial/ethnic groups, if they exist.54 The relatively small number

of variants that we examined for each gene also served as a limitation. Further fine mapping in all three racial/ethnic subpopulations may be warranted. Finally, this Thiamet G study is cross-sectional, allowing us to test for disease susceptibility but not incidence or severity. Therefore, it will be important to examine these findings in additional populations and to assess whether these variants are also associated with other factors or characteristics associated with increased risk of hepatitis A infection, some of which may be unrelated to biological susceptibility. For example, some variants may simply be of higher prevalence among Mexican Americans who are of lower socioeconomic status (a risk factor for hepatitis A infection itself) or those who have a higher proportion of Native American ancestry. In conclusion, this study is the first to examine genetic associations with risk of HAV infection using a population-based and nationally representative sample of the United States population. We found significant associations between susceptibility to HAV infection and variants in TGFB1, XRCC1, and ABCB1 among Mexican Americans. It would be prudent to examine these findings in diverse populations. Furthermore, NHANES can be used to facilitate the population-level assessment of new and validated genetic variants for viral hepatitis susceptibility.

(Hepatology 2013;58:1779–1789) The cytokine tumor necrosis factor alpha GDC-0068 price (TNFα; TNF) mediates pleiotropic effects by triggering inflammation and cell proliferation by way of nuclear factor kappa B (NF-κB), apoptosis through caspase-8 (Casp8), or activation of cJun N-terminal kinases (JNK). It has been identified as a crucial mediator for the priming phase of liver regeneration. Genetic inactivation of TNF-receptor 1 (TNF-R1) results in decreased NF-κB and JNK signaling leading to impaired hepatocyte proliferation

after 70% partial hepatectomy (PH).[1] In the adult liver, hepatocytes are long-lived and rarely undergo proliferation, yet they retain a remarkable ability to proliferate.[2] This allows the liver to restore its original mass selleck chemical within 7 to 10 days after PH. The regenerative response is initiated by a series of signaling events that allow the quiescent hepatocytes to reenter the cell cycle and undergo several

rounds of proliferation until the original liver mass is restored.[3] Binding of TNF to TNF-R1 rapidly initiates assembly of a plasma membrane bound complex-I, composed of TNF-R1, the tumor necrosis factor receptor type 1-associated death domain protein (TRADD), the protein kinase RIP1, and the TNF receptor-associated factor 2 (TRAF2). Complex-I induces immediate downstream activation of both the JNK and NF-κB signaling pathways and prevents apoptosis in part by inducing antiapoptotic proteins such as FLIPL.[4] Upon inhibition of NF-κB signaling, a competing

complex (complex-II) is formed immediately after TNF ligation. Complex-II includes the adapter proteins TRADD, FADD (Fas-associated protein with death domain), and the proapoptotic protease pro-caspase-8, which eventually initiates the apoptotic signal cascade.[5] Constitutive targeted disruption of Casp8 results in embryonic lethality presumably due to an abundance of developmental defects.[6] More recent studies revealed that Casp8 plays also an essential role for prevention of an alternative mode of programmed cell death, termed necroptosis.[7] We recently reported that loss of Casp8 in hepatocytes protects from acute Fas and lipopolysaccharide (LPS)-induced liver injury but also triggers increased check nonapoptotic cell death in mice lacking the NF-κB essential modulator (NEMO) involving enhanced RIP1 kinase activity and necroptosis.[8] The aim of the present study was to investigate the consequences of genetic Casp8 inactivation in hepatocytes for liver regeneration following PH. We demonstrate that loss of Casp8 leads to an accelerated onset of hepatocyte priming and DNA synthesis following PH without affecting proper termination of liver growth. We provide evidence that this protective effect is due to early NF-κB activation associated with premature expression of the upstream RIP1 kinase. Our findings may have an impact for the evaluation of human therapies using low-molecular caspase-inhibitors.

8%, p = 0.009). The percentage of transient PHG in group B was significant higher than that in group A (42.9% vs 9.1%, p = 0.009). Severe PHG was not exacerbated after

ligation. The percentage of bleeding from PHG in group B was not significant lower than that in group A (7.1% vs 15.2%, p = 0.328). Conclusion: Most of PHG after ligation was transient and persistent, which was not very severe. Severe PHG was not exacerbated after ligation. Key Word(s): 1. esophageal varices; 2. ligation; 3. PHG; Presenting Author: DANPING SONG Additional Authors: BINGXIA GAO Corresponding Author: DANPING SONG, BINGXIA GAO Affiliations: Beijing Bureau of Health find more Objective: Background: Portal hypertension (PHT) is characterized as obstruction of portal vein flow is due to prehepatic, posthepatic

or intrahepatic etiologies, and an increase in portal pressure (> 10 mm Hg). Increasing of portal pressure is caused by prehepatic (portal vein or spleen vein), posthepatic (hepatic vein or inferior vena cava) or intrahepatic (hepatic sinusoid, before, after). LEE011 datasheet Clinical manifestation of portal hypertension are upper gastrointestinal hemorrhage, splenomegaly, ascites and hepatic encephalopathy, etc, 80% of PHT is cirrhosis, Non-cirrhotic portal hypertension only 5–10%. Need to identify Non-cirrhotic portal hypertension, find etiologies, and take a treatment in time. Purpose: Probe role of biliary system cancer in portal hypertension development, and mechanism. Forskolin in vitro Methods: Review 2 cases of PHT caused by biliary system cancer. Results: 2 cases of portal hypertension happened 0.5 year / 1 year after the operation for extrahepatic cholangiocarcinoma / gallbladder neck cancer respectively. Manifestation are Esophageal variceal bleeding, or together with gastric varices; ascites; non-splenomegaly; cirrhosis is not supported by biochemical test & iconography; high possibility of tumour recurrence is found. Patients died in 2 cases caused by tumor recurrence. To discuss possible

mechanism: 1. tumor recurrence constricts portal vein; 2. Part of tissue structure changes after operation impacts portal vein flow; 3. portal vein cancer embolus; 4. Portal pressure increases by obstructive jaundice. Conclusion: Biliary system cancer (gallbladder cancer, cholangiocarcinoma) is one of the rare reasons of non-cirrhotic portal hypertension. portal hypertension after operation probably indicates the tumor recurrence. Take emergency endoscopy as far as possible if find upper gastrointestinal hemorrhage on this kind of patients, and take corresponding endoscopical therapy to extend their life. Key Word(s): 1. portal hypertension; 2. cholangiocarcinoma; 3.

8%, p = 0.009). The percentage of transient PHG in group B was significant higher than that in group A (42.9% vs 9.1%, p = 0.009). Severe PHG was not exacerbated after

ligation. The percentage of bleeding from PHG in group B was not significant lower than that in group A (7.1% vs 15.2%, p = 0.328). Conclusion: Most of PHG after ligation was transient and persistent, which was not very severe. Severe PHG was not exacerbated after ligation. Key Word(s): 1. esophageal varices; 2. ligation; 3. PHG; Presenting Author: DANPING SONG Additional Authors: BINGXIA GAO Corresponding Author: DANPING SONG, BINGXIA GAO Affiliations: Beijing Bureau of Health MK-8669 molecular weight Objective: Background: Portal hypertension (PHT) is characterized as obstruction of portal vein flow is due to prehepatic, posthepatic

or intrahepatic etiologies, and an increase in portal pressure (> 10 mm Hg). Increasing of portal pressure is caused by prehepatic (portal vein or spleen vein), posthepatic (hepatic vein or inferior vena cava) or intrahepatic (hepatic sinusoid, before, after). PD98059 clinical trial Clinical manifestation of portal hypertension are upper gastrointestinal hemorrhage, splenomegaly, ascites and hepatic encephalopathy, etc, 80% of PHT is cirrhosis, Non-cirrhotic portal hypertension only 5–10%. Need to identify Non-cirrhotic portal hypertension, find etiologies, and take a treatment in time. Purpose: Probe role of biliary system cancer in portal hypertension development, and mechanism. (-)-p-Bromotetramisole Oxalate Methods: Review 2 cases of PHT caused by biliary system cancer. Results: 2 cases of portal hypertension happened 0.5 year / 1 year after the operation for extrahepatic cholangiocarcinoma / gallbladder neck cancer respectively. Manifestation are Esophageal variceal bleeding, or together with gastric varices; ascites; non-splenomegaly; cirrhosis is not supported by biochemical test & iconography; high possibility of tumour recurrence is found. Patients died in 2 cases caused by tumor recurrence. To discuss possible

mechanism: 1. tumor recurrence constricts portal vein; 2. Part of tissue structure changes after operation impacts portal vein flow; 3. portal vein cancer embolus; 4. Portal pressure increases by obstructive jaundice. Conclusion: Biliary system cancer (gallbladder cancer, cholangiocarcinoma) is one of the rare reasons of non-cirrhotic portal hypertension. portal hypertension after operation probably indicates the tumor recurrence. Take emergency endoscopy as far as possible if find upper gastrointestinal hemorrhage on this kind of patients, and take corresponding endoscopical therapy to extend their life. Key Word(s): 1. portal hypertension; 2. cholangiocarcinoma; 3.

We should fully consider adaptation of ESD and we should choose other treatment methods. The colorectal ESD for old patient has been proven to be effective and safe. Key Word(s): 1. ESD elderly patients Presenting Author: ZHINING FAN Additional Authors: YIN ZHANG, ZHINING FAN Corresponding Author: ZHINING FAN Affiliations: The First People’s Hospital of Changzhou, The First Affiliated Hospital of NJMU Objective: Gastric submucosal tumors (SMTs) originating from the muscularis propria layer are treated endoscopically. The successful closure of the wall defect is a critical step. This study evaluated the safety and feasibility of endoscopic purse-string

suture (EPSS) method with an endoloop and several metallic clips after endoscopic RG7204 nmr full-thickness resection (EFTR) or perforation due to endoscopic submucosal dissection Abiraterone manufacturer (ESD). Methods: Thirty patients with SMT originating from the muscularis propria layer receiving EFTR or ESD were retrospectively analyzed from December 2009 to April 2013. After successful

tumor resection, an endoloop was anchored onto the circumferential margin of the gastric defect with several metallic clips and tightened gently. Patient characteristics, tumor size, en bloc resection, and postoperative complications were evaluated. Results: EPSS was successfully performed in all the 30 patients following EFTR or perforation due to ESD. The mean size of the resected specimen was 1.9 cm in diameter. No severe complications occurred during Carnitine palmitoyltransferase II or after the procedure. One month after the procedure, the healed lesions were endoscopically confirmed. Conclusion: EPSS with an endoloop and clips is an effective

and safe technique for closing the gastric defect after EFTR or perforation due to ESD. Key Word(s): 1. complete defect closure with purse-string sutures in gastric submucosal tumors Presenting Author: ZHINING FAN Additional Authors: YIN ZHANG, ZHINING FAN Corresponding Author: ZHINING FAN Affiliations: The First People’s Hospital of Changzhou, The First Affiliated Hospital of NJMU Objective: The use of self-expanding metallic stents (SEMSs) is the current treatment of choice for malignant gastrointestinal obstructions. However, the stents can only promote the drainage but have no antitumor effect. Some studies have reported that drug-eluting SEMS may have the potential of tumor inhibition. The aim of the study was to evaluate the efficiency and safety of paclitaxel-eluting SEMS (PEMS) in rabbit esophageal cancer model. Methods: A PEMS was covered with a paclitaxel- incorporated membrane in which the concentration of paclitaxel was 10% (wt/vol). The rabbit models were created endoscopically. And then PEMS or SEMS was endoscopically inserted into rabbit esophagus.

We should fully consider adaptation of ESD and we should choose other treatment methods. The colorectal ESD for old patient has been proven to be effective and safe. Key Word(s): 1. ESD elderly patients Presenting Author: ZHINING FAN Additional Authors: YIN ZHANG, ZHINING FAN Corresponding Author: ZHINING FAN Affiliations: The First People’s Hospital of Changzhou, The First Affiliated Hospital of NJMU Objective: Gastric submucosal tumors (SMTs) originating from the muscularis propria layer are treated endoscopically. The successful closure of the wall defect is a critical step. This study evaluated the safety and feasibility of endoscopic purse-string

suture (EPSS) method with an endoloop and several metallic clips after endoscopic learn more full-thickness resection (EFTR) or perforation due to endoscopic submucosal dissection Cabozantinib molecular weight (ESD). Methods: Thirty patients with SMT originating from the muscularis propria layer receiving EFTR or ESD were retrospectively analyzed from December 2009 to April 2013. After successful

tumor resection, an endoloop was anchored onto the circumferential margin of the gastric defect with several metallic clips and tightened gently. Patient characteristics, tumor size, en bloc resection, and postoperative complications were evaluated. Results: EPSS was successfully performed in all the 30 patients following EFTR or perforation due to ESD. The mean size of the resected specimen was 1.9 cm in diameter. No severe complications occurred during L-NAME HCl or after the procedure. One month after the procedure, the healed lesions were endoscopically confirmed. Conclusion: EPSS with an endoloop and clips is an effective

and safe technique for closing the gastric defect after EFTR or perforation due to ESD. Key Word(s): 1. complete defect closure with purse-string sutures in gastric submucosal tumors Presenting Author: ZHINING FAN Additional Authors: YIN ZHANG, ZHINING FAN Corresponding Author: ZHINING FAN Affiliations: The First People’s Hospital of Changzhou, The First Affiliated Hospital of NJMU Objective: The use of self-expanding metallic stents (SEMSs) is the current treatment of choice for malignant gastrointestinal obstructions. However, the stents can only promote the drainage but have no antitumor effect. Some studies have reported that drug-eluting SEMS may have the potential of tumor inhibition. The aim of the study was to evaluate the efficiency and safety of paclitaxel-eluting SEMS (PEMS) in rabbit esophageal cancer model. Methods: A PEMS was covered with a paclitaxel- incorporated membrane in which the concentration of paclitaxel was 10% (wt/vol). The rabbit models were created endoscopically. And then PEMS or SEMS was endoscopically inserted into rabbit esophagus.