BMDC, bone marrow-derived DC; DC, dendritic www.selleckchem.com/products/Rapamycin.html cells; HCV, hepatitis C virus; IFN-α, interferon alpha; IL-10, interleukin 10; MoDC, monocyte derived dendritic cells; PBMC, peripheral blood mononuclear cells. Phages from a library expressing 15-mer random peptides near the N-terminus of phage surface

protein pIII (a kind gift of GP Smith, University of Missouri-Columbia)19 were allowed to interact with biotinylated recombinant IL-10 (rIL-10) (Amersham Pharmacia Biotech, UK) as described.20 Three rounds of panning were carried out using 2.5, 0.02, and 0.002 μg/mL of rIL-10, respectively. After the third round, phages were eluted and their region coding for the 15-mer peptides was sequenced as described.20 Peptides identified using the phage library and used in initial screening assays as well as the human leukocyte antigen (HLA)-A2 restricted cytotoxic T lymphocyte (CTL) epitope from HCV NS3 1073-1081 and HCV NS3 peptide pools M2 and M4 were synthesized as described.21 Their purity was always above 80%. C-terminal amidated peptides p9 and p13, as well as control selleck kinase inhibitor peptide p301 (amino

acids 301-315 of HIV-1 gp120), were also purchased from NeoMPS (Strasbourg, France). MC/9 murine mast cell line (ATCC; Manassas, VA) was grown in Dulbecco’s modified Eagle’s medium (DMEM) containing 2 mM L-glutamine, 0.05 mM 2-mercaptoethanol, 10% fetal bovine serum (complete medium; CM), and 5% rat T-STIM (BD-Biosciences, San Diego, CA). In IL-10-dependent proliferation assays, 2 × 104 cells were cultured in round-bottomed 96-well plates in CM containing

0.5 ng/mL of murine IL-4 (Peprotech, UK) and 1.25 ng/mL of human or murine rIL-10 (eBioscience, San Diego, CA), previously incubated for 2 hours with or without peptides. After 24 hours, 1 μCi of (methyl-3H)-thymidine (Amersham Life Science, Buckinghamshire, UK) was added per well and incubated for 12 additional hours before harvesting. Cells grown with or without IL-10 were used as positive (PC) and negative control (NC), respectively. Percentage of inhibition of IL-10 was calculated as: 100 × (cpmPC − cpmPT) / (cpmPC − cpmNC), where cpmPT corresponds to cpm obtained in the presence of IL-10 and peptides tested. Toxicity of the peptides was analyzed using similar bioassays with MC/9 MCE公司 cells but instead of rIL-10, murine GM-CSF (Peprotech, UK) at 0.01 ng/mL was used as stimulus. Peptide binding to IL-10 was analyzed by surface plasmon resonance using a BIAcore X Biosensor (BIAcore, AB, Uppsala, Sweden). IL-10 (R&D Systems) was covalently immobilized onto the surface of flow cell 2 (FC2) of a CM5 chip (BIAcore) as described.20 Flow cell 1 (FC1) without IL-10 was used as the reference flow cell. Peptide solutions (10 μM) were injected three times in 10 mM Hepes, 150 mM NaCl, 0.005% (v/v) Tween-20, 0.1 mg/mL BSA, pH 7.4 at a flow of 30 μL/min.

Sharma, Subodh Bn, Debasish Basu Introduction: Current UK guidelines, in line with many other countries, do not support routine antenatal screening for hepatitis C virus (HCV). At St Mary’s Hospital, UK all mothers attending antenatal screening are offered HCV testing. We discuss

the outcomes over the last 10 years. Methods: All pregnancies with antenatal booking dates from the 1st November 2003 to the 1st March 2013 were included for retrospective analysis. Records of patients with antenatal screening HCV positive results are stored on a maternity unit anonymised encrypted database. Data on these women from hospital reporting software and clinic

notes were used to make the audit BIBW2992 cell line dataset. Results: Within the audited Ipilimumab in vitro period a total of 35,455 women had booked in for antenatal care. A total of 119 (0.003%) HCV antibody positive results were recorded. 44 (37%) of these were new cases of HCV, as confirmed by PCR testing, 32 (27%) cases were in patients who had previously been diagnosed with HCV and 43 (36%) were spontaneous clearers. Of the newly diagnosed HCV mothers 10 reported a history of injecting drug use, 1 had possibly been infected via blood transfusion. 12 women were born in the United Kingdom and 32 born outside the UK. As of December 2013, 19 of the 44 newly diagnosed women underwent treatment for HCV and 2 are currently undergoing treatment, with 14 achieving SVR (74%). Of nine women

with genotype 1 HCV, eight were treated with interferon and ribavirin without protease inhibitor and one during a clinical trial involving alisporivir. 7 (78%) women with genotype 1 achieved SVR. Of the 23 women that currently haven’t been treated 20 are in active follow-up. All newly diagnosed women assessed with either liver biopsy or fibroscan had mild to moderate disease only. 4 vertical transmissions were identified MCE公司 from the 119 HCV antibody positive mothers (3.4% [95% CI 0.9-8.4%]). Out of the 44 deliveries by newly diagnosed mothers, 3 babies were infected vertically (6.8% [95%CI 1.4-18.7%]), as confirmed by PCR at 15 months of age. Conclusion: We demonstrate that antenatal screening provides an opportunity to identify healthy women infected with HCV at an early stage of their disease, who may not have otherwise been identified. Compliance to follow-up and SVR rates are superior to quoted rates in high-risk targeted groups. Disclosures: Claire Thorne – Grant/Research Support: AbbVie, Janssen, Public Health England, European Commission, PENTA Foundation Mark R. Thursz – Advisory Committees or Review Panels: Gilead, BMS, Abbott Laboratories Ashley S.

Sharma, Subodh Bn, Debasish Basu Introduction: Current UK guidelines, in line with many other countries, do not support routine antenatal screening for hepatitis C virus (HCV). At St Mary’s Hospital, UK all mothers attending antenatal screening are offered HCV testing. We discuss

the outcomes over the last 10 years. Methods: All pregnancies with antenatal booking dates from the 1st November 2003 to the 1st March 2013 were included for retrospective analysis. Records of patients with antenatal screening HCV positive results are stored on a maternity unit anonymised encrypted database. Data on these women from hospital reporting software and clinic

notes were used to make the audit selleck products dataset. Results: Within the audited Talazoparib supplier period a total of 35,455 women had booked in for antenatal care. A total of 119 (0.003%) HCV antibody positive results were recorded. 44 (37%) of these were new cases of HCV, as confirmed by PCR testing, 32 (27%) cases were in patients who had previously been diagnosed with HCV and 43 (36%) were spontaneous clearers. Of the newly diagnosed HCV mothers 10 reported a history of injecting drug use, 1 had possibly been infected via blood transfusion. 12 women were born in the United Kingdom and 32 born outside the UK. As of December 2013, 19 of the 44 newly diagnosed women underwent treatment for HCV and 2 are currently undergoing treatment, with 14 achieving SVR (74%). Of nine women

with genotype 1 HCV, eight were treated with interferon and ribavirin without protease inhibitor and one during a clinical trial involving alisporivir. 7 (78%) women with genotype 1 achieved SVR. Of the 23 women that currently haven’t been treated 20 are in active follow-up. All newly diagnosed women assessed with either liver biopsy or fibroscan had mild to moderate disease only. 4 vertical transmissions were identified 上海皓元医药股份有限公司 from the 119 HCV antibody positive mothers (3.4% [95% CI 0.9-8.4%]). Out of the 44 deliveries by newly diagnosed mothers, 3 babies were infected vertically (6.8% [95%CI 1.4-18.7%]), as confirmed by PCR at 15 months of age. Conclusion: We demonstrate that antenatal screening provides an opportunity to identify healthy women infected with HCV at an early stage of their disease, who may not have otherwise been identified. Compliance to follow-up and SVR rates are superior to quoted rates in high-risk targeted groups. Disclosures: Claire Thorne – Grant/Research Support: AbbVie, Janssen, Public Health England, European Commission, PENTA Foundation Mark R. Thursz – Advisory Committees or Review Panels: Gilead, BMS, Abbott Laboratories Ashley S.

Proportional analysis of percentage drop in serum bilirubin versus Imax was measured using Fisher’s exact test. In all, 20 patients were recruited into the study over 18 months (14 men and 6 women were recruited). All patients were required to have an MdF score of >32 as defined by the study inclusion criteria. There was no correlation between baseline bilirubin, MdF, Lille score, or GAHS and mortality at 6 months (P = 0.45, P = 0.54; P = 0.70, and P = 0.97, respectively; Fig. 1) in this cohort of SAH. A drop in serum levels of bilirubin in the first 7 days of treatment

with steroids (clinical steroid sensitivity) has been shown to correlate with outcome in SAH.25 Consistent with this, we saw a strong correlation between this parameter and 6-month mortality in our patient cohort (Fig. 1), indicating check details that our cohort is similar to those previously studied in SAH. Subjects were categorized as steroid-resistant by in vitro criteria (Imax <60%). The overall prevalence of clinical steroid resistance in this patient cohort was high (68%)—higher than the values seen in other inflammatory conditions and the in vitro steroid resistance seen in the general population (about 30%).13, 15, 26,

27 No statistical differences in baseline MdF, Lille score, GAHS, or baseline (day 0) bilirubin were seen between the in vitro steroid-resistant and steroid-sensitive groups (Fig. 2). Talazoparib However, in vitro steroid resistance, as indicated by Imax <60%, was significantly associated with outcome in response to steroid therapy as determined by mortality at 6 months (P = 0.03) (Fig. 3). 82% (9/11) of in vitro steroid-resistant patients were dead at 6 months as compared to 21% (2/9) of steroid-sensitive patients (P = 0.03). In

patients who survived for 6 months following their treatment, only 2 of 11 (21%) had an Imax value of lower than 60%. Consistent with this finding, patients who had a serum bilirubin fall of < 25% in the first 7 days of steroid treatment also had a lower Imax (Fig. 4). 91% (10/11) of in vitro steroid-resistant Rho patients failed to show a significant fall in bilirubin at day 7 as compared to 44% (4/9) of steroid-sensitive patients (P < 0.05). In those patients demonstrating in vitro steroid resistance as measured by an Imax value <60% (n = 11), competitive inhibition of IL-2 at the high-affinity CD25 receptor with 10 μg/mL basiliximab improved lymphocyte suppression in the presence of high-dose dexamethasone, P = 0.002 (Fig. 5). Basiliximab improved Imax in 91% (10/11) of in vitro steroid-resistant patients (P = 0.002). We have shown here that in a cohort of patients with SAH (MdF/Maddrey score >32 at baseline) treated with a standard steroid regime, clinical outcome (survival at 6 months) correlates with an in vitro measure of lymphocyte steroid resistance (DILPA).

This study highlights the role of chronic iron overload, not acute parenteral injection, as a ‘second hit’ in the development of NASH in a mouse model with metabolic syndrome. Disclosures: Kris V. Kowdley – Advisory Committees or Review Panels: AbbVie, Gilead, Merck, Novartis, Trio Health, Boeringer Ingelheim, Ikaria, Janssen; Grant/Research Support: AbbVie, Beckman, Boeringer Ingelheim, BMS, Gilead Sciences, Ikaria, Janssen, Merck, Mochida, Vertex The following people have nothing to disclose: Priya Handa, Vicki Morgan-Stevenson, Bryan D. Maliken, James E. Nelson, Matthew M. Yeh Background: The NLRP3 inflammasome, http://www.selleckchem.com/products/H-89-dihydrochloride.html a caspase-1

activation platform critical for processing key pro-inflammatory cytokines, is of great importance in innate immunity. While its activation has been linked to the development acute and chronic liver diseases, regulatory pathways that mediate this process are poorly understood. Therefore,

our AIM was to investigate the role of IL-17 and TNF-α in NLRP3 dependent liver damage. Methods: Nlrp3A350VneoR knock-in mice were bred onto IL-17 and TNF-α knockout backgrounds. The resultant mice were then crossed with IL-17 or TNF-α knockout mice expressing a Cre recombinase under the Lysozyme promoter allowing for mutant Nlrp3 expression in myeloid derived cells in mice deficient in IL-17 or TNF-α. Results: Mice expressing the Nlrp3A350V mutation in myeloid derived cells were smaller than non-mutant littermates, showed a marked inflammatory infiltrate in liver samples and had elevated levels of IL-17 Enzalutamide molecular weight and TNF-α when compared to littermate controls. Mutants lacking

IL-17 showed a slight improvement in weight differential, while TNF-α knockout mutants were not distinguishable from their non-mutant knockout littermates. Livers of intact Nlrp3A350V mutants showed strong neutrophilic infiltrations, while IL-17 loss of function mutants showed fewer neutrophils when compared to intact Nlrp3A350V mutants, but still significantly more than their non-mutant IL-17 knockout littermates. The amount of neutrophils and regulating chemokines in TNF-α deficient mutants did not differ from non-mutant knockout littermates. An increase in hepatic macrophages was only present in intact Nlrp3A350V mutants, while values in Bay 11-7085 IL-17 and TNF-α deficient mutants were similar to corresponding littermates. However, inflammatory macrophage polarization with increased mRNA levels of TNF-α and iNOS was present in inact Nlr-p3A350V mutants and IL-17 lacking mutants. Moreover, intact Nlrp3A350Vmutants showed fibrosis, as evidenced by Sirius red staining and increased mRNA levels of CTGF and TIMP-1. IL-17 lacking mutants exhibited amelioration of the aforementioned fibrosis, while TNF-α deficient mutants showed no signs of fibrosis when compared to littermate controls.

7%, 1-year survival 29.2%, no severe toxicity) [40]. The effect of sunitinib as second-line treatment in patients with GC has been assessed in a German phase II trial [41]. The overall response rate was 3.9% with a PFS of 1.28 months, an OS of 5.81 months, and a 1-year survival rate of 23.7%. These results do not support the application of sunitinib in this setting. Efforts are made to use the rapidly developing biostatistical approaches of gene-coexpression network profiling for the

identification of novel target genes or promising candidate compounds for the treatment of advanced GC [42]. Several studies have suggested that chronic infection with H. pylori may moderately increase the risk for colorectal cancer [43-45]. The background for this hypothesis is that infection with H. pylori leads to an increase of plasma gastrin levels. Hypergastrinemia stimulates mucosal cell proliferation. Chronic H. pylori www.selleckchem.com/products/Maraviroc.html HIF-1�� pathway infection results in gastric atrophy, cell

mutation, and transformation of gastric mucosal cells into gastrin-producing cells, which also express gastrin receptors serving to stimulate cell proliferation and tumor growth [46-48]. Two meta-analysis reported that there is a modest increase in the risk of colorectal cancer owing to H. pylori infection [49, 50]. However, the studies had several weaknesses as thus included a small sample size of studies with high heterogeneity and made note or confounding controls. Recently, a large population-based case control study was conducted in Germany to investigate the association between H. pylori and colorectal cancer [51]. Serum anti-H. pylori antibodies and anti-CagA antibodies were measured in 1712 patients with colorectal cancer and 1669 controls. There was a high MG-132 cost H. pylori seroprevalence in the study population (mean age 69 years) with more than 40% in both arms. Overall, H. pylori infection

was more prevalent in colorectal cancer cases (46.1%) than in controls (40.1%). The authors performed a stratified analysis which showed risk elevation to be essentially confined to left-sided colorectal cancer, with an odds ratio (OR) of 1.22 (95% CI: 1.02–1.45). The results of this large population-based study suggest that H. pylori infection may be associated with an increased risk for the selected group after the neoplasia of the left colorectum. Colorectal cancer development is based on the adenoma-carcinoma sequence. Thus, a study investigated correlation between H. pylori infection or chronic atrophic gastritis (CAG) and risk of colorectal adenoma [52]. In this study, H. pylori infection was a risk factor for adenoma as a whole. The analysis of distal adenoma cases showed that adenoma risk was significantly increased in the presence of H. pylori infection when chronic atrophic gastritis was present. In a large cross-sectional study from Korea, 2195 eligible subjects undergoing screening colonoscopy have been evaluated for the prevalence of H.

7%, 1-year survival 29.2%, no severe toxicity) [40]. The effect of sunitinib as second-line treatment in patients with GC has been assessed in a German phase II trial [41]. The overall response rate was 3.9% with a PFS of 1.28 months, an OS of 5.81 months, and a 1-year survival rate of 23.7%. These results do not support the application of sunitinib in this setting. Efforts are made to use the rapidly developing biostatistical approaches of gene-coexpression network profiling for the

identification of novel target genes or promising candidate compounds for the treatment of advanced GC [42]. Several studies have suggested that chronic infection with H. pylori may moderately increase the risk for colorectal cancer [43-45]. The background for this hypothesis is that infection with H. pylori leads to an increase of plasma gastrin levels. Hypergastrinemia stimulates mucosal cell proliferation. Chronic H. pylori Sorafenib Rapamycin infection results in gastric atrophy, cell

mutation, and transformation of gastric mucosal cells into gastrin-producing cells, which also express gastrin receptors serving to stimulate cell proliferation and tumor growth [46-48]. Two meta-analysis reported that there is a modest increase in the risk of colorectal cancer owing to H. pylori infection [49, 50]. However, the studies had several weaknesses as thus included a small sample size of studies with high heterogeneity and made note or confounding controls. Recently, a large population-based case control study was conducted in Germany to investigate the association between H. pylori and colorectal cancer [51]. Serum anti-H. pylori antibodies and anti-CagA antibodies were measured in 1712 patients with colorectal cancer and 1669 controls. There was a high Tau-protein kinase H. pylori seroprevalence in the study population (mean age 69 years) with more than 40% in both arms. Overall, H. pylori infection

was more prevalent in colorectal cancer cases (46.1%) than in controls (40.1%). The authors performed a stratified analysis which showed risk elevation to be essentially confined to left-sided colorectal cancer, with an odds ratio (OR) of 1.22 (95% CI: 1.02–1.45). The results of this large population-based study suggest that H. pylori infection may be associated with an increased risk for the selected group after the neoplasia of the left colorectum. Colorectal cancer development is based on the adenoma-carcinoma sequence. Thus, a study investigated correlation between H. pylori infection or chronic atrophic gastritis (CAG) and risk of colorectal adenoma [52]. In this study, H. pylori infection was a risk factor for adenoma as a whole. The analysis of distal adenoma cases showed that adenoma risk was significantly increased in the presence of H. pylori infection when chronic atrophic gastritis was present. In a large cross-sectional study from Korea, 2195 eligible subjects undergoing screening colonoscopy have been evaluated for the prevalence of H.

In addition, the currently available liver chemistries, such as serum alanine aminotransferase (ALT), do not reliably distinguish between mild and transient DILI, which is of no consequence for the patient who can continue to receive the drug safely, versus DILI that will progress to life-threatening injury if drug therapy is not promptly stopped.3 In addition, currently available tests generally cannot distinguish which specific drug is causing the DILI in patients on multiple drug therapy. What is clearly needed are better biomarkers of DILI to help clinicians, as well as provide more meaningful liver safety data in

clinical trials of new drugs. We believe that the peripheral blood (PB) transcriptome may contain information that could address the shortcomings of currently available DILI diagnostic tools. Support for the PB transcriptomic approach comes from several recent findings. In an in-life rat MLN8237 study of eight hepatoxicants, we recently demonstrated that PB cell gene expression can be successfully utilized to detect the presence and severity of toxic responses in the liver.4 In fact, these studies suggested that PB transcriptomic data might be more sensitive to liver injury than traditional clinical tests and therefore able to detect DILI earlier. In addition, the pattern of PB cell transcriptomic response varied across

toxicants, indicating the existence Akt inhibitor of “signatures” that could be useful in identifying the specific drug responsible for DILI. With specific respect to acetaminophen (APAP), the most common identifiable causative agent of acute liver failure in the US, we have shown that in rats treated with toxic doses, PB transcriptomic signatures, particularly in immune and inflammatory pathways, outperform traditional histological or clinical chemistry Selleckchem DAPT markers in detecting DILI. Furthermore, by probing human whole blood transcriptomic data from clinical overdose patients with human

orthologs of this rat PB signature, we were also able to differentiate these patients from nonexposed individuals.5 The hypothesis tested in the current study was that a supratherapeutic but not overtly toxic APAP dose would result in readily detectable changes in the human PB transcriptome and that these changes would be qualitatively similar to changes we have demonstrated in rats and humans after toxic doses of APAP.5 ALT, alanine aminotransferase; APAP, acetaminophen; AUC, area under the curve; CBC, complete blood counts; CYP2E1, cytochrome P4502E1; DEGs, differentially expressed genes; DILI, drug-induced liver injury; GSA, gene set analysis; GSH, glutathione; IPA, ingenuity pathways analysis; NAPQI, N-acetyl-p-benzoquinone-imide; PB, peripheral blood. Subjects were healthy volunteers from 18-55 years old weighing 55 to 85 kg and not taking any over-the-counter or prescription medications.

Key Word(s): 1. HIF-1α; 2. the hypoxia; 3. gastric cancer; 4. ASODN; Presenting Author: WANG XI Corresponding Author: WANG XI Affiliations: Department of Gastroenterology, the First Affiliated Hospital, Harbin Medical University this website Objective: To study the expression and interaction of ΔNp63, p21WAF1 and PCNA in esophageal squamous carcinoma, and to explore their role in occurrence and development of the cancer. Methods: Immunohistochemical method was carried out to

detect the expression of ΔNp63, p21WAF1 and PCNA for 42 patients from endoscopic mucosa biopsies. The 42 cases included the esophageal cancer, adjacent cancer and far cancer tissues. Results: The positive incidence of ΔNp63 and PCNA was 78.6% and 100% in the esophageal cancer tissues, 52.4% and 59.5% in the adjacent cancer tissues, 26.2% and 31.0% in far cancer tissues, respectively. The positive incidence of p21WAF1 was 54.8% in the esophageal cancer tissues, 76.2% in the adjacent cancer tissues and 90.5% in far cancer tissues. There was positive correlation between and PCNA expression in the esophageal cancer tissue. Conclusion: The expression of ΔNp63 and PCNA was high in the cancer tissues, and higher with decreasing of cancer differentiation. However, the expression of p21 was low in the

cancer tissues, and lower with decreasing of cancer differentiation. click here There was negative correlation between p21 expression and ΔNp63/PCNA expression in esophageal Clomifene cancer. The overexpression of ΔNp63 in esophageal cancer may not only exist in the invasive stage but also play an important role in the early stage of esophageal carcinoma. Key Word(s): 1. esophageal cancer; 2. ΔNp63; 3. p21WAF1; 4. PCNA; Presenting

Author: MAZHI BIN Corresponding Author: MAZHI BIN Affiliations: The First Affiliated Hospital of Harbin Medical University Objective: To study the impact of the apoptosis of the human gastrointestinal carcinoma cells induced by arsenic trioxide, and the changes of Survivin, BCL-2 expression after the chemotherapy with it. Methods: To select 20 Patients diagnosed gastrointestinal carcinoma through endoscopy and biopsy, including 9 gastric cancer and 11 colorectal cancer, and hold malignant tissue of them by endoscopy and biospy. They were given As2O3 intravenous administration (10 mg/d) for three days before operated. After that, all the patients received Surgery. Take pathologies in the preoperative and intraoperative, we observed the cytological morphology, and calculated the apoptosis index(AI) under the light microscope, and detected the positive expression rate of the Survivin, BCL-2 with immunohistochemical method. Results: Apoptosis of post-chemotherapy gastrointestinal cancer cells are 17.04%, more significant than pre-chemotherapy 6.07%,the difference is significant statistic- allly(P < 0.

Key Word(s): 1. HIF-1α; 2. the hypoxia; 3. gastric cancer; 4. ASODN; Presenting Author: WANG XI Corresponding Author: WANG XI Affiliations: Department of Gastroenterology, the First Affiliated Hospital, Harbin Medical University selleck screening library Objective: To study the expression and interaction of ΔNp63, p21WAF1 and PCNA in esophageal squamous carcinoma, and to explore their role in occurrence and development of the cancer. Methods: Immunohistochemical method was carried out to

detect the expression of ΔNp63, p21WAF1 and PCNA for 42 patients from endoscopic mucosa biopsies. The 42 cases included the esophageal cancer, adjacent cancer and far cancer tissues. Results: The positive incidence of ΔNp63 and PCNA was 78.6% and 100% in the esophageal cancer tissues, 52.4% and 59.5% in the adjacent cancer tissues, 26.2% and 31.0% in far cancer tissues, respectively. The positive incidence of p21WAF1 was 54.8% in the esophageal cancer tissues, 76.2% in the adjacent cancer tissues and 90.5% in far cancer tissues. There was positive correlation between and PCNA expression in the esophageal cancer tissue. Conclusion: The expression of ΔNp63 and PCNA was high in the cancer tissues, and higher with decreasing of cancer differentiation. However, the expression of p21 was low in the

cancer tissues, and lower with decreasing of cancer differentiation. 3-MA molecular weight There was negative correlation between p21 expression and ΔNp63/PCNA expression in esophageal MRIP cancer. The overexpression of ΔNp63 in esophageal cancer may not only exist in the invasive stage but also play an important role in the early stage of esophageal carcinoma. Key Word(s): 1. esophageal cancer; 2. ΔNp63; 3. p21WAF1; 4. PCNA; Presenting

Author: MAZHI BIN Corresponding Author: MAZHI BIN Affiliations: The First Affiliated Hospital of Harbin Medical University Objective: To study the impact of the apoptosis of the human gastrointestinal carcinoma cells induced by arsenic trioxide, and the changes of Survivin, BCL-2 expression after the chemotherapy with it. Methods: To select 20 Patients diagnosed gastrointestinal carcinoma through endoscopy and biopsy, including 9 gastric cancer and 11 colorectal cancer, and hold malignant tissue of them by endoscopy and biospy. They were given As2O3 intravenous administration (10 mg/d) for three days before operated. After that, all the patients received Surgery. Take pathologies in the preoperative and intraoperative, we observed the cytological morphology, and calculated the apoptosis index(AI) under the light microscope, and detected the positive expression rate of the Survivin, BCL-2 with immunohistochemical method. Results: Apoptosis of post-chemotherapy gastrointestinal cancer cells are 17.04%, more significant than pre-chemotherapy 6.07%,the difference is significant statistic- allly(P < 0.