Browsing by Author "Yuceyar, H"
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Item Is administration of n-3 fatty acids by mucosal enema protective against trinitrobenzene-induced colitis in rats?Yuceyar, H; Ozutemiz, O; Huseyinov, A; Saruç, M; Alkanat, M; Bor, S; Coker, I; Batur, YWe investigated the protective role of fish oil (FO-source of n-3 FA) enriched diet tin the first protocol in 20 rats and FO administration intrarectally (in the second protocol) in 40 rats with trinitrobennzene (TNB) colitis. All colonic specimens were pathologically evaluated, myeloperoxidase enzyme activities were measured, leukotriene B4 (LTB4) and LTC4 levels were determined by radioimmunoassay. In the first protocol 10 rats (group Al) were fed with 8% sunflower and cotton oil enriched diet and (group A2) with 8% FO enriched diet for 6 weeks. At the end of this period, TNB (30 mg in 0.25 mi of 30% ethanol) were intrarectally administered. After 2 weeks, rats were sacrificed. MPO activities (2.47 versus 30.17), LTB4 (34.5 versus 903.3) and LTC4 (77.7 versus 456.0) levels were significantly reduced in group A2 compared with group Al (P < 0.005). There was also a significant difference in pathologic scores (1.55 versus 2.12, P < 0.0002) between two groups. In the first part of the second protocol, 20 male rats were randomized into two equal groups (B1 and B2) and TNB colitis was induced. After 1 day, 1 mi of saline (group B1) or n-3 FA enemas (group B2) were administered every day for 2 weeks. At the end of this period, rats were sacrificed and evaluated as done for previous groups. Although there was no significant difference between the two groups in comparison with MPO enzyme activities and pathologic scores, the LTB4 (130.1 versus 971.0) and LTC4 (126.0 versus 532.0) levels of FO group were significantly reduced (P < 0.005). In the second part of the second protocol, 20 male rats were randomized into two groups. One millilitre of saline (group B3) or FO enemas (group B4) were administered to rats every day for 3 days. At the fourth day, TNB-colitis was induced and after 24 h rats were sacrificed. We could not find any significant difference in MPO activities, pathologic scores, LTB4 and LTC4 levels between groups B3 and B4. In conclusion; FO enriched diet decreased both pathologic damage and tissue LT levels. The second protocol of our study revealed that the long-term FO enemas decreased the LTB4 and LTC4 levels; however, did not have any beneficial effect on the tissue lesions. Short periods of FO enemas did not have a protective role in the occurrence of experimental colitis. The present study showed that FO enemas significantly decreased LT levels. The protective effect of FO (oral and enema) in TNB colitis may open a new insight into the treatment of inflammatory bowel disease. (C) 1999 Harcourt Publishers Ltd.Item Combination thymosin-α1 and interferon-α2b in the treatment of anti-HBe-positive chronic hepatitis B in TurkeySaruc, M; Yuceyar, H; Kucukmetin, N; Demir, MA; Kandiloglu, ARBackground/Aims: The most prevalent type of chronic hepatitis B in Turkey is anti-HBe-positive. No consistently effective therapy is yet available for the treatment of these patients. The aim of this study was to assess the efficacy and safety of interferon-alpha and thymosin-alpha(1) combination in the treatment of naive anti-HBe-positive and HBV DNA-positive chronic hepatitis B patients. Methodology: Twenty-one patients were enrolled in the study. All patients had documented anti-HBe-positive, HBV DNA-positive chronic active hepatitis B without evidence of cirrhosis. Patients received a 26-week combination course of 1.6mg thymosin-alpha(1) subcutaneously twice a week and 10 MIU interferon-alpha subcutaneously three times a week, followed by interferon-alpha monotherapy at the same dose for another 26 weeks. After treatment patients were observed for a further 26 weeks. Endpoints were a normalization of alanine aminotransferase and negativity of HBV DNA at weeks 52 and 78, as well as an improvement in liver histology at week 78. Results: Eighteen (87.7%) of the 21 patients responded by losing serum HBV DNA and normalizing alanine aminotransferase values at the end of the 52-week treatment period. Sixteen (76.2%) of these patients became sustained responders, with normal alanine aminotransferase and negative HBV DNA at the end of 78 weeks. Two patients were non-responders, two relapsed and one had a breakthrough during therapy. Significant improvements in the Knodell histological activity index were observed in the responders. No adverse events other than those seen previously with interferon monotherapy were reported. Conclusions: Combination interferon-Q2b and thymosin-alpha(1) treatment may provide a safe and effective therapeutic approach for the difficult-to-treat antiHBe-positive chronic hepatitis B patients. Further controlled studies are needed to assess the full role of this treatment strategy.Item GSTP1 Gene Methylation Profiles in Helicobacter pylori (+) and (-) Antral Intestinal Metaplasia and Distal Gastric Tumour Patients in Turkish PopulationAsik-Sen, G; Kasap, E; Orenay-Boyacioglu, S; Korkmaz, M; Kahraman, E; Unsal, B; Yüksel-Saritas, E; Yuceyar, HBackground/Aims: Gastric cancer (GC) is the second most common malignancy worldwide, with a high mortality rate. The incidence of GC has declined in the western countries during the last decades. The glutathione S-transferases comprise a group of enzymes that are critical in the detoxification of carcinogens. In this study we aimed at the relationship GSTP-1 methylation in patients with intestinal metaplasia with and without Helicobacter pylori infection, gastric cancer and controls. Methodology: The methylation status of GSTP1 gene was analyzed by methylation specific PCR after bisulfate modification in H. pylori (+) (n=25) and (-) (n=25) intestinal metaplasia (IM) patients, GC (n=25) and control subjects (n=15) between September 2009 to November 2011. Results: During the study period 90 patients who underwent endoscopic examination were included in the study. When we considered the GSTP1 gene methylation profile in all of the groups; 26 (28%) patients had methylated GSTP1 gene, 31 (34%) patients had unmethylated GSTP1 gene and 33 (36%) patients had heterogeneously methylated GSTP1 gene. Conclusions: GSTP1 gene methylation profile is not appropriate for early diagnosis of cases with gastric cancer.Item Long-term outcomes of thymosin-α1 and interferon α-2b combination therapy in patients with hepatitis B e antigen (HBeAg) negative chronic hepatitis BSaruc, M; Ozden, N; Turkel, N; Ayhan, S; Hock, LM; Tuzcuoglu, I; Yuceyar, HHepatitis B e antibody (HbeAb) and hepatitis B virus (HBV) DNA positive chronic hepatitis is a clinical entity, distinct from classical hepatitis B e antigen (HbeAg) positive chronic hepatitis B. Our aim was to evaluate the long-term therapeutic efficacy of the combination of interferon alpha-2b and thymosin-alpha1 compared with lamivudine plus interferon alpha-2b and interferon alpha-2b alone. Fifty-two patients with HbeAg-negative chronic hepatitis B were assigned to three different groups in a nonrandomized manner. Group 1 (n = 27) received thymosin-alpha1 [1.6 mg subcutaneously (sc), twice a week] and interferon alpha-2b (10 MIU sc, three times per week) for 26 weeks, subsequently followed by interferon alpha-2b monotherapy at the same dosage for an additional 26 weeks. Group 2 (n = 10) received interferon alpha-2b (10 MIU sc, three times per week) for 52 weeks. Group 3 (n = 15) received interferon a-2b (10 MIU sc, three times per week) and lamivudine [100 mg orally (po), q.d.] for, 62 weeks, followed by continuous lamivudine (100 mg po, q.d.) therapy. By the end of 78 weeks, a sustained response (SR-6 mo) was seen in 74% (20/27) of the patients within Group 1. On the contrary, Groups 2 and 3 had sustained response rates of 40 (4/10) and 53.3% (8/15), respectively (p = 0.13). At the end of 12 months post-treatment in Group 1, a virological and biochemical response rate was seen in 70.3% of patients (19/27); in contrast, Groups 2 and 3 had response rates of 20 (2/10) and 26.6% (4/15), respectively (p = 0036). At the end of the 18-month post-treatment follow-up period, 71.4% (19/27) of patients in Group 1, 10% of patients in Group 2 (1/10), and 20% of patients in Group 3(3/15) preserved their sustained response (p = 0.0003). Interferon alpha-2b and thymosin-alpha1 combination therapy results in significant virological and biochemical response rates compared with standard therapeutic regimens and is well tolerated.Item An experimental model of hemolysis-induced acute pancreatitisSaruc, M; Yuceyar, H; Turkel, N; Ozutemiz, O; Tuzcuoglu, I; Yuce, G; Huseyinov, AThe literature indicates that acute pancreatitis is a complication of massive hemolysis with a prevalence of about 20%. We describe an experimental model of hemolysis-induced acute pancreatitis. Hemolytic anemia was induced in rats by a single ip injection of 60 mg/kg of 20 mg/ml acetylphenylhydrazine (APH) in 20% (v/v) ethanol on the first experimental day (day 0). One hundred and fifty Wistar albino rats weighing 180-200 g were divided into three groups of 50 animals each: groups 1, 2 and 3 were injected ip with APH, 20% ethanol, and physiological saline, respectively. Ten rats from each group were sacrificed on study days 1, 2, 3, 4 and 5. Serum amylase, lipase levels and pancreatic tissue tumor necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF) contents were determined and a histological examination of the pancreas was performed. No hemolysis or pancreatitis was observed in any of the rats in groups 2 and 3. In group 1, massive hemolysis was observed in 35 (70%) of 50 rats, moderate hemolysis in seven (14%), and no hemolysis in eight (16%). Thirty-three of 35 (94.2%) rats with massive hemolysis had hyperamylasemia, and 29 of these rats (82.8%) had histologically proven pancreatitis. The most severe pancreatitis occurred on day 3, as demonstrated by histology. Tissue TNF-alpha and PAF levels were statistically higher in group 1 than in groups 2 and 3. Acute massive hemolysis induced acute pancreatitis, as indicated by histology, in almost 80% of cases. Hemolysis may induce acute pancreatitis by triggering the release of proinflammatory and immunoregulatory cytokines.Item The systemic cellular immune response in the Helicobacter pylori-associated duodenal ulcer and chronic antral gastritisYuceyar, H; Saruc, M; Kokuludag, A; Terzioglu, E; Goksel, G; Isisag, ABackground/Aims: The exact pathogenesis of Helicobacter pylori infection is not fully understood. This study aims to evaluate the specific subset composition of peripheral blood lymphocytes in patients with H. pylori-positive duodenal ulcer n=14), chronic antral gastritis n=28), since reports so far have led to inconclusive and conflicting results. Methodology: 42 patients with dyspepsia and 50 controls underwent the following procedures: 1) gastroscopy and gastric biopsy (five specimens) 2) histology, 3) serologic test for anti-H. pylori antibodies IgG (Pyloriset EIA-G, Orion Diagnostica) and anti-cytotoxin associated gene A (cag A) IgG antibodies (VIVA Diagnositika by ELISA), 4) analysis of the peripheral blood lymphocytes using monoclonal antibodies reacting with lymphocyte cell surface antigens (anti-CD3, anti-CD19, anti-CD4, anti-CD8, anti-CD16 + CD56, anti-HLA DR) by flow-cytometry (Becton-Dickinson) to detect possible changes in the lymphocytes subpopulation in patients with duodenal ulcer and chronic antral gastritis. Results: We found no alteration in total T and B lymphocytes and CD4(+) T, CD8(+) T lymphocytes and natural killer cells of both duodenal ulcer and chronic antral gastritis patients compared to normal persons. although there was a slight increase in the proportion of active T lymphocytes in duodenal ulcer and chronic antral gastritis groups comparing to healthy subjects the difference was not statistically significant. Conclusions: These data indicate that there is no systemic alteration in the specific immune system in response to H. pylori in patients with duodenal ulcer and chronic antral gastritis.Item Mean platelet volume can indicate dietary adherence and disease severity of celiac diseaseGerceker, E; Baykan, AR; Cerrah, S; Yuceyar, HOBJECTIVE: At present, there is no reliable indicator for dietary compliance and disease severity in patients with celiac disease (CD). The aim of this study is to evaluate mean platelet volume (MPV) level as a biomarker for detection of disease activation, dietary adherence, and assessment of disease severity. METHODS: Eighty-one patients with CD and 50 healthy subjects were enrolled in this study. The diagnosis of CD was estab-lished by both positive antibodies against endomysium or gliadin and histopathological criteria (lymphocytic infiltration and total villous atrophy in duodenal biopsies). RESULTS: MPV was observed to be significantly higher among CD patients when compared to healthy controls (8.14 +/- 0.26 fL vs. 7.82 +/- 0.29 fL and p=0.001). Overall dietary adherence rate was 72.8% (58/81 CD patients). After induction of a gluten-free diet, the MPV was significantly lower in the dietary adherent group than non-adherent patients (7.86 +/- 0.17 fL vs. 8.07 +/- 0.30 fL and p=0.001). The increase of MPV was correlated with Marsh classification (Marsh 3 active CD vs. Marsh 2 active CD vs. Marsh 1 active CD; 8.32 +/- 0.27 fL vs. 8.12 +/- 0.19 fL vs. 7.98 +/- 0.19 fL; p=0.004 and p=0.009). CONCLUSION: Based on these data, we believe that increased MPV can provide additional benefit to screening in patients with CD. It can indicate the activation of the disease and adherence to the diet.Item Aurora kinase A (AURKA) and never in mitosis gene A-related kinase 6 (NEK6) genes are upregulated in erosive esophagitis and esophageal adenocarcinomaKasap, E; Boyacioglu, SÖ; Korkmaz, M; Yuksel, ES; Ünsal, B; Kahraman, E; Özütemiz, Ö; Yuceyar, HGastroesophageal reflux disease is a risk factor for esophageal adenocarcinoma yet studies that have investigated the relationship between erosive esophagitis and esophageal adenocarcinoma have usually focused on symptom-related evidence or polymorphisms. There are no epigenetic gene expression studies on this topic. In this study, we aimed to evaluate the relationship between erosive esophagitis and esophageal adenocarcinoma to identify whether there is a genetic predisposition for esophageal adenocarcinoma. The Human Epigenetic Chromatin Modification Enzyme RT2 Profiler (TM) PCR array (PAHS-085A) was used to detect the expression of 84 key genes encoding enzymes. This was carried out prospectively for samples from 60 patients (20 patients as a control group, 20 patients with erosive esophagitis and 20 patients with esophageal adenocarcinoma). AURKA, AURKB, NEK6 were expressed at significantly higher levels in esophageal adenocarcinoma compared to the control group. MBD2 was expressed at significantly lower levels in the esophageal adenocarcinoma group compared to the control group. AURKA, AURKC, HDAC9 and NEK6 were expressed at significantly higher levels in erosive esophagitis compared to the control group. There was no difference in unregulated gene expression between the erosive esophagitis and esophageal adenocarcinoma. MBD2 was significantly downregulated in esophageal adenocarcinoma compared to erosive esophagitis. NEK6 and AURKA were significantly unregulated in esophageal adenocarcinoma and erosive esophagitis compared to the control group. This is a novel study on the genetic predisposition for erosive esophagitis and esophageal adenocarcinoma. AURKA and NEK6 are two promising genetic markers for erosive esophagitis and esophageal adenocarcinoma.Item The role of heme in hemolysis-induced acute pancreatitisSaruç, M; Yuceyar, H; Turkel, N; Ozutemiz, O; Tuzcuoglu, I; Ayhan, S; Yuce, G; Coker, I; Huseyinov, ABackground: The aim was to reveal the mechanism of hemolysis-induced acute pancreatitis and to evaluate the role of heme and heme oxygenase activity in inducing pancreatic inflammation in an experimental hemolysis model. Material/Methods: Hemolytic anemia was induced in rats by intraperitoneal injection of 60 mg/kg acetylphenylhydrazine (APH). To evaluate the toxic effect of free heme after hemolysis, heme oxygenase inhibitor (HOI) was used to inhibit the enzyme which decreases the free heme concentration after hemolysis. One hundred and fifty rats were divided into two treatment and three control groups. Rats in the hemolysis group were given APH intraperitoneally. Rats in the HOI+hemolysis group were given Cr(III)mesoporphyrin IX chloride as HOI and then APH intraperitoneally. Serum amylase and lipase levels as well as pancreatic tissue cytokine content were determined and histological examination performed. Results: No hemolysis or pancreatitis was seen in the control groups. Massive hemolysis was seen in 22 of the 30 rats of the hemolysis group and 20 of the 30 rats of the HOI+hemolysis group. The total pancreatitis rates were 60% and 76.6% in the hemolysis and HOI+hemolysis groups, respectively (p<0.05). Pancreatic cytokine levels were significantly higher in the HOI+hemolysis and hemolysis groups than in all control groups. The highest ICAM-1 and MCP-1 levels were in the HOI+hemolysis group. Histological signs of acute pancreatitis were also more severe in this group. Conclusions: Acute massive hemolysis can induce acute pancreatitis. Excess of free vascular heme seems to be an inducer of inflammation by modulating ICAM-1 and MCP-1.Item Functional dyspepsiaSaruc, M; Ozden, N; Turkel, N; Ayhan, S; Demir, MA; Tuzcuoglu, I; Akarca, US; Yuceyar, HThe etiology of functional dyspepsia is not known. The objective of the present study was to determine the characteristics of functional dyspepsia in Western Turkey. We divided 900 patients with functional dyspepsia into three subgroups according to symptoms: ulcer-like (UL), 321 (35.6%), motility disorder-like (ML), 281 (31.2%), and the combination (C) of these symptoms, 298 (33.1%). All patients were submitted to endoscopic evaluation, with two biopsies taken from the cardia and corpus, and four from the antrum of the stomach. All biopsy samples were studied for Helicobacter pylori (Hp) density, chronic inflammation, activity, intestinal metaplasia, atrophy, and the presence of lymphoid aggregates by histological examination. One antral biopsy was used for the rapid urease test. Tissue cagA status was determined by PCR from an antral biopsy specimen by a random sampling method. We also determined the serum levels of tumor necrosis factor-alpha (TNF-alpha) and gastrin by the same method. Data were analyzed statistically by the Kolmogorov-Smimov test and by analysis of variance. Hp and cagA positivity was significantly higher in the UL subgroup than in the others. The patients in the ML subgroup had the lowest Hp and cagA positivity and Hp density. The ML subgroup also showed the lowest level of Hp-induced inflammation among all subgroups. The serum levels of TNF-alpha and gastrin did not reveal any difference between groups. Our findings show a poor association of Hp with the ML subgroup of functional dyspepsia, but a stronger association with the UL and C subgroups.Item ASSOCIATION OF INTERLEUKIN 12B RS3212227 POLYMORPHISM WITH GASTRIC CANCER, INTESTINAL METAPLASIA, AND Helicobacter pylori INFECTIONOrenay-Boyacioglu, S; Kasap, E; Yuceyar, H; Korkmaz, MInterleukin 12 (IL-12) has a key function in promoting Th1 immune response in the gastrointestinal mucosa. Although cytokine gene polymorphisms are associated with increased risk of gastric cancer (GC), studies on different geographic regions and ethnic groups are not able to draw a consistent result. The current case-control study aims to find out an association between a functional IL-12B rs3212227 polymorphism and the susceptibility and clinical features of the study groups, which are GC, Helicobacter pylori-infected and H. pylori-uninfected intestinal metaplasia (IM). In this study, IL-12B rs3212227 polymorphism was genotyped in 35 GC cases, 25 H. pylori-infected IM patients, 25 H. pylori-uninfected IM patients, and 25 control subjects. PCR-RFLP analysis was performed to find out and compare the polymorphism profiles of case biopsies. There was statistical significance in genotype distributions and allelic frequencies in GC patients with proximal arrest in stomach (p=0.042). The rs3212227 genotypes and allelic frequencies were not correlated with any of the study groups (p>0.05). Other clinical features examined in the GC patients were also not correlated with the rs3212227 genotypes and allelic frequencies (p>0.05). Current findings suggest that IL-12B rs3212227 polymorphism may play a role in GC development.Item The effect of CagA status on response to Helicobacter pylori eradication therapy in Western TurkeySaruç, M; Goksel, G; Ozkaya, S; Guclu, F; Ozbakkaloglu, B; Yuceyar, HIf cyto toxin-associated gene A (CagA) status affects the response rates of therapy, then it may be possible to predict Helicobacter pylori eradication rates. We aimed to evaluate the response to eradication treatment of H. pylori infection in CagA-positive and CagA-negative patients. A total of 184 patients (93 males, 91 females, mean age 42.6 +/- 12.8 years) with H. pylori-positive chronic gastritis were studied. Subjects underwent a gastroscopy and biopsy specimens were taken from the gastric antrum, body, and fundus. Before the eradication therapy was given all patients were tested for CagA, TNF-alpha and gastrin levels. They were then prescribed lansoprazole (30 mg bid), clarithromycin (500 mg bid), and amoxicillin (1.0 mg bid) for one week. On the 8th week a second endoscopy was performed and further biopsy specimens were obtained from the same sites as in the initial endoscopy. One hundred and twenty-seven patients (69.1%) were found to be CagA positive and 57 patients (30.9%) were CagA negative. The total eradication rate was 82.6%. In the CagA-positive group this rate was 87.4%, and in the CagA-negative group it was 71.9% (P = 0.019). TNF-alpha levels were higher in the CagA-positive than in the Cag-A-riegative group (P = 0.001). However, gastrin levels were not different between groups (P = 0.421). Our findings revealed that CagA-negative status might be a risk factor for failure of H. pylori triple therapies. The CagA pathogenicity island gives a growth advantage to H. pylori strains and has been associated with an increase in the inflammatory response at the gastric mucosal level. These properties could make CagA-positive H. pylori strains more susceptible to antibiotics.Item Never in mitosis gene A-related kinase 6 and aurora kinase A: New gene biomarkers in the conversion from ulcerative colitis to colorectal cancerGerçeker, E; Boyacioglu, SO; Kasap, E; Baykan, A; Yuceyar, H; Yildirim, H; Ayhan, S; Ellidokuz, E; Korkmaz, MUlcerative colitis (UC) is an important risk factor for colorectal cancer (CRC). Histone modifications are one of the epigenetic mechanisms that may have key roles in the carcinogenesis of CRC. At present, there are no studies comparing histone modification patterns of UC and CRC in the literature. Therefore the aim of the present study was to investigate whether genes, particularly those involved in histone modification, have value in patient monitoring with regards to CRC development in UC. Key gene expressions of the histone modification enzyme were assessed and compared in CRC, UC and control groups using the RT-PCR array technique. Patients were divided into subgroups based on the extent and duration of the disease and inflammatory burden, which are considered risk factors for CRC development in UC patients. In UC and CRC groups, a significantly higher overexpression of the NEK6 and AURKA genes compared to the control group was identified. In addition, there was a significantly higher overexpression of HDAC1 and PAK1 genes in the UC group, and of HDAC1, HDAC7, PAKI and AURKB genes in the CRC group. NEK6, AURKA, HDAC1 and PAK1 were significantly overexpressed in patients with a longer UC duration. Overexpression of AURKA and NEK6 genes was significantly more pronounced in UC patients with more extensive colon involvement. HDAC1, HDAC7, PAK1, NEK6, AURKA and AURKB are important diagnostic and prognostic markers involved in the carcinogenesis of CRC. HDAC1, PAK1, NEK6 and AURKA may be considered as diagnostic markers to be used in CRC screening for UC patients.Item The potential role of the NEK6, AURKA, AURKB, and PAK1 genes in adenomatous colorectal polyps and colorectal adenocarcinomaKasap, E; Gerceker, E; Boyacioglu, SÖ; Yuceyar, H; Yildirm, H; Ayhan, S; Korkmaz, MColorectal adenomatous polyp (CRAP) is a major risk factor for the development of sporadic colorectal cancer (CRC). Histone modifications are one of the epigenetic mechanisms that may have key roles in the carcinogenesis of CRC. The objective of the present study is to investigate the alternations in the defined histone modification gene expression profiles in patients with CRAP and CRC. Histone modification enzyme key gene expressions of the CRC, CRAP, and control groups were evaluated and compared using the reverse transcription PCR (RT-PCR) array method. Gene expression analysis was performed in the CRAP group after dividing the patients into subgroups according to the polyp diameter, pathological results, and morphological parameters which are risk factors for developing CRC in patients with CRAP. PAK1, NEK6, AURKA, AURKB, HDAC1, and HDAC7 were significantly more overexpressed in CRC subjects compared to the controls (p < 0.05). PAK1, NEK6, AURKA, AURKB, and HDAC1 were significantly more overexpressed in the CRAP group compared to the controls (p < 0.005). There were no significant differences between the CRAP and CRC groups with regards to PAK1, NEK6, AURKA, or AURKB gene overexpression. PAK1, NEK6, AURKA, and AURKB were significantly in correlation with the polyp diameter as they were more overexpressed in polyps with larger diameters. In conclusion, overexpressions of NEK6, AURKA, AURKB, and PAK1 genes can be used as predictive markers to decide the colonoscopic surveillance intervals after the polypectomy procedure especially in polyps with larger diameters.Item Comparison of interferonα2β monotherapy with the combination of thymosinα1 and interferonα2β in the treatment of anti-HBe-positive chronic hepatitis B in Turkey.Saruc, M; Yuceyar, H; Kucukmetin, N; Demir, MA; Kandiloglu, ARItem Expression profiles of histone modification genes in gastric cancer progressionOrenay-Boyacioglu, S; Kasap, E; Gerceker, E; Yuceyar, H; Demirci, U; Bilgic, F; Korkmaz, MGastric cancer (GC) development can be attributed to several risk factors including atrophic gastritis (AG), intestinal metaplasia (IM), and the presence of Helicobacter pylori (HP). Also, histone modification is an epigenetic mechanism that plays a pivotal role in GC carcinogenesis. In this preliminary study, we aimed to describe the expression profiles of histone modification in the AG, IM, and GC patient groups. A total of 80 patients with AG (n = 27), IM (n = 25), and GC (n = 28) with an additional 20 control subjects were included in the study. Expression profiles of three histone phosphorylation genes (PAK1, NEK6, and AURKA) and five histone deacetylation genes (HDACs 1, 2, 3, 5, and 7) were examined based on the results of Real Time qPCR method. It was observed that AURKA and HDAC2 genes were significantly overexpressed in all groups compared to the control (P < 0.05). In GC patients, overexpression of HDAC2 gene was detected in the absence of metastasis, and overexpression of AURKA, HDAC2, and NEK6 genes was detected in the presence of metastasis. When cancer involvements were compared, significant overexpression of the HDAC2 gene was noted in overall and corpus involvements (P < 0.05). In addition, overexpression of AURKA, NEK6, HDAC1, and HDAC2 genes and underexpression of HDAC5 gene were detected in the antrum involvement (P < 0.05). In conclusion, decreased expression of HDAC5 in GC is reported for the first time in this study, while supporting the existing literature in AURKA, NEK6, HDAC1, and HDAC2 up regulations during GC development.Item Alteration in Methylation Pattern of Retinoblastoma 1 Gene Promotor Region in Intestinal Metaplasia with or without Helicobacter pylori and Gastric Cancer PatientsBoyacioglu, SO; Kasap, E; Yuceyar, H; Korkmaz, MBackground. Helicobacter pylori, intestinal metaplasia (IM), and gene methylation play important roles in gastric carcinogenesis. However, the association among H. pylori infection, IM, gastric cancer (GC), and gene methylation is not fully understood. Cell cycle control involving retinoblastoma 1 (RB1) gene is one of the main regulatory pathways reported to be altered in gastric carcinogenesis. Objectives. The purpose of this research is to assess the methylation status of RB1 gene in GC and IM with or without H. pylori infection, and to discuss the possible role of H. pylori-induced RB1 gene methylation in the mechanism of gastric carcinogenesis. Material and Methods. The methylation profile of RB1 gene was analyzed by sodium bisulfite modification and methylation-specific PCR in GC (n = 24), IM patients with H. pylori positive (n = 20) and negative (n = 20), and control subjects (n = 20). Results. According to methylation levels in RB1 gene; the high correlation values were detected between H. pylori positive-IM group and GC group, and between H. pylori positive-IM and H. pylori negative-IM groups (p < 0.05). No correlations between H. pylori negative-IM and GC groups and between GC and control groups were detected in methylation status of RB1 gene. Conclusions. High methylation levels in RB1 gene in H. pylori positive individuals may suggest an elevated risk of gastric cancer occurrence.