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| 1 | Alterations of glutathione S-transferase and matrix metalloproteinase-9 expressions are early events in esophageal carcinogenesis显示文摘AIM: To investigate the role of glutathione S-transferase (GST) and matrix metalloproteinase-9 (MMP-9) expres-sions in the development and progression of reflux es-ophagitis-Barrett’s metaplasia-dysplasia-adenocarcinoma sequence in the esophagus.METHODS: GST and MMP-9 expressions were analyzed in 51 paraffin-embedded tissue samples by immunohisto-chemistry including patients with reflux esophagitis (n = 7), Barrett’s metaplasia (n = 14), Barrett and esophagi-tis (n = 8), Barrett and dysplasia (n = 7), esophageal adenocarcinoma (n = 8) and a control group without any histological changes (n = 7). Immunostaining was determined semiquantitatively. Statistical analysis with one-way ANOVA, LSD test and correlation analysis were performed. P value of < 0.05 was considered significant.RESULTS: GST expression was significantly higher while MMP-9 expression was significantly lower in control group compared to Barrett’s metaplasia and the other groups. No major changes were observed between Bar-rett, esophagitis, and Barrett and concomitant esophagi-tis. Barrett and concomitant dysplasia, and adenocarci-noma revealed a significant lower expression of GST and higher levels of MMP-9 compared to all other groups. Adenocarcinoma showed almost no expression of GST and significantly higher levels of MMP-9 than Barrett and concomitant dysplasia. Alterations of GST and MMP-9 were inversely correlated (r = - 0.82).CONCLUSION: Decreased GST and increased ex-pression of MMP-9 in Barrett’s metaplasia-dysplasia-adenocarcinoma sequence as compared to normal tissue suggest their association with esophageal tumorigenesis. Loss of GST and gain of MMP-9 in Barrett with dyspla-sia compared to non-dysplastic metaplasia indicate that these alterations may be early events in carcinogenesis. Quantification of these parameters in Barrett’s esopha-gus might be useful to identify patients at higher risk for progression to cancer. | Laszlo Herszenyi Istvan Hritz Istvan Pregun Ferenc Sipos Mark Juhasz Bela Molnar Zsolt Tulassay | 2007 | World Journal of Gastroenterology2007，13，5： | 37 |
| 2 | Diagnostic and prognostic potential of tissue and circulating long non-coding RNAs in colorectal tumors显示文摘Long non-coding RNAs(lncRNAs)are members of the non-protein coding RNA family longer than 200 nucleotides.They participate in the regulation of gene and protein expression influencing apoptosis,cell proliferation and immune responses,thereby playing a critical role in the development and progression of various cancers,including colorectal cancer(CRC).As CRC is one of the most frequently diagnosed malignancies worldwide with high mortality,its screening and early detection are crucial,so the identification of disease-specific biomarkers is necessary.LncRNAs are promising candidates as they are involved in carcinogenesis,and certain lncRNAs(e.g.,CCAT1,CRNDE,CRCAL1-4)show altered expression in adenomas,making them potential early diagnostic markers.In addition to being useful as tissue-specific markers,analysis of circulating lncRNAs(e.g.,CCAT1,CCAT2,BLACAT1,CRNDE,NEAT1,UCA1)in peripheral blood offers the possibility to establish minimally invasive,liquid biopsy-based diagnostic tests.This review article aims to describe the origin,structure,and functions of lncRNAs and to discuss their contribution to CRC development.Moreover,our purpose is to summarise lncRNAs showing altered expression levels during tumor formation in both colon tissue and plasma/serum samples and to demonstrate their clinical implications as diagnostic or prognostic biomarkers for CRC. | Orsolya Galamb Barbara K Barták Alexandra Kalmár Zsófia B Nagy Krisztina A Szigeti Zsolt Tulassay Peter Igaz Béla Molnár | 2019 | World Journal of Gastroenterology2019，25，34： | 18 |
| 3 | Changes of the cytokine profile in inflammatory bowel diseases显示文摘Cytokines are indispensable signals of the mucosaassociated immune system for maintaining normal gut homeostasis.An imbalance of their profile in favour of inflammation initiation may lead to disease states,such as that is observed in inflammatory bowel diseases(IBD).Although Crohn's disease(CD) is often described as a prototype of T-helper 1-type diseases,and ulcerative colitis(UC) is traditionally viewed as a T-helper 2-mediated condition,the classic paradigm,which categorises cytokines into pro-and anti-inflammatory groups,has recently been changed.The inflammation regulatory pathways may not be mutually exclusive as individual cytokines can have diverse and even opposing functions in various clinical and immunological settings.None the less there are many common immunological responses in IBD that are mediated by cytokines.Although they regulate and influence the development,course and recurrence of the inflammatory process,the concrete pathogenic role of these small signaling molecules is sometimes not unambiguous in the subtypes of the disease.Our aim is to review the current information about pro-and anti-inflammatory effects of traditionally studied and recently discovered cytokines in the pathogenesis of UC and CD.The better understanding of their production and functional activity may lead to the development of new therapeutic modalities. | Gyrgyi Mzes Béla Molnár Zsolt Tulassay Ferenc Sipos | 2012 | World Journal of Gastroenterology2012，18，41： | 16 |
| 4 | Epithelial toll-like receptor 9 signaling in colorectal inflammation and cancer: Clinico-pathogenic aspects显示文摘Toll-like receptors (TLRs) recognize specific motifs which are frequently present in bacteria, fungi, prokaryotes and viruses. Amongst TLRs, TLR9 can be activated by such bacterial or viral DNA fragments, immunoglobulin-DNA complexes or synthetic oligonucleotides, which all contain unmethylated cytosineguanine nucleotide sequences (CpGs). Emerging data indicate that TLR9 signaling has a role in, and may influence, colorectal carcinogenesis and colonic inflammation. CpGs are classified into three groups according to their influence on both the antigen-specific humoraland cellular immunity, and the production of type 1 interferons and proinflammatory cytokines. TLR9 activation via CpGs may serve as a new therapeutic target for several cancerous and various inflammatory conditions. Due to its probable anti-cancer effects, the application possibilities of TLR9-signaling modulation may be extremely diverse even in colorectal tumors. In this review we aimed to summarize the current knowledge about TLR-signaling in the pathogenesis and therapy of inflammatory bowel diseases and colorectal cancer. Due to the species-specific differences in TLR9 expression, however, one must be careful in translating the animal model data into the human system, because of the differences between CpG-oligodeoxynucleotide-responsive cells. TLR9 agonist DNA-based immunomodulatory sequences could also represent a promising therapeutic alternative in systemic inflammatory conditions and chronic colonic inflammations as their side effects are not significant. | István Fri Ferenc Sipos Tiana M Germann Alexandra Kalmár Zsolt Tulassay Béla Molnár Gyrgyi Mzes | 2013 | World Journal of Gastroenterology2013，19，26： | 14 |
| 5 | Toll-like receptor 4 and NOD2/CARD15 mutations in Hungarian patients with Crohn's disease: Phenotype-genotype correlations显示文摘AIM: To determine common NOD2/CARD15 mutations and TLR4 D299G polymorphism in Hungarian patients with CD.METHODS: A total of 527 unrelated patients with CD (male/female: 265/262, age: 37.1 (SD 7.6) years) and 200 healthy subjects were included. DNA was screened for possible NOD2/CARD15 mutations by denaturing highperformance liquid chromatography (confirmed by direct sequencing). TLR4 D299G was tested by PCR-RFLP.RESULTS: NOD2/CARD15 mutations were found in 185patients (35.1%) and in 33 controls (16.5%, P<0.0001).SNP8/R702W (10.8% vs 6%, P = 0.02), SNP13/3020insC (19.4% vs 5%, P<0.0001) and exon4 R703C (2.1% vs 0%, P = 0.02) mutations were more frequent in CD, while the frequency of SNP12/G908R was not increased. The frequency of TLR4 D299G was not different (CD: 9.9% vscontrols: 12.0%). Variant NOD2/CARD15 allele was associated with an increased risk for CD (ORhet = 1.71,95%CI = 1.12-2.6, P= 0.0001, ORtwo-riskalleles = 25.2,95%CI = 4.37- , P<0.0001), early disease onset (carrier:26.4 years vs non-carrier: 29.8 years, P = 0.0006), ileal disease (81.9% vs 69.5%, OR = 1.99, 95%CI = 1.29-3.08,P = 0.02, presence of NOD2/CARD15 and TLR4: 86.7% vs64.8%), stricturing behavior (OR = 1.69, 95%CI = 1.13-2.55,P = 0.026) and increased need for resection (OR=1.71,95%CI: 1.13-2.62, P= 0.01), but not with duration, extraintestinal manifestations, familial disease or smoking. TLR4exhibited a modifier effect: age of onset in wt/TLR4 D299G carriers: 27.4 years vs NOD2mut/TLR D299G: 23 years (P= 0.06), in NOD2mut/wt: 26.7 years.CONCLUSION: These results confirm that variant NOD2/CARD15 (R702W, R703C and 3020insC) alleles are associated with earlier disease onset, ileal disease,stricturing disease behavior in Hungarian CD patients. In contrast, although the frequency of TLR4 D299G polymorphism was not different from controls, NOD2/TLR4mutation carriers tended to present at earlier age. | Peter Laszlo Lakatos Laszlo Lakatos Ferenc Szalay Claudia Willheim-Polli Christoph (O|¨)sterreicher Zsolt Tulassay Tamas Molnar Walter Reinisch Janos Papp Gyula Mozsik Hungarian IBD Study Group Peter Ferenci | 2005 | World Journal of Gastroenterology2005，11，10： | 14 |
| 6 | Helicobacter pylori infection: New pathogenetic and clinical aspects显示文摘Helicobacter pylori(H.pylori)infects more than half of the world’s human population,but only 1%to3%of infected people consequently develop gastric adenocarcinomas.The clinical outcome of the infection is determined by host genetic predisposition,bacterial virulence factors,and environmental factors.The association between H.pylori infection and chronic active gastritis,peptic ulcer disease,gastric cell carcinoma,and B cell mucosa-associated lymphoid tissue lymphoma has been well established.With the exception of unexplained iron deficiency anemia and idiopathic thrombocytopenic purpura,H.pylori infection has no proven role in extraintestinal diseases.On the other hand,there is data showing that H.pylori infection could be beneficial for some human diseases.The unpredictability of the long-term consequences of H.pylori infection and the economic challenge in eradicating it is why identification of high-risk individuals is crucial. | Krisztina Hagymási Zsolt Tulassay | 2014 | World Journal of Gastroenterology2014，20，21： | 13 |
| 7 | 埃索美拉唑在十二指肠球部溃疡中根除幽门螺杆菌和愈合溃疡的疗效显示文摘 | Tulassay Z Kryszewski A Dite P Kleczkowski D Rudzinski J Bartuzi Z Hasselgren G Larko A Wrangstadh M 钟捷 | 2002 | 中华消化杂志2002，22，10： | 11 |
| 8 | Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer显示文摘Metabolic syndrome(Met S), as a chronic inflammatory disorder has a potential role in the development of inflammatory and cancerous complications of the colonic tissue. The interaction of DNA damage and inflammation is affected by the insulin-like growth factor 1 receptor(IGF1 R) signaling pathway. The IGF1 R pathway has been reported to regulate autophagy, as well, but sometimes through a bidirectional context. Targeting the IGF1 R-autophagy crosstalk could represent a promising strategy for the development of new antiinflammatory and anticancer therapies, and may help for subjects suffering from Met S who are at increased risk of colorectal cancer. However, therapeutic responses to targeted therapies are often shortlived, since a signaling crosstalk of IGF1 R with other receptor tyrosine kinases or autophagy exists, leading to acquired cellular resistance to therapy. From a pharmacological point of view, it is attractive to speculate that synergistic benefits could be achieved by inhibition of one of the key effectors of the IGF1 R pathway, in parallel with the pharmacological stimulation of the autophagy machinery, but cautiousness is also required, because pharmacologic IGF1 R modulation can initiate additional, sometimes unfavorable biologic effects. | Ferenc Sipos Hajnal Székely Imre Dániel Kis Zsolt Tulassay Gyorgyi Muzes | 2017 | World Journal of Gastroenterology2017，23，46： | 9 |
| 9 | Contribution of TLR signaling to the pathogenesis of colitisassociated cancer in inflammatory bowel disease显示文摘In the intestine a balance between proinflammatory and repair signals of the immune system is essential for the maintenance of intestinal homeostasis. The innate immunity ensures a primary host response to microbial invasion, which induces an inflammatory process to localize the infection and prevent systemic dissemination of pathogens. The key elements of this process are the germline encoded pattern recognition receptors inclu-ding Toll-like receptors(TLRs). If pathogens cannot be eliminated, they may elicit chronic inflammation, which may be partly mediated via TLRs. Additionally, chronic inflammation has long been suggested to trigger tissue tumorous transformation. Inflammation, the seventh hallmark of cancer, may affect all phases of tumor development, and evade the immune system. Inflammation acts as a cellular stressor and may trigger DNA damage or genetic instability. Furthermore, chronic inflammation can provoke genetic mutations and epigenetic mechanisms that promote malignant cell transformation. Colorectal cancers in inflammatory bowel disease patients are considered typical examples of inflammation-related cancers. Although data regarding the role of TLRs in the pathomechanism of cancer-as-sociated colitis are rather conflicting, functionally these molecules can be classified as 'largely antitumorigenic' and 'largely pro-tumorigenic' with the caveat that the underlying signaling pathways are mainly context(i.e., organ-, tissue-, cell-) and ligand-dependent. | Ferenc Sipos István Fri Miklós Constantinovits Zsolt Tulassay Gyrgyi Mzes | 2014 | World Journal of Gastroenterology2014，20，36： | 9 |
| 10 | Long-term omeprazole and esomeprazole treatment does not significantly increase gastric epithelial cell proliferation and epithelial growth factor receptor expression and has no effect on apoptosis and p53 expression显示文摘AIM: To study the effect of proton pump inhibitor (PPI)treatment on patients with reflux esophagitis and its in vivo effect on apoptosis, p53- and epidermal growth factor receptor (EGFR) expression.METHODS: After informed consent was obtained, gastric biopsies of the antrum were taken from patients with reflux oesophagitis prior to and after 6 mo of 20 mg omeprazole (n = 14) or 40 mg esomeprazole (n = 12) therapy.Patients did not take any other medications known to affect the gastric mucosa. All patients were Helicobacter pylori negative as confirmed by rapid urease test and histology,respectively. Cell proliferation, apoptosis, EGFR, and p53expression were measured by immunohistochemical techniques. At least 600 glandular epithelial cells were encountered and results were expressed as percentage of total cells counted. Was considered statistically significant.RESULTS: Although there was a trend towards increase of cell proliferation and EGFR expression both in omeprazole and esomeprazole treated group, the difference was not statistically significant. Neither apoptosis nor p53 expression was affected.CONCLUSION: Long-term PPI treatment does not significantly increase gastric epithelial cell proliferation and EGFR expression and has no effect on apoptosis and p53 expression. | Istvan Hritz Laszlo Herszenyi Bela Molnar Zsolt Tulassay Laszlo Pronai | 2005 | World Journal of Gastroenterology2005，11，30： | 7 |
| 11 | Aging related methylation influences the gene expression of key control genes in colorectal cancer and adenoma显示文摘AIM To analyze colorectal carcinogenesis and age-related DNA methylation alterations of gene sequences associated with epigenetic clock CpG sites. METHODS In silico DNA methylation analysis of 353 epigenetic clock Cp G sites published by Steve Horvath was performed using methylation array data for a set of 123 colonic tissue samples [64 colorectal cancer(CRC), 42 adenoma, 17 normal; GEO accession number: GSE48684]. Among the differentially methylated agerelated genes, secreted frizzled related protein 1(SFRP1) promoter methylation was further investigated in colonic tissue from 8 healthy adults, 19 normal children, 20 adenoma and 8 CRC patients using bisulfite-specific PCR followed by methylation-specific high resolution melting(MS-HRM) analysis. m RNA expression of age-related 'epigenetic clock' genes was studied using Affymetrix HGU133 Plus2.0 whole transcriptome data of 153 colonic biopsy samples(49 healthy adult, 49 adenoma, 49 CRC, 6 healthy children)(GEO accession numbers: GSE37364, GSE10714, GSE4183, GSE37267). Whole promoter methylation analysis of genes showing inverse DNA methylationgene expression data was performed on 30 colonic samples using methyl capture sequencing.RESULTS Fifty-seven age-related Cp G sites including hypermethylated PPP1R16 B, SFRP1, SYNE1 and hypomethylated MGP, PIPOX were differentially methylated between CRC and normal tissues(P < 0.05, ?β≥ 10%). In the adenoma vs normal comparison, 70 CpG sites differed significantly, including hypermethylated DKK3, SDC2, SFRP1, SYNE1 and hypomethylated CEMIP, SPATA18(P < 0.05, ?β≥ 10%). In MS-HRM analysis, the SFRP1 promoter region was significantly hypermethylated in CRC(55.0% ± 8.4 %) and adenoma tissue samples(49.9% ± 18.1%) compared to normal adult(5.2% ± 2.7%) and young(2.2% ± 0.7%) colonic tissue(P < 0.0001). DNA methylation of SFRP1 promoter was slightly, but significantly increased in healthy adults compared to normal young samples(P < 0.02). This correlated with significantly increased SFRP1 m RNA levels in children compared to normal adult samples(P < 0.05). In CRC tissue the mR NA expression of 117 agerelated genes were changed, while in adenoma samples 102 genes showed differential expression compared with normal colonic tissue(P < 0.05, logF C > 0.5). The change of expression for several genes including SYNE1, CLEC3 B, LTBP3 and SFRP1, followed the same pattern in aging and carcinogenesis, though not for all genes(e.g., MGP). CONCLUSION Several age-related DNA methylation alterations can be observed during CRC development and progression affecting the m RNA expression of certain CRC- and adenoma-related key control genes. | Orsolya Galamb Alexandra Kalmár Barbara Kinga Barták árpád V Patai Katalin Leiszter Bálint Péterfia Barnabás Wichmann Gábor Valcz Gábor Veres Zsolt Tulassay Béla Molnár | 2016 | World Journal of Gastroenterology2016，22，47： | 7 |
| 12 | Interplay of autophagy and innate immunity in Crohn's disease: A key immunobiologic feature显示文摘Crohn's disease representing a clinical phenotype of inflammatory bowel disease is a polygenic immune disorder with complex multifactor etiology. Recent genome-wide association studies of susceptibility loci have highlighted on the importance of the autophagy pathway, which previously had not been implicated in disease pathology. Autophagy represents an evolutionarily highly conserved multi-step process of cellular self-digestion due to sequestration of excessive, damaged, or aged proteins and intracellular organelles in double-membranous vesicles of autophagosomes, terminally self-digested in lysosomes. Autophagy is deeply involved in regulation of cell development and differentiation, survival and senescence, and it also fundamentally affects the inflammatory pathways, as well as the innate and adaptive arms of immune responses. Autophagy is mainly activated due to sensors of the innate immunity, i.e., by pattern recognition receptor signaling. The interplay of genes regulating immune functions is strongly influenced by the environment, especially gut resident microbiota. The basic challenge for intestinal immune recognition is the requirement of a simultaneous delicate balance between tolerance and responsiveness towards microbes. On the basis of autophagy-related risk genetic polymorphisms (ATG16L1, IRGM , NOD2 , XBP1 ) impaired sensing and handling of intracellular bacteria by innate immunity, closely interrelated with the autophagic and unfolded protein pathways seem to be the most relevant immunobiologic events. Autophagy is now widely considered as a key regulator mechanism with the capacity to integrate several aspects of Crohn's disease pathogenesis. In this review, recent advances in the exciting crosstalk of susceptibility coding variants-related autophagy and innate immunity are discussed. | Gyrgyi Müzes Zsolt Tulassay Ferenc Sipos | 2013 | World Journal of Gastroenterology2013，19，28： | 6 |
| 13 | Plasma carnitine ester profile in adult celiac disease patients maintained on long-term gluten free diet显示文摘AIM: To determine the fasting plasma carnitine ester in patients with celiac disease.METHODS: We determined the fasting plasma carnitine ester profile using ESI triple quadrupol mass spectrometry in 33 adult patients with biopsy-confirmed maturity onset celiac disease maintained on long term gluten free diet.RESULIS: The level of free camitine did not differ as the celiac disease patients were compared with the healthy controls, whereas the acetylcarnitine level was markedly reduced (4.703 ± 0.205 vs 10.227 ± 0.368 nmol/mL,P<0.01). The level of propionylcarnitine was 61.5%,butyrylcarnitine 56.9%, hexanoylcarnitine 75%,octanoylcarnitine 71.1%, octenoylcarnitine 52.1%,decanoylcarnitine 73.1%, cecenoylcarnitine 58.3%,lauroylcarnitine 61.5%, miristoylcarnitine 66.7%,miristoleylcarnitine 62.5% and oleylcarnitine 81.1%in the celiac disease patients compared to the control values, respectively (P<0.01).CONCLUSION: The marked decrease of circulating acetylcarnitine with 50-80 % decrease of 11 other carnitine esters shows that the carnitine ester metabolism can be influenced even in clinically asymptomatic and well being adult celiac disease patients, and gluten withdrawal alone does not necessarily normalize all elements of the disturbed carnitine homeostasis. | Judit Bene Katalin Komlósi Beáta Gasztonyi Márk Juhász Zsolt Tulassay Béla Melegh | 2005 | World Journal of Gastroenterology2005，11，42： | 5 |
| 14 | 含埃索美拉唑的一周三联治疗能有效根除幽门螺杆菌感染显示文摘 | Tulassay Z Kryszewski A Dite P Kleczkowski D Rudzinski J Bartuzi Z Hasselgren G Larko A Wrangstadh M 钟捷 | 2003 | 中华消化杂志2003，23，2： | 5 |
| 15 | Serrated pathway:Alternative route to colorectal cancer显示文摘Serrated polyps have been an area of intense focus for gastroenterologists over the past several years. Contrary to what was thought before,a growing body of literature indicates that these polyps can be precursors of colorectal cancer(CRC).Most of these lesions, particularly those in the proximal colon,have so far been under-recognized and missed during colonoscopy,qualifying these lesions to be the main cause of interval cancers.It is estimated that 10%-20%of CRCs evolve through this alternative,serrated pathway, with a distinct genetic and epigenetic profile.Aberrant DNA methylation plays a central role in the development of this CRC subtype.This characteristic molecular background is reflected in a unique pathological and clinical manifestation different from cancers arising via the traditional pathway.In this review we would like to highlight morphological,molecular and clinical features of this emerging pathway that are essential for gastroenterologists and may influence their everyday practice. | rpád V Patai Béla Molnár Zsolt Tulassay Ferenc Sipos | 2013 | World Journal of Gastroenterology2013，19，5： | 4 |
| 16 | Difference of interleukin-23 receptor gene haplotype variants in ulcerative colitis compared to Crohn’s disease and psoriasis显示文摘 | Eniko Safrany Melinda Szabo Marta Szell Lajos Kemeny Katalin Sumegi Bela I. Melegh Lili Magyari Petra Matyas Maria Figler Agnes Weber Zsolt Tulassay Bela Melegh | 2013 | Inflammation Research2013，，2： | 3 |
| 17 | Impact of proteolytic enzymes in colorectal cancer development and progression显示文摘Tumor invasion and metastasis is a highly complicated, multi-step phenomenon. In the complex event of tumor progression, tumor cells interact with basement membrane and extracellular matrix components. Proteolytic enzymes(proteinases) are involved in the degradation of extracellular matrix, but also in cancer invasion and metastasis. The four categories of proteinases(cysteine-, serine-, aspartic-, and metalloproteinases) are named and classified according to the essential catalytic component in their active site. We and others have shown that proteolytic enzymes play a major role not only in colorectal cancer(CRC) invasion and metastasis, but also in malignant transformation of precancerous lesions into cancer. Tissue and serumplasma antigen concentrations of proteinases might be of great value in identifying patients with poor prognosis in CRC. Our results, in concordance with othersindicate the potential tumor marker impact of proteinases for the early diagnosis of CRC. In addition, proteinases may also serve as potential target molecules for therapeutic agents. | László Herszényi Loránd Barabás István Hritz Gábor István Zsolt Tulassay | 2014 | World Journal of Gastroenterology2014，20，37： | 3 |
| 18 | Elevated insulin-like growth factor 1 receptor, hepatocyte growth factor receptor and telomerase protein expression in mild ulcerative colitis显示文摘 | Ferenc Sipos Orsolya Galamb László Herszényi Béla Molnár Norbert Solymosi Tamás Zágoni Lajos Berczi Zsolt Tulassay | 2008 | Scandinavian Journal of Gastroenterology2008，，3： | 2 |
| 19 | mRNA expression, functional profiling and multivariate classification of colon biopsy specimen by cDNA overall glass microarray显示文摘AIM: To understand the local pathophysiological altera- tions and gene ontology-based functional classification of colonic biopsies into inflammatory and neoplastic dis- eases. METHODS: Total RNA was extracted from frozen biop- sies and amplified by T7-method. Expression profile was evaluated by Atlas Glass 1K microarrays. After microar- ray quality control, applicable data were available from 10 adenomas, 6 colorectal adenocarcinomas (CRCs), and 6 inflammatory bowel diseases (IBDs). Multivariate statistical and cell functional analyses were performed. Real-time RT-PCR and immunohistochemistry were used for validation. RESULTS: Discriminant analysis of selected genes, could correctly reclassify all 22 samples using 4 parameters (heat shock transcription factor-1, bystin-like, calgranu- lin-A, TRAIL receptor 3). IBD samples were characterized by overregulated chemokine (C-X-C motif) ligand 13, replication protein A1, E74-like factor 2 and downregu- lated TNF receptor-associated factor 6, BCL2-interacting killer genes. In adenomas upregulation of TNF receptor- associated factor 6, replication protein A1, E74-like factor 2 and underexpression of BCL2-associated X protein, cal- granulin-A genes were found. CRC cases had significantly increased epidermal growth factor receptor, topoisomer- ase-1, v-jun, TNF receptor-associated factor 6 and TRAIL receptor 3, and decreased RAD51 and RAD52 DNA repair gene, protein phosphatase-2A and BCL2-interacting killer mRNA levels. Epidermal growth factor receptor RT-PCR and immunohistochemistry, topoisomerase-1 RT-PCRconfirmed the chip results. CONCLUSION: Different histological alterations can be reclassified by functional, multivariate analysis using cDNA microarrays. Further studies with expanded sample number are needed for subclassification of pathological alterations. | Orsolya Galamb Ferenc Sipos Elek Dinya Sandor Spisak Zsolt Tulassay Bela Molnar | 2006 | World Journal of Gastroenterology2006，12，43： | 2 |
| 20 | Insulin induced translocation of Na^+/K^+-ATPase is decreased in the heart of streptozotocin diabetic rats显示文摘 | Klara ROSTA Eszter TULASSAY Anna ENZSOLY Katalin RONAI Ambrus SZANTHO Tamas PANDICS Andrea FEKETE Peter MANDL Agota VER | 2009 | Acta Pharmacologica Sinica2009，30，12： | 2 |
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