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| 1 | 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 |
| 2 | 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 |
| 3 | Therapeutic aspects of c-MYC signaling in inflammatory and cancerous colonic diseases显示文摘Colonic inflammation is required to heal infections, wounds, and maintain tissue homeostasis. As the seventh hallmark of cancer, however, it may affect all phases of tumor development, including tumor initiation, promotion, invasion and metastatic dissemination, and also evasion immune surveillance. Inflammation acts as a cellular stressor and may trigger DNA damage or genetic instability, and, further, chronic inflammation can provoke genetic mutations and epigenetic mechanisms that promote malignant cell transformation. Both sporadical and colitis-associated colorectal carcinogenesis are multi-step, complex processes arising from the uncontrolled proliferation and spreading of malignantly transformed cell clones with the obvious ability to evade the host's protective immunity. In cells upon DNA damage several protooncogenes, including c-MYC are activated in parelell with the inactivation of tumor suppressor genes. The target genes of the c-MYC protein participate in different cellular functions, including cell cycle, survival, protein synthesis, cell adhesion, and microRNA expression. The transcriptional program regulated by c-MYC is context dependent, therefore the final cellular response to elevated c-MYC levels may range from increased proliferation to augmented apoptosis. Considering physiological intestinal homeostasis, c-MYC displays a fundamental role in the regulation of cell proliferation and crypt cell number. However, c-MYC gene is frequently deregulated in inflammation, and overexpressed in both sporadic and colitis-associated colon adenocarcinomas. Recent results demonstrated that endogenous c-MYC is essential for efficient induction of p53-dependent apoptosis following DNA damage, but c-MYC function is also involved in and regulated by autophagy-related mechanisms, while its expression is affected by DNA-methylation, or histone acetylation. Molecules directly targeting c-MYC, or agents acting on other genes involved in the c-MYC pathway could be selected for combined regiments. However, due to its context-dependent cellular function, it is clinically essential to consider which cytotoxic drugs are used in combination with c-MYC targeted agents in various tissues. Increasing our knowledge about MYCdependent pathways might provide direction to novel anti-inflammatory and colorectal cancer therapies. | Ferenc Sipos Gábor Firneisz Györgyi Mũzes | 2016 | World Journal of Gastroenterology2016，22，35： | 9 |
| 4 | 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 |
| 5 | Regulatory T cells in inflammatory bowel diseases and colorectal cancer显示文摘Regulatory T cells(T regs) are key elements in immunological self-tolerance.The number of T regs may alter in both peripheral blood and in colonic mucosa during pathological circumstances.The local cellular,microbiological and cytokine milieu affect immunophenotype and function of T regs.Forkhead box P3+ T regs function shows altered properties in inflammatory bowel diseases(IBDs).This alteration of T regs function can furthermore be observed between Crohn's disease and ulcerative colitis,which may have both clinical and therapeutical consequences.Chronic mucosal inflammation may also influence T regs function,which together with the intestinal bacterial flora seem to have a supporting role in colitis-associated colorectal carcinogenesis.T regs have a crucial role in the immunoevasion of cancer cells in sporadic colorectal cancer.Furthermore,their number and phenotype correlate closely with the clinical outcome of the disease,even if their contribution to carcinogenesis has previously been controversial.Despite knowledge of the clinical relationship between IBD and colitis-associated colon cancer,and the growing number of immunological aspects encompassing sporadic colorectal carcinogenesis,the molecular and cellular links amongst T regs,regulation of the inflammation,and cancer development are still not well understood.In this paper,we aimed to review the current data surrounding the role of T regs in the pathogenesis of IBD,colitis-associated colon cancer and sporadic colorectal cancer. | Gyrgyi Mzes Béla Molnár Ferenc Sipos | 2012 | World Journal of Gastroenterology2012，18，40： | 7 |
| 6 | 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 |
| 7 | Relevance of α-defensins(HNP1-3) and defensin β-1 in diabetes显示文摘AIM: To investigate the genetic background of human defensin expression in type 1 and 2 diabetes.METHODS: Associations between DEFA1/DEFA3 gene copy number polymorphism and diabetes as well as between the promoter polymorphisms of DEFB1 and diabetes were studied. The copy number variation of the DEFA1/DEFA3 genes was determined in 257 diabetic patients(117 patients with type 1 and 140 with type 2 diabetes). The control group consisted of 221 age- and gender-matched healthy blood donors. The cumulative copy numbers of the DEFA1/DEFA3 genes were detected by using quantitative PCR analysis. To evaluate the HNP 1-3(human neutrophil peptide 1-3 or α-defensin) levels in the circulation, plasma HNP 1-3 concentrations were measured by ELISA. The expression of DEFA1/A3 in peripheral leukocytes of the diabetic patients was measured by quantitative RT PCR analysis. Three SNPs of the human DEFB1(human defensin β-1) gene: DEFB1 G-20A(rs11362), DEFB1 C-44G(rs1800972) and DEFB1 G-52A(rs1799946) were genotyped by Custom TaqMan? Real Time PCR assay.RESULTS: Significant differences were observed in HNP1-3 levels between the healthy subjects and both groups of diabetic patients. The mean ± SE was 28.78 ± 4.2 ng/mL in type 1 diabetes, and 29.82 ± 5.36 ng/mL in type 2 diabetes, vs 11.94 ± 2.96 ng/mL in controls; P < 0.01 respectively. There was no significant difference between patients with type 1 and type 2 diabetes in the high plasma concentrations of HNP1-3. The highest concentrations of α-defensin were found in diabetic patients with nephropathy(49.4 ± 4.8 ng/mL), neuropathy(38.7 ± 4.8 ng/mL) or cardiovascular complications(45.6 ± 1.45 ng/L). There was no significant difference in the cumulative copy numbers of DEFA1/DEFA3 genes between controls and patients, or between patients with the two types of diabetes. Comparisons of HNP 1-3 plasma level and DEFA1/A3 copy number of the same patient did not reveal significant relationship between defensin-α levels and the gene copy numbers(r2 = 0.01). Similarly, no positive correlation was observed between the copy numbers and the mRNA expression levels of DEFA1/A3. Regarding the C-44G polymorphism of DEFB1, the GG 'protective' genotype was much less frequent(1%-2%) among both groups of patients than among controls(9%).CONCLUSION: Elevated HNP1-3 levels in diabetes are independent of DEFA1/DEFA3 copy numbers, but GG genotype of C-44G SNP in DEFB1 gene may result in decreased defensin β-1 production. | Balázs Csaba Németh Tamás Várkonyi Ferenc Somogyvári Csaba Lengyel Katalin Fehértemplomi Szabolcs Nyiraty Péter Kempler Yvette Mándi | 2014 | World Journal of Gastroenterology2014，20，27： | 4 |
| 8 | Isolated lymphoid follicles in colon: Switch points between inflammation and colorectal cancer?显示文摘Gut-associated lymphoid tissue is supposed to play a central role in both the organization of colonic repair mechanisms and colorectal carcinogenesis. In inflammatory conditions, the number, diameter and density of isolated lymphoid follicles (ILFs) increases. They are not only involved in immune surveillance, but their presence is also indispensable in normal mucosal regeneration of the colon. In carcinogenesis, ILFs may play a dual role. On the one hand they may support tumor growth and the metastatic process by vascular endothelial growth factor receptor signaling and producing a specific cytokine and cellular milieu, but on the other hand their presence is sometimes associated with a better prognosis. The relation of ILFs to bone marrow derived stem cells, follicular dendritic cells, subepithelial myofibroblasts or crypt formation, which are all involved in mucosal repair and carcinogenesis, has not been directly studied. Data about the putative organizer role of ILFs is scattered in scientific literature. | Ferenc Sipos Gyrgyi Müzes | 2011 | World Journal of Gastroenterology2011，17，13： | 4 |
| 9 | ESPEN Guidelines on Enteral Nutrition: Liver disease显示文摘 | M. Plauth E. Cabré O. Riggio M. Assis-Camilo M. Pirlich J. Kondrup P. Ferenci E. Holm S. vom Dahl M.J. Müller W. Nolte | 2006 | Clinical Nutrition2006，，2： | 3 |
| 10 | Intratumoral functional heterogeneity and chemotherapy显示文摘Intratumoral heterogeneity including genetic and nongenetic mechanisms refers to biological differences amongst malignant cells originated within the same tumor.Both,cell differentiation hierarchy and stochasticity in gene expression and signaling pathways may result in phenotypic differences of cancer cells.Since a tumor consists of cancer cell clones that display distinct behaviours,changes in clonal proliferative behavior may also contribute to the phenotypic variability of tumor cells.There is a need to reveal molecular actions driving chemotherapeutic resistance in colon cancer cells.In general,it is widely hypothesized that therapeutic resistance in colorectal cancer is a consequence of the preferential survival of cancer stem cells.However,recent data regarding colorectal cancer suggest that resistance to anticancer therapy and post-therapeutic tumor reappearence could be related to variations of clonal dynamics.Understanding the interaction of genetic and nongenetic determinants influencing the functional diversity and therapy response of tumors should be a future direction for cancer research. | Ferenc Sipos Miklós Constantinovits Gyrgyi Müzes | 2014 | World Journal of Gastroenterology2014，20，10： | 3 |
| 11 | Frequency and prognostic role of mucosal healing in patients with Crohn's disease and ulcerative colitis after one-year of biological therapy显示文摘AIM:To assess the endoscopic activity before and after a one-year period of biological therapy and to evaluate the frequency of relapses and need for retreatment after stopping the biologicals in patients with Crohn’s disease(CD)and ulcerative colitis(UC).METHODS:The data from 41 patients with CD and 22 patients with UC were assessed.Twenty-four CD patients received infliximab,and 17 received adalimumab.The endoscopic severity of CD was quantified with the simplified endoscopic activity score for Crohn’s disease in CD and with the Mayo endoscopic subscore in UC.RESULTS:Mucosal healing was achieved in 23 CD and7 UC patients.Biological therapy had to be restarted in78%of patients achieving complete mucosal healing with CD and in 100%of patients with UC.Neither clinical remission nor mucosal healing was associated with the time to restarting the biological therapy in either CD or UC.CONCLUSION:Mucosal healing did not predict sustained clinical remission in patients in whom the biological therapies had been stopped. | Klaudia Farkas Péter László Lakatos Mónika Szcs va Pallagi-Kunstár Anita Bálint Ferenc Nagy Zoltán Szepes Noémi Vass Lajos S Kiss Tibor Wittmann Tamás Molnár | 2014 | World Journal of Gastroenterology2014，20，11： | 2 |
| 12 | ABT-450, Ritonavir, Ombitasvir, and Dasabuvir Achieves 97% and 100% Sustained Virologic Response With or Without Ribavirin in Treatment-experienced Patients with HCV Genotype 1b Infection显示文摘 | Pietro Andreone Massimo G. Colombo Jeffrey V. Enejosa Iftihar Koksal Peter Ferenci Andreas Maieron Beat Müllhaupt Yves Horsmans Ola Weiland Henk W. Reesink Lino Rodrigues Yiran B. Hu Thomas Podsadecki Barry Bernstein | 2014 | Gastroenterology2014，，： | 2 |
| 13 | Association of hepatocyte-derived growth factor receptor/caudal type homeobox 2 co-expression with mucosal regeneration in active ulcerative colitis显示文摘AIM:To characterize the regeneration-associated stem cell-related phenotype of hepatocyte-derived growth factor receptor(HGFR)-expressing cells in active ulcerative colitis(UC).METHODS:On the whole 38 peripheral blood samples and 38 colonic biopsy samples from 18 patients with histologically proven active UC and 20 healthy control subjects were collected.After preparing tissue microarrays and blood smears HGFR,caudal type homeobox 2(CDX2),prominin-1(CD133) and Musashi-1conventional and double fluorescent immunolabelings were performed.Immunostained samples were digitalized using high-resolution Mirax Desk instrument,and analyzed with the Mirax TMA Module software.For semiquantitative counting of immunopositive lamina propria(LP) cells 5 fields of view were counted at magnification x 200 in each sample core,then mean ± SD were determined.In case of peripheral blood smears,30 fields of view with 100 μm diameter were evaluated in every sample and the number of immunopositive cells(mean ± SD) was determined.Using 337 nm UVA Laser MicroDissection system at least 5000 subepithelial cells from the lamina propria were collected.Gene expression analysis of HGFR,CDX2,CD133,leucine-rich repeat-containing G-protein coupled receptor 5(Lgr5),Musashi-1 and cytokeratin20(CK20) were performed in both laser-microdisscted samples and blood samples by using real time reverse transcription polymerase chain reaction(RT-PCR).RESULTS:By performing conventional and double fluorescent immunolabelings confirmed by RT-PCR,higher number of HGFR(blood:6.7 ± 1.22 vs 38.5 ±3.18;LP:2.25 ± 0.85 vs 9.22 ± 0.65;P < 0.05),CDX2(blood:0 vs 0.94 ± 0.64;LP:0.75 ± 0.55 vs 2.11± 0.75;P < 0.05),CD133(blood:1.1 ± 0.72 vs 8.3± 1.08;LP:11.1 ± 0.85 vs 26.28 ± 1.71;P < 0.05)and Musashi-1(blood and LP:0 vs scattered) positive cells were detected in blood and lamina propria of UC samples as compared to controls.HGFR/CDX2(blood:0 vs 1± 0.59;LP:0.8 ± 0.69 vs 2.06 ± 0.72,P < 0.05)and Musashi-1/CDX2(blood and LP:0 vs scattered) coexpressions were found in blood and lamina propria of UC samples.HGFR/CD133 and CD133/CDX2 coexpressions appeared only in UC lamina propria samples.CDX2,Lgr5 and Musashi-1 expressions in UC blood samples were not accompanied by CK20 mRNA expression.CONCLUSION:In active UC,a portion of circulating HGFR-expressing cells are committed to the epithelial lineage,and may participate in mucosal regeneration by undergoing mesenchymal-to-epithelial transition. | Ferenc Sipos Miklós Constantinovits Gábor Valcz Zsolt Tulassay Gy?rgyi M?zes | 2015 | World Journal of Gastroenterology2015，21，28： | 2 |
| 14 | A Short Amino-Terminal Part of Arabidopsis Phytochrome A Induces Constitutive Photomorphogenic Response显示文摘Phytochrome A (phyA ) 是在 Arabidopsis thaliana 察觉到的 far-red 光的主导的光敏电阻器。phyA 在发信号的变白的幼苗,和导致光的 phyA 的细胞质在高水平积累被一个复杂规章的网络调停。这包括光 -- 并且进在 vivo 的原子核的本国的 phyA 的 FHY1/FHL 蛋白质依赖者 translocation。phyA (PHYA406 ) 的短 N 终端碎片对 phenocopy 足够,这也被显示出在 vitro 的这个高度调整的细胞的过程。为了测试这 N 终端的生物活动,在 planta phyA 碎裂,我们生产了表示 PHYA406YFP 的转基因的 phyA-201 植物(黄荧光灯蛋白质) DD, PHYA406YFPDDNLS (原子本地化信号) ,和 PHYA406YFPDDNES (原子出口信号) 熔化蛋白质。这里,我们报导 PHYA406YFPDD 被进口进原子核,而 PHYA406YFPDDNLS 和 PHYA406YFPDDNES 显示期望的组成的本地化模式,这进程部分是轻依赖者的。我们的结果证明这些截断的 phyA 蛋白质是轻马厩的,当局部性时,他们在他们的原子核,和两个都不触发组成的象 photomorphogenic 一样回答导致合适的 phyA 发信号。我们证明在 vitro 并且在 vivo PHYA406, Pfr 和 Pr 绑 COP1, photomorphogenesis 的一个一般抑压者,并且在原子身体与它共同本地化。因此,我们断定在 planta,截断的 PHYA406 蛋白质以一种光无关的方式在原子核使 COP1 失去活性。 | Andra's Viczia'n E'va Ada'm Iris Wolf Ja'nos Bindics Stefan Kircher Marc Heijde Roman Ulm Eberhard Scha'fer Ferenc Nagy | 2012 | Molecular Plant2012，5，3： | 2 |
| 15 | Early on-treatment prediction of response to peginterferon alfa-2a for HBeAg-negative chronic hepatitisB using HBsAg and HBV DNA levels 显示文摘 | Rijckborst V Hansen BE Cakaloglu Y Ferenci P Tabak F Akdogan M Simon K Akarca US Flisiak R Verhey E Van Vuuren AJ Boucher CA ter Borg MJ Janssen HL | 2010 | Hepatology2010，52，2： | 1 |
| 16 | A haz- ard perception test for novice drivers显示文摘 | Scialfa C T Desehenes M C Ference J | 2011 | Accident A- nalysis and Prevention2011，43，1： | 1 |
| 17 | Disagreements in the therapeutic use of mesenchymal stem cellderived secretome显示文摘In a recent article,the authors provide a detailed summary of the characteristics and biological functions of mesenchymal stem cells(MSCs),as well as a discussion on the potential mechanisms of action of MSC-based therapies.They describe the morphology,biogenesis,and current isolation techniques of exosomes,one of the most important fractions of the MSC-derived secretome.They also summarize the characteristics of MSC-derived exosomes and highlight their functions and therapeutic potential for tissue/organ regeneration and for kidney,liver,cardiovascular,neurological,and musculoskeletal diseases,as well as cutaneous wound healing.Despite the fact that MSCs are regarded as an important pillar of regenerative medicine,their regenerative potential has been demonstrated to be limited in a number of pathological conditions.The negative effects of MSC-based cell therapy have heightened interest in the therapeutic use of MSC-derived secretome.On the other hand,MSC-derived exosomes and microvesicles possess the potential to have a significant impact on disease development,including cancer.MSCs can interact with tumor cells and promote mutual exchange and induction of cellular markers by exchanging secretome.Furthermore,enzymes secreted into and activated within exosomes can result in tumor cells acquiring new properties.As a result,therapeutic applications of MSC-derived secretomes must be approached with extreme caution. | Ferenc Sipos Györgyi Műzes | 2022 | World Journal of Stem Cells2022，14，6： | 1 |
| 18 | Analysis of TGF beta protein expression in aggressive fibromatosis (desmoid tumor)显示文摘 | Ferenc T Stalinska L Turant M Sygut J Tosik D Dziki A | 2006 | Pol J Pathol2006，57，： | 1 |
| 19 | Hepato eellular carcinoma (HCC):a global perspective显示文摘 | Ferenci P Fried M Labrecque D | 2010 | J Clin Gastroenterol2010，44，4： | 1 |
| 20 | The effects of predation risk on the use of social foraging tactics显示文摘 | Zoltán Barta András Liker Ferenc Mónus | 2004 | Animal Behaviour2004，，： | 1 |
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