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| 1 | 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 |
| 2 | 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 |
| 3 | Fusion of fungal protoplasts显示文摘 | Ferenczy L Kevei F Zsolt J | 1974 | Nature1974，248，： | 1 |
| 4 | Fusion of fungal protoplasts 显示文摘 | Ferenczy L Kevei F Zsolt J | 1974 | Nature1974，248，： | 1 |
| 5 | Molecular patholocly of tumor metastasis显示文摘 | ZSOLT O ORSOLYA C OZSE F | 2002 | Pathol Oncol Res2002，8，： | 1 |
| 6 | Elevated extracellular HSP70(HSPA1A)level as an independent prognostic marker of mortality in patients with heart failure显示文摘 | Jenei Z M Tímea G Zsolt F | 2013 | Cell Stress&Chaperones2013，18，6： | 1 |
| 7 | Fusion of fungal Protoplast显示文摘 | Ferencezy L Kevei F Zsolt J | 1974 | Nature1974，248，： | 1 |
| 8 | Fusion of fungal Protoplast 显示文摘 | Ferencezy L Kevei F Zsolt J | 1974 | Nature1974，248，： | 1 |
| 9 | Fusion of fungal protoplasts显示文摘 | Ferenczy L Kevei F Zsolt J | 1974 | Nature1974，248，5451： | 1 |
| 10 | Molecular basis of the cotton effects induced by the binding of curcumin to human serum albu- min 显示文摘 | Zsila F Zsolt B Simonyi M | 2003 | Tetrahedron-Asymmetr2003，14，16： | 1 |
| 11 | Assessment of the current intensity for preventing ice accretion on overhead conductors显示文摘 | Zsolt P Masoud F Laszlo I K | 2007 | IEEE Trans on Power Delivery2007，22，1： | 1 |
| 12 | Assessment of the current intensity for preventing ice accretion on overhead conductors显示文摘 | Zsolt P Masoud F | 2007 | IEEE Transactions on Power Delivery2007，22，1： | 1 |
| 13 | Single-exposure dual-energy subtraction chest radiography:detection of pulmonary nodules and masses in clinical practice显示文摘 | Zsolt S F Michael A Seyran Y H | 2008 | Eur Radiol2008，18，1： | 1 |
| 14 | Fusion of fungal protop last显示文摘 | Ferencezy L Kevei F Zsolt J | 1974 | Nature1974，248，： | 1 |
| 15 | Fusion of fungal protoplast显示文摘 | FERENCZY L KEVEI F ZSOLT J | 1974 | Nature1974，，248： | 1 |
| 16 | Fusion of fungal protoplasts显示文摘 | FERENCZY L KEVEI F ZSOLT J | 1974 | Nature1974，248，： | 1 |
| 17 | Fusion of fungal protoplast显示文摘 | FERENCZY L KEVEI F ZSOLT J | 1974 | Nature1974，248，5847： | 1 |
| 18 | Interaction of serum 70kDa heat shock protein levels and HspA1B (+1267) gene polymorphism with disease severity in patients with chronic heart failure显示文摘 | Tímea G Zsolt F Zoltán P | 2008 | Cell Stress Chaperones2008，13，2： | 1 |
| 19 | Fusion of fungal protoplasts 显示文摘 | FERENCZY L KEVEI F ZSOLT J | 1974 | Nature1974，，248： | 1 |
| 20 | Low back- ground and high contrast PET imaging of amyloid- βwith AZD2995 and AZD2184 in Alzheimer's disease patients显示文摘 | Anton F Anders J Zsolt C | 2013 | Eur J Nucl Med Mol Imaging2013，40，： | 1 |
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