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| 1 | Association between polymorphisms in the Toll-like receptor 4,CD14,and CARD15/NOD2and inflammatory bowel disease in the Greek population显示文摘AIM: Crohn's disease(CD)and ulcerative colitis(UC)are multifactorial diseases with a significant genetic background.Apart from CARD15/NOD2 gene, evidence is accumulating that molecules related to the innate immune response such as CD14 or Toll-like receptor 4 (TLR4), are involved in their pathogenesis. In further exploring the genetic background of these diseases, we investigated the variations in the CARD15/NOD2 gene (Arg702Trp,Gly908Arg and Leu1007fsinsC), and polymorphisms in the TLR4 gene (Asp299Gly and Thr399Ile) as well as in the promoter of the CD14 gene (T/C at position -159) in Greek patients with CD and UC.METHODS: DNA was obtained from 120 patients with CD,85 with UC and 100 healthy individuals. Genotyping was performed by allele specific PCR or by PCR-RFLP analysis.RESULTS: The 299Gly allele frequency of the TLR4 gene and the T allele and TT genotype frequendes of the CD14 promoter were significantly higher in CD patients only compared to healthy individuals (P = 0.026<0.05; P = 0.0048<0.01 and P= 0.047<0.05 respectively). Concerning the NOD2/CARD15mutations the overall presence in CD patients was significantly higher than that in UC patients or in controls.Additionally, 51.67% of the CD patients were carriers of a TLR4 and/or CD14 polymorphic allele and at least one variant of the NOD2/CARD15, compared to 27% of the UC patients. It should be pointed out that both frequencies significantly increased as compared with the 10% frequency of multiple carriers found in healthy controls. A possible interaction of the NOD2/CARD15 with TLR4 and especially CD14, increased the risk of developing inflammatory bowel disease (IBD).CONCLUSION: Our results indicate that co-existence of a mutation in either the TLR4 or CD14 gene, and in NOD2/CARD15is associated with an increased susceptibility to developing CD compared to UC, and to developing either CD or UC compared to healthy individuals. | Maria Gazouli Gerassimos Mantzaris Athanassios Kotsinas Panayotis Zacharatos Efstathios Papalambros Athanassios Archimandritis John Ikonomopoulos Vassilis G Gorgoulis | 2005 | World Journal of Gastroenterology2005，11，5： | 17 |
| 2 | E2F transcription factors and digestive system malignancies:How much do we know?显示文摘The E2F proteins comprise a family of 8 members that function as transcription factors.They are key targets of the retinoblastoma protein(RB)and were initially divided into groups of activators and repressors.Accumulating data suggest that there is no specific role for each individual E2F member.Instead,each E2F can exert a variety of cellular effects,some of which represent opposing ones.For instance,specific E2Fs can activate transcription and repression,promote or hamper cell proliferation,augment or inhibit apoptosis,all being dependent on the cellular context.This complexity reflects the importance that these transcription factors have on a cell’s fate.Thus,delineating the specific role for each E2F member in specific malignancies,although not easy,is a challenging and continuously pursued task,especially in view of potential E2F targeted therapies.Therefore,several reviews are continuously trying to evaluate available data on E2F status in various malignancies.Such reviews have attempted to reach a consensus,often in the simplistic form of oncogenes or tumor suppressor genes for the E2Fs.However they frequently miss spatial and temporal alterations of these factors during tumor development,which should also be considered in conjunction with the status of the regulatory networks that these factors participate in.In the current‘‘Letter to the Editor’’,we comment on the flaws,misinterpretations and omissions in one such review article published recently in the World Journal of Gastroenterology regarding the role of E2Fs in digestive system malignancies. | Konstantinos Evangelou Sophia Havaki Athanassios Kotsinas | 2014 | World Journal of Gastroenterology2014，20，29： | 2 |
| 3 | p53 activates ICAM-1 (CD54) expression in an NFkB independent manner 显示文摘 | Gorgoulis VG Zacharatos P Kotsinas A | 2003 | EMBO J2003，22，7： | 1 |
| 4 | The 3' UTR IGF2R- A2/B2 variant is associated with increased tumor growth and advanced stages in non-small cell lung cancer 显示文摘 | Kotsinas A Evangelou K Sideridou M | 2008 | Cancer Lett2008，259，2： | 1 |
| 5 | E2F1 overexpression correlates with decreased prolifer- ation and better prognosis in adenocarcinomas of Bar- rett oesophagus显示文摘 | Evangelou K Kotsinas A Mariolis-Sapsakos T | 2008 | J Clin Pathol2008，61，： | 1 |
| 6 | PIG3: a novel link between oxidative stress and DNA damage response in cancer显示文摘 | Kotsinas A Aggarwal V Tan EJ | 2012 | Cancer Lett2012，327，12： | 1 |
| 7 | E2F-1 overexpression correlates with decreased proliferation and better prognosis in adenocarcinomas of Barrett oesophagus显示文摘 | Evangelou K Kotsinas A Mariolis-Sapsakos T | 2008 | J Clin Pathol2008，61，5： | 1 |
| 8 | Modulatation of wild-type p53activity by mutant p53 (R273H) depends on the p53 responsive element (p53RE)显示文摘 | Zacharatos P V Corgoulis V G Kotsinas A | 1999 | Anticancer Res1999，19，1： | 1 |
| 9 | Distinct expression patterns of the transcription factor E2F1 in relation to tumour growth parameters in common human carcinomas显示文摘 | Zacharatos P Kotsinas A Evangelou K | 2004 | J Pathol2004，203，3： | 1 |
| 10 | P53 activates ICAM-1 (CD54)expression in an NF-KB-independent manner 显示文摘 | Gorgoulis VG Zacharatos P Kotsinas A | 2003 | EMBO J2003，22，7： | 1 |
| 11 | p53 activates ICAM-1 (CD54) expression in an NFkB independent manner 显示文摘 | Gorgoulis V G Zacharatos P Kotsinas A | 2003 | EMBO J2003，22，7： | 1 |
| 12 | The stress kinase MKK7 couples oncogenic stress to p53 stability and tumor suppression显示文摘 | SCHRAMEK D KOTSINAS A MEIXNER A | 2011 | Nat Genet2011，43，3： | 1 |
| 13 | Distinct expression patterns of the transcription factor E2F-1 in relation to tumour growth parameters in common human carcinomas 显示文摘 | Zacharatos P Kotsinas A Evangelou K | 2004 | J Pathol2004，203，3： | 1 |
| 14 | Pragmaticalization:The case of ba' and you know显示文摘 | Erman B Kotsinas U B | 1993 | New Series1993，，10： | 1 |
| 15 | Why is p53- inducible gene 3 rarely affected in cancer? 显示文摘 | Kotsinas A Pateras IS Galanos PS | 2010 | Oncogene2010，29，37： | 1 |
| 16 | Distinct expression patterns of the transcription factor E2F-1 in relation to tumour growth parameters in common human carcinomas 显示文摘 | Zaeharatos P Kotsinas A Evangelou K | 2004 | J Pathol2004，203，3： | 1 |
| 17 | Distinct expression patterns of the transcription factor E2F-1 in relation to tumour growth parameters in common human carcinomas显示文摘 | Zacharatos P Kotsinas A Evangelou K | 2004 | J Pathol2004，203，3： | 1 |
| 18 | Association of allelic imbalance at locus D13s171 (BRCA2) and p53 alterations with tumor kinetics and chromosomal instability in non-small cell lung catcinoma显示文摘 | Gorgoulis VG Kotsinas A Zacharatos P | 2000 | Cancer2000，89，9： | 1 |
| 19 | E2F-1 overexpression correlates with decreased proliferation and better prognosis in adenocarcinomas of Barrett oesophagus显示文摘 | Evangelou K Kotsinas A Mariolis-Sapsakos T | | 0，，： | 1 |
| 20 | The 3' UTR IGF2R-A2/B2 variant is associated with increased tumor growth and advanced stages in non-small cell lung cancer显示文摘 | Kotsinas A Evangelou K Sideridou M | 2008 | Cancer Lett2008，259，2： | 1 |
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