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| 1 | Epidemiology of esophageal cancer显示文摘Esophageal cancer(EsC)is one of the least studied and deadliest cancers worldwide because of its extremely aggressive nature and poor survival rate.It ranks sixth among all cancers in mortality.In retrospective studies of EsC,smoking,hot tea drinking,red meat consumption,poor oral health,low intake of fresh fruit and vegetables,and low socioeconomic status have been associated with a higher risk of esophageal squamous cell carcinoma.Barrett’s esophagus is clearly recognized as a risk factor for EsC,and dysplasia remains the only factor useful for identifying patients at increased risk,for the development of esophageal adenocarcinoma in clinical practice.Here,we investigated the epidemiologic patterns and causes of EsC.Using population based cancer data from the Surveillance,Epidemiology and End Results Program of the United States;we generated the most up-to-date stage distribution and 5-year relative survival by stage at diagnosis for 1998-2009.Special note should be given to the fact that esophageal cancer,mainly adenocarcinoma,is one of the very few cancers that is contributing to increasing death rates(20%)among males in the United States.To further explore the mechanism of development of EsC will hopefully decrease the incidence of EsC and improve outcomes. | Yuwei Zhang | 2013 | World Journal of Gastroenterology2013，19，34： | 74 |
| 2 | Th1/Th2 cytokines and their genotypes as predictors of hepatitis B virus related hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC), the predominant type of primary liver cancer, is one of the most serious lifethreatening malignancies, worldwide. In majority of the cases, HCC develops after prolonged and persistent chronic liver disease. hepatitis B virus(HBV) or HCV infection is prominent etiological factors, attributing to this condition. It has been well documented that HBV, being the inducer of chronic inflammation, is the main causative agent in causing HCC, particularly in Asian countries. The HBV infection leads to a wide range of clinical symptoms from carrier state to malignancy. Cytokines being immune-modulatory molecules, are the key mediators in the defense mechanism against viral infection. In this regard, this review will detail the substantial role of key Th1: interleukin 1(IL-1), IL-2, IL-12, tumor necrosis factor-α, interferon-γ; Th2: IL-4, IL-10 and non Th1/Th2: IL-6, transforming growth factor-β1 cytokines genotypes in analyzing the variability in the clinical manifestations in an HBV-afflicted individual, which might finally, culminates into HCC. Since cytokine production is regulated genetically, the cytokine promoter region single-nucleotide polymorphisms induced changes, greatly affects the cytokine production, thus resulting into differential outcome of immune balance. | Roli Saxena Jyotdeep Kaur | 2015 | World Journal of Hepatology2015，7，11： | 50 |
| 3 | The relation between HLA-DQA1 genes and genetic susceptibility to duodenal ulcer in Wuhan Hans显示文摘AIM To study the genetic susceptibility of HLA-DQA1 alleles to duodenal ulcer in Wuhan Hans.METHODS Seventy patients with duodenalulcer and fifty healthy controls were examinedfor HLA-DQA1 genotypes.HLA-DQA1 typing wascarried out by digesting the locus specificpolymerase chain reaction amplified productswith alleles specific restriction enzymes(PCR-RFLP),i.e.,Apal Ⅰ,Bsaj Ⅰ,Hph Ⅰ,Fok Ⅰ,Mbo Ⅱ and Mnl Ⅰ.RESULTS The allele frequencies of DQA1 * 0301and DQA1 * 0102 in patients with duodenal ulcerwere significantly higher and lower respectivelythan those in healthy controls(0.40 vs 0.20,P = 0.003,mcorret = 0.024)and(0.05 vs 0.14,P = 0.012,but Pcorret>0.05),respectively.CONCLUSION DQA1 * 0301 is a susceptiblegene for duodenal ulcer in Wuhan Hans,andthere are immunogenetic differences in HLA-DQA1 locus between duodenal ulcer patients andhealthy controls. | Du YP Deng CS Lu DY Huang MF Guo SF Hou W | 2000 | World Journal of Gastroenterology2000，6，1： | 37 |
| 4 | CYP2C19 polymorphism influences Helicobacter pylori eradication显示文摘The known factors that have contributed to the decline of Helicobacter pylori(H.pylori)eradication rate include antibiotic resistance,poor compliance,high gastric acidity,high bacterial load,and cytochrome P450 2C19(CYP2C19)polymorphism.Proton pump inhibitor(PPI)is important in the eradication regimen.The principal enzyme implicated in the metabolism of PPIs is CYP2C19.The effects of PPI depend on metabolic enzyme,cytochrome P450 enzymes,and CYP2C19 with genetic differences in the activity of this enzyme(the homozygous EM,heterozygous EM(Het EM),and poor metabolizer).The frequency of the CYP2C19 polymorphism is highly varied among different ethnic populations.The CYP2C19genotype is a cardinal factor of H.pylori eradication in patients taking omeprazole-based or lansoprazolebased triple therapies.In contrast,the CYP2C19 polymorphism has no significant effect on the rabeprazolebased or esomeprazole-based triple therapies.The efficacy of levofloxacin-based rescue triple therapy might be also affected by the CYP2C19 polymorphism,but CYP2C19 genotypes did not show obvious impact on other levofloxacin-based rescue therapies.Choice of different PPIs and/or increasing doses of PPIs should be individualized based on the pharmacogenetics background of each patient and pharmacological profile of each drug.Other possible factors influencing gastric acid secretion(e.g.,IL-1β-511 polymorphism)would be also under consideration. | Chao-Hung Kuo Chien-Yu Lu Hsiang-Yao Shih Chung-Jung Liu Meng-Chieh Wu Huang-Ming Hu Wen-Hung Hsu Fang-Jung Yu Deng-Chyang Wu Fu-Chen Kuo | 2014 | World Journal of Gastroenterology2014，20，43： | 33 |
| 5 | Polymorphism of p16INK4a gene and rare mutation of p15INK4b gene exon2 in primary hepatocarcinoma显示文摘INTRODUCTION Hepatocellular carcinoma(HCC)is the mostcommon cause of death from cancer in China.Themechanisms of hepatocarcinogenesis are not yetknown clearly,p16INK4a gene,the multiple tumorsuppressor gene 1(MTS1),encodes P16 protein,which acts as an inhibitor by binding directly toCDK4 and CDK6 and preventing its association | Yang Qin Bo Li Yong Shu Tan Zhi Lin Sun Feng Qiong Zuo Ze Fang Sun Institute of Biochemistry and Molecular Biology,West China University of Medical Sciences,Chengdu 610041,Sichuan Province,China Department of General Surgery,The First Affiliated Hospital,West China University of Medical Sciences,Chengdu 610041,Sichuan Province,China Department of Pathology,The First Affiliated Hospital,West China University of Medical Sciences,Chengdu 610041,Sichuan Province,China | 2000 | World Journal of Gastroenterology2000，6，3： | 30 |
| 6 | Glutathione S-transferases M1,T1 genotypes and the risk of gastric cancer:A case-control study显示文摘AIM Glutathione S-transferases (GSTs are involved in the detoxification of many potential carcinogens and appear to play a critical role in the protection from the effects of carcinogens. The contribution of glutathione Stransferases M1 and T1 genotypes to susceptibility to the risk of gastric cancer and their interaction with cigarette smoking are still unclear. The aim of this study was to determine whether there was any relationship between genetic polymorphisms of GSTM1 and GSTT1 and gastric cancer.METHODS A population based case - control study was carried out in a high-risk area, Changle County, Fujian Province, China. The epidemiological data were collected by a standard questionnaire and blood samples were obtained from 95 incidence gastric cancer cases and 94 healthy controls. A polymerase chain reaction method was used to detect the presence or absence of the GSTM1 and GSTT1 genes in genomic DNA. Logistic regression model was employed in the data analysis.RESULTS An increase in risk for gastric cancer was found among carriers of GSTM1 null genotype. The adjusted odds ratio (OR) was 2.63 [95% Confidence Interval (95% CI) 1.17-5.88], after controlling for age,gender, cigarette smoking, alcohol drinking, and fish sauce intake. The frequency of GSTT1 null genotype in cancer cases (43.16%) was not significantly different from that in controls (50.00%). However, the risk for gastric cancer in those with GSTM1 null and GSTT1 nonnull genotype was significantly higher than in those with both GSTM1 and GSTT1 non-null genotype (OR = 2.77,95% Cl 1.15- 6.77). Compared with those subjects who never smoked and had normal GSTM1 genotype, Ors were 1.60 (95% CI: 0.62- 4.19) for never smokers with GSTM1 null type, 2.33 (95% CI 0.88- 6.28) for smokers with normal GSTM1, and 8.06 (95% CI 2.83- 23.67) for smokers with GSTM1 null type.CONCLUSIONS GSTM1 gene polymorphisms may be associated with genetic susceptibility of stomach cancer and may modulate tobacco-related carcinogenesis of gastric cancer. | Lin Cai Shun-Zhang Yu Zuo-Feng Zhang Department of Epidemiology.Fujian Medical University,Fuzhou 350004,Fujian Province,ChinaDepartment of Epidemiology,Shanghai Medical University,Shanghai 200032,China Department of Epidemiology,UCLA School of Public Health,Los Angeles California,USA | 2001 | World Journal of Gastroenterology2001，7，4： | 22 |
| 7 | Platelets and depression in cardiovascular disease:A brief review of the current literature显示文摘Major depression is an independent risk factor for cardiovascular mortality and morbidity. The exact mechanisms linking depression and increased cardiovascular risk remain poorly understood. Several mechanisms have been proposed including increased platelet reactivity. This review focuses on the current literature that examines the platelet hypothesis of depression. To date studies show increased serotonin response, increased platelet serotonin receptor density, decreased serotonin transporter binding, and decreased platelet serotonin levels in individuals with depression. However other studies have shown no change in serotonin uptake. In addition to platelet serotonin specific pathways, other platelet pathways that have shown significant changes in depressed individuals include blunting of the platelet adenosine response, increased platelet thrombin response, increased glycoprotein Ⅰb expression, increased P-selectin, β thromboglobulin, and platelet factor four, as well as decreased platelet brain derived neurotrophic factor. However there are other studies that show conflicting evidence of increased platelet activation as measured by integrin receptor α2b β3. Other conflictingdata include α adrenergic density and platelet response to augmented serotonin. The direction of future research in platelet functional changes in depression and coronary artery disease should continue to focus on serotonin specific pathways with emphasis on potential mechanisms of specific pathway changes. | Marlene S Williams | 2012 | World Journal of Psychiatry2012，2，6： | 21 |
| 8 | PNPLA3 I148M polymorphism and progressive liver disease显示文摘The 148 Isoleucine to Methionine protein variant(I148M)of patatin-like phospholipase domain-containing 3(PNPLA3),a protein is expressed in the liver and is involved in lipid metabolism,has recently been identified as a major determinant of liver fat content.Several studies confirmed that the I148M variant predisposes towards the full spectrum of liver damage associated with fatty liver:from simple steatosis to steatohepatitis and progressive fibrosis.Furthermore,the I148M variant represents a major determinant of progression of alcohol related steatohepatitis to cirrhosis,and to influence fibrogenesis and related clinical outcomes in chronic hepatitis C virus hepatitis,and possibly chronic hepatitis B virus hepatitis,hereditary hemochromatosis and primary sclerosing cholangitis.All in all,studies suggest that the I148M polymorphism may represent a general modifier of fibrogenesis in liver diseases.Remarkably,the effect of the I148M variant on fibrosis was independent of that on hepatic steatosis and inflammation,suggesting that it may affect both the quantity and quality of hepatic lipids and the biology of non-parenchymal liver cells besides hepatocytes,directly promoting fibrogenesis.Therefore,PNPLA3 is a key player in liver disease progression.Assessment of the I148M polymorphism will possibly inform clinical practice in the future,whereas the determination of the effect of the 148M variant will reveal mechanisms involved in hepatic fibrogenesis. | Paola Dongiovanni Benedetta Donati Roberta Fares Rosa Lombardi Rosellina Margherita Mancina Stefano Romeo Luca Valenti | 2013 | World Journal of Gastroenterology2013，19，41： | 17 |
| 9 | HMGB1 gene polymorphisms in patients with chronic hepatitis B virus infection显示文摘AIM: To characterize high mobility group box chromosomal protein 1(HMGB1) polymorphisms in patients infected with hepatitis B virus(HBV) and determine the different patterns in patient subgroups.METHODS: A total of 1495 unrelated Han Chinese HBV carriers were recruited in this hospital-based casecontrol study.The HMGB1 1176 G/C polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism assay.RESULTS: A significant association was observed between HMGB1 1176 G/C polymorphism and outcome of HBV infection.The subjects bearing 1176G/G genotype had an increased risk of susceptibility to chronic hepatitis B,liver cirrhosis and severe hepatitis B when compared with those bearing at least one 1176C allele.CONCLUSION: Patients with 1176G/G genotype of HMGB1 gene are more likely to have a progressive status in HBV infection. | Chun-Qing Deng Guo-Hong Deng Yu-Ming Wang | 2013 | World Journal of Gastroenterology2013，19，31： | 15 |
| 10 | SSR Analysis of Genetic Relationship and Classification in Chrysanthemum Germplasm Collection显示文摘To further test the accuracy and rationality of the Chinese classification system for chrysanthemum(Chrysanthemum morifolium), 10 simple sequence repeat(SSR) markers were used to identify a collection of 88 chrysanthemum and its related genera accessions. In total, 42 effective alleles across 88 accessions were detected; 3 429 bands were obtained by PCR amplification, including 2 630 polymorphic bands. The similarity coefficient ranged from 0.53 to 0.88. Cluster analysis based on UPGMA illustrated that the wild species and large-flower cultivars were first divided into two clusters, then the large-flower cultivars formed five distinct groups according to petal type, indicated that petal type can be a classification criterion. In the wild species cluster, C. vestitum and C. zawadaskii grouped with A. trilobata, suggested that the Ajania genera was closely related to the Chrysanthemum genera. ‘Hangbaiju’, ‘Gongju’ and ‘Chuju’ were grouped together, and ‘Boju’, O. longilobus and C. mongolicum constituted another branch, showed a correlation with geographic region of origin. Population structure analysis was subsequently performed with K values ranging from 2 to 10, and the most likely estimate for the population structure is five subpopulations, which is nearly consistent with the clustering results. Principle component analysis was further performed to verify the classification results. The results showed that these SSR markers are very powerful for studying genetic relationships and will be useful tools in the identification and classification of chrysanthemum. | LUO Chang CHEN Dongliang CHENG Xi LIU Hua LI Yahui HUANG Conglin | 2018 | Horticultural Plant Journal2018，4，2： | 15 |
| 11 | pms3 is the locus causing the original photoperiod-sensitive male sterility mutation of‘Nongken 58S'显示文摘Photoperiod-sensitive genic male sterile (PSGMS) rice is a very useful germplasm for hybrid rice development. It was first found as a spontaneous mutant in a japonica cultivar ’Nongken 58’. pms3 on chromosome 12 was determined to be the locus where the original PSGMS mutation occurred, changing the normal cultivar Nongken 58 to PSGMS Nongken 58S. Large amounts of RAPD and AFLP analyses were also conducted for the fine mapping of the pms3 genomic region, which resulted in 4 molecular markers linked to pms3. Although these markers somewhat increased the marker density of this region, the pms3 locus is still located in a marker-sparse region. | 梅明华 陈亮 章志宏 李子银 徐才国 张启发 | 1999 | Science China(Life Sciences)1999，42，3： | 14 |
| 12 | Severe irinotecan-induced toxicity in a patient with UGT1A1*28 and UGT1A1*6 polymorphisms显示文摘Many studies have demonstrated the impact of UGT1A1 on toxicity of irinotecan. In particular, patients bear-ing UGT1A1*28 (TA 7/7) have a higher risk of severe neutropenia and diarrhea. Based on this, prescribers of irinotecan are advised that patients with UGT1A1*28 (TA 7/7) should start with a reduced dose of irinotecan, although a particular dose is not specified. Research in Asian countries has shown a lower incidence of UG-T1A1*28 (TA 7/7), while UGT1A1*6 (A/A) is more often found and is associated with severe irinotecan-related neutropenia. We report here a case of a metastatic colorectal cancer patient who is heterozygous for the UGT1A1*28 polymorphism (TA 6/7) as well as the UG-T1A1*6 polymorphism (G/A). The patient was treated with FOLFIRI for 9 cycles and underwent two irinote-can dose reductions according to pharmacokinetic data regarding exposure to the active metabolite, SN-38. Simultaneous heterozygous UGT1A1*28 and UGT1A1*6 polymorphisms may produce higher exposure to SN-38 and a higher risk of adverse effects related to irinote-can. Additional studies will be necessary to determine the optimal starting dose of irinotecan for patients with both UGT1A1*28 and UGT1A1*6 polymorphisms. | Jian-Ming Xu Yan Wang Fei-Jiao Ge Li Lin Ze-Yuan Liu Manish R Sharma | 2013 | World Journal of Gastroenterology2013，19，24： | 14 |
| 13 | Rheumatoid arthritis susceptibility genes: An overview显示文摘Rheumatoid arthritis(RA) is a chronic, inflammatory autoimmune disease sustained by genetic factors. Various aspects of the genetic contribution to the pathogenetics and outcome of RA are still unknown. Several genes have been indicated so far in the pathogenesis of RA. Apart from human leukocyte antigen, large genome wide association studies have identified many loci involved in RA pathogenesis. These genes include protein tyrosine phosphatase, nonreceptor type 22, Peptidyl Arginine Deiminase type Ⅳ, signal transducer and activator of transcription 4, cytotoxic T-lymphocyte-associated protein 4, tumor necrosis factor-receptor associated factor 1/complement component 5, tumor necrosis factor and others. It is important to determine whether a combination of RA risk alleles are able to identify patients who will develop certain clinical outcomes, such myocardium infarction, severe infection or lymphoma, as well as to identify patients who will respond to biological medication therapy. | Izabela Korczowska | 2014 | World Journal of Orthopedics2014，5，4： | 14 |
| 14 | XbaⅠpolymorphisms of apolipoprotein B gene:Another risk factor of gallstone formation after radical gastrectomy显示文摘AIM:To prospectively investigate the association between the XbaⅠpolymorphisms of apolipoprotein B (APOB)gene and gallstone formation following gastrectomy.METHODS:The study was conducted between January 2005 and December 2006.A total of 186 gastric cancer patients who had undergone radical gastrectomy were grouped according to XbaⅠpolymorphisms of APOB gene(X+X-group,n=24 and X-X-group,n =162)and compared.The XbaⅠpolymorphisms of APOB gene were detected by polymerase chain reaction-restriction fragment length polymorphism(PCRRFLP).RESULTS:The incidence of gallstone was significantly higher in the X + X-group than in the X-X-group[54.2% vs 9.3%,RR=5.85(2.23-15.32),P<0.001].The serum levels of total cholesterol(TC)and low-density lipoprotein(LDL)were higher in the X + X-than in the X-X-group(4.02±1.12 vs 3.48±0.88,P=0.004 before surgery and 3.88±1.09 vs 3.40±0.86,P=0.008 after surgery).LDL was 2.21±0.96 vs 1.89±0.84(P =0.042)before surgery and 2.09±0.95 vs 1.72±0.85 (P=0.029)after surgery in the two groups.No relationship was found between XbaⅠpolymorphisms and gallbladder motility.CONCLUSION:In Chinese patients after radical gastrectomy,X + allele of APOB gene is another risk factor for the development of gallstone besides the gallbladder motility disorder after surgery. | Feng-Lin Liu,Wen-Bin Lu,Wei-Xin Niu,Department of General Surgery,Zhongshan Hospital,Fudan University,Shanghai 200032,China | 2010 | World Journal of Gastroenterology2010，16，20： | 14 |
| 15 | Correlation between pre-miR-146a C/G polymorphism and gastric cancer risk in Chinese population显示文摘AIM:To investigate the association between pre-miR- 146a C/G polymorphism and gastric cancer risk. METHODS:We performed a hospital-based,case-control study using polymerase chain reaction-restriction fragment length polymorphism method in 608 individuals(304 gastric cancer patients and 304 age and sex matched cancer-free controls).RESULTS:The frequencies of pre-miR-146a C/G genotypes in the case group were significantly different from those in the control groups(P=0.037).Compared with CC genotype carriers,subjects with the variant genotypes(GC+GG)had a 58%increased risk of gastric cancer(adjusted OR=1.58,95%CI:1.11-2.20,P= 0.009).Moreover,a higher gastric cancer risk was especially evident in younger individuals aged≤58 years, nonsmokers,and males(adjusted OR=1.76,95%CI: 1.08-2.87,P=0.024;adjusted OR=1.55,95%CI: 1.06-2.28,P=0.025;adjusted OR=1.53,95%CI: 1.04-2.27,P=0.033;respectively). CONCLUSION:Pre-miR-146a C/G polymorphism might be associated with an elevated risk of gastric cancer in Chinese population. | Ying Zeng Nan-Nan Liu Guang-Hui Dong Jie Chen Bin Wang Qing-Min Sun Li Yang | 2010 | World Journal of Gastroenterology2010，16，28： | 14 |
| 16 | Epidemiological studies of esophageal cancer in the era of genome-wide association studies显示文摘Esophageal cancer(EC) caused about 395000 deaths in 2010. China has the most cases of EC and EC is the fourth leading cause of cancer death in China. Esophageal squamous cell carcinoma(ESCC) is the predominant histologic type(90%-95%), while the incidence of esophageal adenocarcinoma(EAC) remains extremely low in China. Traditional epidemiological studies have revealed that environmental carcinogens are risk factors for EC. Molecular epidemiological studies revealed that susceptibility to EC is influenced by both environmental and genetic risk factors. Of all the risk factors for EC, some are associated with the risk of ESCC and others with the risk of EAC. However, the details and mechanisms of risk factors involved in the process for EC are unclear. The advanced methods and techniques used in human genome studies bring a great opportunity for researchers to explore and identify the details of those risk factors or susceptibility genes involved inthe process of EC. Human genome epidemiology is a new branch of epidemiology, which leads the epidemiology study from the molecular epidemiology era to the era of genome wide association studies(GWAS). Here we review the epidemiological studies of EC(especially ESCC) in the era of GWAS, and provide an overview of the general risk factors and those genomic variants(genes, SNPs, miRNAs, proteins) involved in the process of ESCC. | An-Hui Wang Yuan Liu Bo Wang Yi-Xuan He Ye-Xian Fang Yong-Ping Yan | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，3： | 14 |
| 17 | Insights into CYP2B6-mediated drug–drug interactions显示文摘Mounting evidence demonstrates that CYP2B6 plays a much larger role in human drug metabolism than was previously believed.The discovery of multiple important substrates of CYP2B6 as well as polymorphic differences has sparked increasing interest in the genetic and xenobiotic factors contributing to the expression and function of the enzyme.The expression of CYP2B6 is regulated primarily by the xenobiotic receptors constitutive androstane receptor(CAR) and pregnane X receptor(PXR) in the liver.In addition to CYP2B6,these receptors also mediate the inductive expression of CYP3A4,and a number of important phase II enzymes and drug transporters.CYP2B6 has been demonstrated to play a role in the metabolism of 2%–10% of clinically used drugs including widely used antineoplastic agents cyclophosphamide and ifosfamide,anesthetics propofol and ketamine,synthetic opioids pethidine and methadone,and the antiretrovirals nevirapine and efavirenz,among others.Significant inter-individual variability in the expression and function of the human CYP2B6 gene exists and can result in altered clinical outcomes in patients receiving treatment with CYP2B6-substrate drugs.These variances arise from a number of sources including genetic polymorphism,and xenobiotic intervention.In this review,we will provide an overview of the key players in CYP2B6 expression and function and highlight recent advances made in assessing clinical ramifications of important CYP2B6-mediated drug–drug interactions. | William D.Hedrich Hazem E.Hassan Hongbing Wang | 2016 | Acta Pharmaceutica Sinica B2016，6，5： | 14 |
| 18 | Epigenetics of hepatocellular carcinoma:Role of microRNA显示文摘Hepatocellular carcinoma(HCC)represents a major form of primary liver cancer in adults.MicroRNAs(miRs),small non-coding single-stranded RNAs of 19-24nucleotides in length,negatively regulate the expression of many target genes at the post-transcriptional and/or translational levels and play a critical role in the initiation and progression of HCC.In this review we have summarized the information of aberrantly expressed miRs in HCC,their mechanism of action and relationship to cancer.The recent advances in HCC research reveal that miRs regulate expression of various oncogenes and tumor suppressor genes,thereby contributing to the modulation of diverse biological processes including proliferation,apoptosis,epithelial to mesenchymal transition and metastasis.From a clinical viewpoint,polymorphisms within miR-binding sites are associated with the risk of HCC.Polymorphisms in miR related genes have been shown to correlate with survival or treatment outcome in patients.Furthermore,the review focuses on the potential role of miRs as novel biomarkers and their translational applications for diagnosis and therapy in HCC.With further insights into miR deregulation in HCC,it is expected that novel miR-based therapeutics will arise.Also,we orient the readers to other reviews that may provide better understanding of miR research in HCC. | Sharad Khare Qiong Zhang Jamal A Ibdah | 2013 | World Journal of Gastroenterology2013，19，33： | 12 |
| 19 | 茶树CHS基因结构及编码区单核苷酸多态性分析显示文摘【目的】通过试验获得茶树CHS基因(CsCHS)gDNA序列,以进一步确定CsCHS基因结构;研究CsCHS编码区单核苷酸多态性,并结合茶树多酚含量进行关联分析,寻找基因中可能存在的与茶多酚含量存在显著或极显著相关关系的SNP位点。【方法】根据NCBI数据库中已有CsCHS序列设计特异性引物,再分别以基因组DNA和cDNA为模板进行PCR扩增,经克隆、测序获得CsCHS1、CsCHS2、CsCHS3三个基因的gDNA和cDNA全长序列,通过序列比对方法确定CsCHS结构。利用Compute pI/Mw、SOPMA等软件对所得序列进行生物信息学分析,预测和比较CsCHS1、CsCHS2和CsCHS3三者蛋白质结构。以茶多酚含量差异较大的57份茶树品种为材料,分别以57份材料的cDNA为模板,用特异性引物进行PCR扩增,然后利用PCR产物直接测序法筛查CsCHS编码区序列的单核苷酸多态性。结合CsCHS编码区序列单核苷酸多态性和57份材料多酚含量,利用软件TASSEL进行关联分析,筛选基因中可能与茶多酚含量存在显著或极显著相关关系的SNP位点。【结果】试验获得CsCHS1、CsCHS2和CsCHS3的cDNA序列长度分别为1 277、1 320和1 242 bp,各自均包含一个长度为1 170 bp的开放阅读框;CsCHS1、CsCHS2和CsCHS3的gDNA序列长度分别为1 600、1 330和1 607 bp。通过gDNA序列和cDAN序列比对,结合真核生物内含子GT-AG法则,确定CsCHS1、CsCHS3分别包含2个外显子和1个内含子,内含子大小分别为323和356 bp,CsCHS2可能没有内含子。根据CsCHS1、CsCHS2和CsCHS3 cDNA序列推导三者对应氨基酸序列,比较三条氨基酸序列发现三者氨基酸同源性较高,达到92.6%—95.4%,CHS蛋白亚家族中的特征性保守位点在这三条序列中都能找到,生物信息学分析结果显示CsCHS1、CsCHS2和CsCHS3三者蛋白质结构高度相似。CsCHS1编码区序列中共发现71个SNP位点,SNP出现频率为1SNP/16.48 bp,无Indel,基因核苷酸多样性(π)值为0.01088;CsCHS2编码区序列中共发现55个SNP位点,SNP出现频率分别为1SNP/21.27 bp,CsCHS2核苷酸多样性(π)值(0.00530)明显低于CsCHS1;因扩增CsCHS3 cDNA序列的PCR反应成功率低,未对该基因遗传多样性进行分析。通过关联分析分别从CsCHS1和CsCHS2中找到2个和4个与茶叶多酚含量相关的SNP位点。【结论】CsCHS1和CsCHS3属于保守型CHS基因,且CsCHS1、CsCHS2和CsCHS3蛋白质结构高度相似,推测三者可能在茶树的不同部位或不同生长阶段发挥类似作用;CsCHS1和CsCHS2活跃,二者编码区内可能存在突变热点区。 | 张丽群 韦康 王丽鸳 成浩 刘本英 龚武云 | 2014 | 中国农业科学2014，47，1： | 11 |
| 20 | Pro12Ala polymorphism of the peroxisome proliferator-activated receptor γ2 in patients with fatty liver diseases显示文摘AIM:To test the occurrence of the Pro12Ala mutation of the peroxisome proliferator-activated receptor-γ (PPARγ)2-gene in patients with non-alcoholic fatty liver disease (NAFLD) or alcoholic fatty liver disease (AFLD).METHODS:DNA from a total of 622 specimens including 259 blood samples of healthy blood donors and 363 histologically categorized liver biopsies of patients with NAFLD (n=263) and AFLD (n=100) were analyzed by Real-time polymerase chain reaction using allele-specific probes.RESULTS:In the NAFLD and the AFLD collective,3% of the patients showed homozygous occurrence of the Ala12 PPARγ2-allele,differing from only 1.5% cases in the healthy population.In NAFLD patients,a high incidence of the Ala12 mutant was not associated with the progression of fatty liver disease.However,we observed a significantly higher risk (odds ratio=2.50,CI:1.05-5.90,P=0.028) in AFLD patients carrying the mutated Ala12 allele to develop inflammatory alterations.The linkage of the malfunctioning Ala12-positive PPARγ2 isoform to an increased risk in patients with AFLD to develop severe steatohepatitis and fibrosis indicates a more prominent anti-inflammatory impact of PPARγ2 in progression of AFLD than of NAFLD.CONCLUSION:In AFLD patients,the Pro12Ala single nuclear polymorphism should be studied more extensively in order to serve as a novel candidate in biomarker screening for improved prognosis. | Johannes W Rey Andrea Noetel Aline Hardt Ali Canbay Hakan Alakus Axel zur Hausen Hans Peter Dienes Uta Drebber Margarete Odenthal | 2010 | World Journal of Gastroenterology2010，16，46： | 11 |
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