环状RNA在肝细胞癌发生发展中的作用

肝细胞癌(HCC)是世界上常见的恶性肿瘤之一,研究调控HCC的侵袭迁移机制对于其临床诊断和治疗具有重要意义。环状RNA(circRNA)作为非编码RNA家族的重要成员,因其环状结构高度稳定,在肝细胞中起microRNA(miRNA)海绵作用,以竞争内源性RNA机制调控miRNA或促进靶基因表达,在HCC进展中起重要作用。探讨circRNA在HCC发病中的作用机制,将有助于筛选HCC诊断标志物和研发治疗的有效靶点。     

维生素在胃癌发生中的作用

胃癌是常见的恶性肿瘤,其二级预防之一是增加维生素的摄入。本文从流行病学调查、实验研究及机理研究方面简述维生素在胃癌发生中的作用,为维生素临床防治胃癌的应用提供一定的理论基础。     

可变剪接在胃癌发生和发展中的作用

胃癌已成为严重威胁人类生命健康的恶性肿瘤之一.环境因素和遗传因素的协同作用是胃癌发生和发展的主要诱因,其中环境因素居首要地位.在胃癌的发生和发展过程中常伴随多种肿瘤相关基因结构和表达水平的异常变化,同时伴有多个异常剪接变体的出现.研究剪接变体在胃癌发生中的变化模式有可能为胃癌的早期诊断和病程跟踪提供重要的生物标志物,进...     

微卫星不稳定性在胃癌发生中的作用

胃癌是常见的恶性肿瘤,其发病机制较为复杂,涉及一系列遗传学改变,包括癌基因的激活及抑癌基因的失活。近年来对微卫星不稳定性的研究为胃癌发生的分子学研究开辟了新途径。研究表明,微卫星不稳定性可能是胃癌发生过程中一个新发现的重要机制。     

染色体结构变异在胃癌发生发展中的作用

胃癌的发生是一个多因素多步骤过程,其中染色体结构异常而导致的抑癌基因的失活和癌基因的激活在这个过程中起了重要作用.因此,通过对染色体结构变异的研究寻找肿瘤相关的抑癌基因或癌基因成为胃癌及肿瘤学研究中的重要手段.本文将综述目前胃癌染色体结构异常研究进展,并从方法学上阐述几种分子遗传学及分子生物学常用手段在研究胃癌染色体结构变异中的作用,旨在为读者的实验研究提供有价值的参考.     

竞争性内源RNA在胃癌发生发展中的作用

胃癌是常见的消化系肿瘤之一,在全球癌症死亡中排名第2位.其发病与遗传、环境及生活习惯等多种因素有关.近几年研究发现竞争性内源RNA成员中微小RNA和长链非编码RNA在胃癌的发生发展起着重要作用.本文就竞争性内源RNA在胃癌中作用作一综述.     

环状RNA在肝细胞癌发生发展及诊疗中的作用

肝细胞癌(HCC)作为原发性肝癌最常见的类型,是一种具有侵袭性且致命的恶性肿瘤,其发生发展是一个多基因参与、多步骤、多阶段的过程。环状RNA(circRNA)作为一类内源性非编码RNA,主要通过吸附微小RNA(miRNA)或者RNA结合蛋白(RBP)发挥“海绵作用”,进而调控下游靶基因表达。本文全面介绍了circRNA在HCC信号转导、免疫、代谢、耐药、HBV相关HCC中的作用及意义,及其作为HCC的生物标志物或治疗靶点的潜在价值,为HCC的诊断和治疗提供新思路。     

环状RNA在心房颤动发生中的作用及应用

近年来研究表明,环状RNA在心房组织中的异常表达与心房颤动(简称房颤)结构重构和电重构密切相关。环状RNA与微小RNA相互作用靶向参与调控不同离子通道基因和纤维化相关基因的表达,这为房颤发病的分子机制理解提供了一个新的方向,同时也为未来房颤的诊疗提供了新的诊断标志物和治疗靶点。     

微卫星不稳定性在胃癌发生中的作用

胃癌是常见的恶性肿瘤,其发病机制较为复杂,涉及一系列遗传学改变,包括癌基因的激活及抑癌基因的失活。近年来对微卫星不稳定性的研究为胃癌发生的分子学研究开辟闻新途径。研究表明,微卫星不稳定性可能是胃癌发生过程中一个新发现的重要机制。     

MicroRNA在胃癌中的研究进展

MicroRNA(miRNA)是一类进化过程中高度保守的内源性非编码小RNA.他们具有高度保守性、时序性和组织特异性,通过参与基因表达调控,在肿瘤的发生发展过程中扮演着重要的角色.本文就miRNA在胃癌方面的研究进展作一综述.     

胃黏膜癌变过程中增殖诱导配体及其受体表达水平分析

目的 分析胃癌发生各阶段组织中增殖诱导配体（APRIL）及其受体mRNA的表达水平。方法 在APRIL及其受体基因的高保守区设计相应引物和荧光探针，实时检测PCR产物的荧光强度，根据标准品建立标准曲线，由软件自动计算出待测样本中靶基因mRNA的准确含量，并以靶基因和内参β2微球蛋白（β2M）mRNA含量比值作为评价靶基因表达水平的指标。结果 采用实时荧光定量PCR（RFQ-PCR）检测靶基因mRNA含量的线性范围为10^1～10^9pg／ml，批内和批间重复性测定的变异系数（d）分别为6．52％～12．02％和8．76％～14．16％。APRIL在肠上皮化生、异型增生和胃癌组织中的表达水平显著高于正常胃黏膜（P〈0．05）．在胃癌组织中的表达水平又显著高于肠上皮化生和异型增生（P〈0．05），而其受体B细胞成熟抗原（BCMA）和穿膜蛋白活化物（TACI）在各种胃黏膜病变之间表达水平差异无统计学意义（P〉0．05）。结论 RFQ-PCR检测APRIL及其受体mRNA含量，具有较好的灵敏度和重复性。APRIL在胃癌病变演进过程中呈现累积和渐进趋势，可能在胃癌发生、发展过程中起重要作用．有可能成为胃癌早期诊断和抗癌治疗的靶分子。肿瘤组织可能还表达APRIL未知受体。     

PTEN在胃癌中的研究进展

第10号染色体同源缺失性磷酸酶-张力蛋白基因(phosphatase and tensin homolog deleted on chromosome ten,PTEN)是继p533之后发现的另一重要的抑癌基因,其编码的蛋白质可调控多种细胞信号转导通路或功能分子,构成一个复杂的网络系统,在调控细胞增殖与凋亡、迁移与黏附...     

肥大细胞在胃癌中的功能

肥大细胞在肿瘤发生发展中的作用得到越来越多的重视,但在胃癌中对肥大细胞的研究才刚起步.目前研究表明,肥大细胞在胃癌中的作用可以分为以下3个方面:(1)肥大细胞促进血管生成;(2)肥大细胞的免疫调节作用;(3)肥大细胞与组织重塑,这3方面均与肿瘤生长及转移密切相关,本文拟从此3方面对肥大细胞在胃癌中的研究进展进行综述,并...     

幽门螺杆菌感染与胃癌发病关系的文献计量学分析

目的：了解H pylori感染与胃癌关系研究现状,总结研究热点,提供参考信息．方法：采用引文分析方法对国外2001-2006有关该主题的重要文献进行调查分析,并用SPSS对高频被引文献进行聚类分析,根据各个类中的文献内容分析当前研究的热点．结果：H pylori感染与胃癌关系研究的重要文献多数发表于世界著名的综合性刊物上,肿瘤学与胃肠病学核心期刊次之．检得SCI数据库中相关文献1547篇,其参考文献出现频次高于60次论文42篇．高被引论文聚类分析树图分5类．结论：H pylori感染与胃癌流行病学、胃癌动物模型,H pylori感染的根除与胃癌的关系．H pylori感染、宿主细胞因子多态性与胃癌易感性,以及H pylori致病相关基因的为研究热点．     

Latest insights into the effects of Helicobacter pylori infection on gastric carcinogenesis

There appears to be the strong association between Helicobacter pylori (H pylori) and gastric cancer. We reviewed the latest evidences about the effects of H pylori infection on gastric carcinogenesis, classified into epidemiology, dynamics of gastric mucosal changes, DNA damages, virulence factors, host factors, and source of gastric malignancy. Through the considerable progress made in research into virulence factors resulting from differences between H pylori strains, such as cagA positivity, as well as into host factors, such as gene polymorphisms, a diverse spectrum of H pylori-associated diseases, including gastric cancer, is beginning to lend itself to elucidation. The impact of the novel hypothesis advanced by Houghton et al proposing bone-marrow derived stem cells (BMDC) as a potential source of gastric malignancy on evolving research remains to be seen with interest. Further progress in research into H pylori eradication as a viable prophylaxis of gastric cancer, as well as into the mechanisms of gastric carcinogenesis, is to be eagerly awaited for the current year and beyond.     

MYC and gastric adenocarcinoma carcinogenesis

MYC is an oncogene involved in cell cycle regulation, cell growth arrest, cell adhesion, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function. It has been described as a key element of several carcinogenesis processes in humans. Many studies have shown an association between MYC deregulation and gastric cancer. MYC deregulation is also seen in gastric preneoplastic lesions and thus it may have a role in early gastric carcinogenesis. Several studies have suggested that amplification is the main mechanism of MYC deregulation in gastric cancer. In the present review, we focus on the deregulation of the MYC oncogene in gastric adenocarcinoma carcinogenesis, including its association with Helicobacterpylori （Hpylon] and clinical applications.     

Causal role of Helicobacter pylori infection and eradication therapy in gastric carcinogenesis

Many epidemiological reports indicate that Helicobacterpylori(H pylori)infection plays an important role ingastric carcinogenesis.Several genetic and epigeneticalterations contribute to the initiation,promotion,andprogression of the cancer cells in a multi-step manner.H pylori is known to induce chronic inflammation in thegastric mucosa.Its products,including superoxides,participate in the DNA damage followed by initiation,andthe inflammation-derived cytokines and growth factorscontribute to the promotion of gastric carcinogenesis.By eradicating H pylori,gastric inflammation can becured; the therapy diminishes the levels not onlyof inflammatory cell infiltration,but also atrophy/intestinal metaplasia in part.A randomized controlledtrial revealed that the eradication therapy diminishedthe gastric cancer prevalence in cases without pre-cancerous conditions.In addition,recent epidemiologicalstudies from Japanese groups demonstrated thatthe development of gastric cancer,especially of theintestinal type,was decreased by successful eradicationtherapy,although these were designed in a non-randomized manner.However,it should be mentionedthat endoscopic detection is the only way to evaluate thedegree of gastric carcinogenesis.We have reported thatthe endoscopic and histological morphologies could bemodified by eradication therapy and it might contributeto the prevalence of gastric cancer development.Considering the biological nature of cancer cellproliferation,it is considered that a sufficiently long-termfollow-up would be essential to discuss the anticancereffect of eradication therapy.     

MiR-217 is involved in the carcinogenesis of gastric cancer by down-regulating CDH1 expression

GC is one of the most leading malignancies all over the world, and is also the leading cause of cancer-related mortalities. At present, GC remains difficult to diagnose at an early stage. In this study, we first detected the expression of 9 selected miRNAs in the exosomes from 67 GC patients’ circular exosomes and found 4 miRNAs level was significantly altered. Meanwhile, one out of 4 candidate miRNAs also had a higher expression in the GC tissue samples, and negative correlated with CDH1 expression. Predicted by bioinformatics tools, confirmed by dual luciferase assay and immunoblotting, we identified that CDH1 is a direct target of miR-217. MiR-217 overexpression enhanced gastric cancer cells proliferation, and reduced exosomal CDH1 level which can be delivered into microenvironment. In conclusion, we constructed the negative correlation between miR-217 and CDH1 level in GC patients and cells; unveiled part of the miR-217 function during the pathogenesis of GC. These findings may give insight into understanding the mechanism of GC pathogenesis and provide new biomarkers for clinical diagnosis.