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| 1 | 人口腔鳞状细胞癌和口腔白斑的基因甲基化谱分析显示文摘目的比较人口腔白斑、口腔鳞状细胞癌(oral squamous cell carcinoma,OSCC)与正常口腔黏膜组织中基因的甲基化变化,以明确DNA甲基化在口腔癌发生发展中的作用。
方法从4例正常口腔黏膜、4例口腔白斑以及4例OSCC组织中提取DNA,样本均来自首都医科大学口腔医学院黏膜科。使用Illumina 450K人全基因组甲基化芯片对其进行检测,对CpG位点发生甲基化改变的相关基因进行基因本体分析(gene ontology,GO)和京都基因和基因组百科全书通路富集分析(Kyoto encyclopedia of genes and genomes,KEGG)。
结果口腔白斑及OSCC组织中基因的CpG位点甲基化状态发生了改变。在口腔白斑中,异常CpG位点中的高甲基化改变达86.18%(23 290/27 025);低甲基化改变占13.82%(3 734/27 025)。与口腔白斑相比,OSCC无论是高甲基化还是低甲基化的CpG位点均显著增加。多数发生甲基化改变的CpG位点位于CpG岛的外围,其中大约有1/4位于CpG岛滩(距CpG岛0~2 kb),该部位对于基因调控以及肿瘤的发生至关重要。通路分析表明口腔白斑和OSCC组织中发生甲基化改变的CpG位点有共同的通路富集,其中大部分通路都与肿瘤的发生和进展有关。
结论口腔白斑和OSCC在通路方面及基因中都有相似的甲基化改变,表明在口腔白斑和OSCC的发病过程中,它们的表观遗传学方面可能有类似的分子基础。 | 付洁 宿颖 刘瑶 张辛燕 | 2018 | 中华口腔医学杂志2018，53，4： | 9 |
| 2 | 慢性萎缩性胃炎伴胃黏膜肠上皮化生的中西医诊疗进展显示文摘中医学认为,慢性萎缩性胃炎(CAG)的发病可从外感和内伤两方面探讨。外感方面,当人体正气虚弱,无力抵抗外邪入侵,正所谓'正气存内,邪不可干',若湿阻中焦,气机阻滞,便有利于幽门螺杆菌(Hp)的生长繁殖;六淫过极等因素,易化生为毒,也可导致胃黏膜萎缩、胃黏膜肠上皮化生(GIM)及癌变的发生。内伤方面,长期饮食不节、不洁,七情内伤、劳逸过度、年老体衰等均会导致痰湿、气滞、瘀血、浊毒等病理产物,侵害机体组织,最终导致癌变。目前,中西医治疗CAG伴CIM均取得较好疗效。 | 赵润元 刘小发 | 2018 | 河北中医2018，40，6： | 8 |
| 3 | 胃黏膜肠上皮化生的研究进展显示文摘胃黏膜肠上皮化生(IM)普遍认为是胃腺癌多阶段发生模式的中间阶段,已被视为癌前病变。IM有多种发病因素,且有越来越多的分子被证实参与了其发生机制。流行病学证据显示IM可能具有可逆性,但是目前仍存在争议。笔者就IM的病因、分子机制、是否可逆等方面等研究进展综述文献。 | 余钧辉 郑见宝 孙学军 | 2015 | 中国普通外科杂志2015，24，10： | 7 |
| 4 | 肠上皮化生的中西医诊治进展显示文摘胃黏膜肠上皮化生(intestinal metaplasia,IM)是肠型上皮细胞取代胃黏膜上皮细胞的病理过程,即胃黏膜出现了类似大小肠黏膜的上皮细胞。IM是一个量变的过程,一旦质变即是胃癌癌前病变(precancerous lesions of gastric cancer,PLGC)的重要提示。1978年WHO已将IM作为胃癌的癌前病变,确诊依据为胃镜及组织病理结果。 | 陈云 税典奎 | 2016 | 中医药临床杂志2016，28，7： | 5 |
| 5 | Molecular markers and imaging tools to identify malignant potential in Barrett's esophagus显示文摘Due to its rapidly rising incidence and high mortality, esophageal adenocarcinoma is a major public health concern, particularly in Western countries. The steps involved in the progression from its predisposing condition, gastroesophageal reflux disease, to its premalignant disorder, Barrett's esophagus, and to cancer, are incompletely understood. Current screening and surveillance methods are limited by the lack of population-wide utility, incomplete sampling of standard biopsies, and subjectivity of evaluation. Advances in endoscopic ablation have raised the hope of effective therapy for eradication of high-risk Barrett's lesions, but improvements are needed in determining when to apply this treatment and how to follow patients clinically. Researchers have evaluated numerous potential molecular biomarkers with the goal of detecting dysplasia, with varying degrees of success. The combination of biomarker panels with epidemiologic risk factors to yield clinical risk scoring systems is promising. New approaches to sample tissue may also be combined with these biomarkers for less invasive screening and sur-veillance. The development of novel endoscopic imaging tools in recent years has the potential to markedly improve detection of small foci of dysplasia in vivo. Current and future efforts will aim to determine the combination of markers and imaging modalities that will most effectively improve the rate of early detection of highrisk lesions in Barrett's esophagus. | Michael Bennett Hiroshi Mashimo | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，4： | 0 |
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