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Molecular mechanisms of Barrett's esophagus.巴雷特食管的分子机制。
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2
Proinflammatory cytokine and nuclear factor kappa-B expression along the inflammation-metaplasia-dysplasia-adenocarcinoma sequence in the esophagus.食管中炎症-化生-发育异常-腺癌序列中促炎细胞因子和核因子κB的表达
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Aberrant epithelial-mesenchymal Hedgehog signaling characterizes Barrett's metaplasia.异常的上皮-间充质 Hedgehog 信号特征表现为巴雷特食管化生。
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Distinct esophageal adenocarcinoma molecular subtype has subtype-specific gene expression and mutation patterns.具有独特分子亚型的食管腺癌具有特定的基因表达和突变模式。
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microRNA involvement in the onset and progression of Barrett's esophagus: a systematic review.微小RNA参与巴雷特食管的发生和进展:一项系统综述
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Esophageal Cancer: Genomic and Molecular Characterization, Stem Cell Compartment and Clonal Evolution.食管癌:基因组与分子特征、干细胞区室及克隆进化
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Hnf4α is a key gene that can generate columnar metaplasia in oesophageal epithelium.肝细胞核因子4α(Hnf4α)是一种可在食管上皮中产生柱状化生的关键基因。
Differentiation. 2017 Jan-Feb;93:39-49. doi: 10.1016/j.diff.2016.11.001. Epub 2016 Nov 19.

本文引用的文献

1
Ectopic Cdx2 expression in murine esophagus models an intermediate stage in the emergence of Barrett's esophagus.在小鼠食管模型中异位表达 Cdx2 可模拟 Barrett 食管发生的中间阶段。
PLoS One. 2011 Apr 6;6(4):e18280. doi: 10.1371/journal.pone.0018280.
2
Widespread hypomethylation occurs early and synergizes with gene amplification during esophageal carcinogenesis.广泛的低甲基化发生在早期,并与食管癌发生过程中的基因扩增协同作用。
PLoS Genet. 2011 Mar;7(3):e1001356. doi: 10.1371/journal.pgen.1001356. Epub 2011 Mar 31.
3
Feasibility of mcroRNAs as biomarkers for Barrett's Esophagus progression: a pilot cross-sectional, phase 2 biomarker study.微小 RNA 作为巴雷特食管进展生物标志物的可行性:一项初步的、基于 2 期生物标志物的横断面研究。
Am J Gastroenterol. 2011 Jun;106(6):1055-63. doi: 10.1038/ajg.2011.37. Epub 2011 Mar 15.
4
Essential and redundant functions of caudal family proteins in activating adult intestinal genes.尾部家族蛋白在激活成年肠道基因方面的必要和冗余功能。
Mol Cell Biol. 2011 May;31(10):2026-39. doi: 10.1128/MCB.01250-10. Epub 2011 Mar 14.
5
Signaling through BMP receptors promotes respiratory identity in the foregut via repression of Sox2.BMP 受体信号通过抑制 Sox2 促进前肠的呼吸特征。
Development. 2011 Mar;138(5):971-81. doi: 10.1242/dev.053694.
6
MiR-9 downregulates CDX2 expression in gastric cancer cells.miR-9 下调胃癌细胞中 CDX2 的表达。
Int J Cancer. 2011 Dec 1;129(11):2611-20. doi: 10.1002/ijc.25923. Epub 2011 Mar 25.
7
Roles of Kruppel-like factor 4 in oesophageal epithelial cells in Barrett's epithelium development.Kruppel 样因子 4 在巴雷特食管发育中的食管上皮细胞中的作用。
Gut. 2011 May;60(5):608-17. doi: 10.1136/gut.2010.221648. Epub 2010 Dec 30.
8
Regulation of Krüppel-like factor 4 by the anaphase promoting complex pathway is involved in TGF-beta signaling.后期促进复合物途径对 Kruppel 样因子 4 的调控参与 TGF-β 信号转导。
J Biol Chem. 2011 Mar 4;286(9):6890-901. doi: 10.1074/jbc.M110.179952. Epub 2010 Dec 22.
9
MicroRNA expression profiling in human Barrett's carcinogenesis.人 Barrett 食管癌变过程中的 microRNA 表达谱分析。
Int J Cancer. 2011 Oct 1;129(7):1661-70. doi: 10.1002/ijc.25823. Epub 2011 Mar 11.
10
Cdx genes, inflammation, and the pathogenesis of intestinal metaplasia.Cdx 基因、炎症与肠上皮化生的发病机制。
Prog Mol Biol Transl Sci. 2010;96:231-70. doi: 10.1016/B978-0-12-381280-3.00010-5.

巴雷特食管的分子机制。

Molecular mechanisms of Barrett's esophagus.

机构信息

Cancer Research Program, Julius L. Chambers Biomedical Biotechnology Research Institute, North Carolina Central University, 700 George Street, Durham, NC 27707, USA.

出版信息

Dig Dis Sci. 2011 Dec;56(12):3405-20. doi: 10.1007/s10620-011-1885-6. Epub 2011 Oct 8.

DOI:10.1007/s10620-011-1885-6
PMID:21984436
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3750118/
Abstract

Barrett's esophagus (BE) is defined as the metaplastic conversion of esophageal squamous epithelium to intestinalized columnar epithelium. As a premalignant lesion of esophageal adenocarcinoma (EAC), BE develops as a result of chronic gastroesophageal reflux disease (GERD). Many studies have been conducted to understand the molecular mechanisms of this disease. This review summarizes recent results involving squamous and intestinal transcription factors, signaling pathways, stromal factors, microRNAs, and other factors in the development of BE. A conceptual framework is proposed to guide future studies. We expect elucidation of the molecular mechanisms of BE to help in the development of improved management of GERD, BE, and EAC.

摘要

巴雷特食管(BE)被定义为食管鳞状上皮向肠化生柱状上皮的化生。作为食管腺癌(EAC)的癌前病变,BE 是由于慢性胃食管反流病(GERD)发展而来。许多研究已经致力于理解这种疾病的分子机制。这篇综述总结了涉及鳞状和肠转录因子、信号通路、基质因子、microRNAs 以及 BE 发展过程中的其他因素的最新研究结果。提出了一个概念框架以指导未来的研究。我们期望阐明 BE 的分子机制有助于改善 GERD、BE 和 EAC 的管理。