TL1A在炎症相关结直肠癌中的作用及机制研究
发布时间：2021-11-15 20:37
炎症性肠病（Inflammatory bowel disease,IBD）是一种原因尚不明确的肠道慢性炎症性疾病,具有终身复发的倾向,主要包括溃疡性结肠炎（Ulcerative colitis,UC）和克罗恩病（Crohn’s disease,CD）两种类型。研究证实IBD是结直肠癌发生的确切危险因素之一,病程10年、20年及30年的溃疡性结肠炎患者发生癌变的风险分别为1.2%、3.6%和14.4%,IBD患者平均发生结直肠癌危险度为普通人群的2-4倍,每年平均约有10-15%的IBD患者死于结直肠癌,这种由炎症导致的结直肠癌是IBD最为严重的并发症,严重威胁着人们的生命健康。而由炎症演变而来的结直肠癌与散发性结直肠癌相比,在发病机制、临床特征、病理类型等方面存在明显的不同,因此人们将由结肠炎演变而来的结直肠癌统称为炎症相关结肠癌（colitis-associated colorectal cancer,CAC）。炎症相关结直肠癌的发生通常需要经历“炎症→异型增生→癌”的过程,炎症是CAC发生的始动因素。作为参与炎症最重要炎症介质-肿瘤因子（Tumor necrosis factor,...
【文章来源】：河北医科大学河北省
【文章页数】：116 页
【学位级别】：博士
【部分图文】：
淋系高表达TL1A小鼠的鉴定
图 1-2 淋系高表达TL1A小鼠在AOM+DSS模型中炎症程度较重Fig.1-2 TL1A overexpression mices are more susceptible to AOM+DSSinduced colitis，WT and Tg mice were injected with AOM and treated withfour rounds of DSS for 7days （A）Body weight changes of WT and Tg mice（B）DAI which is consisting of weight loss, stool consistency and FOB, wasmeasured daily. The AOM+DSS/Tg group displayed much severerinflammation compared with AOM+DSS/WT group (2.3±0.76 vs 1.28±0.47,P<0.05) （C）The colonic tissue became hard, poor elasticity, mucouscongestion and edema, localized stenosis, and the size of nodular eminencewas seen, and the lumen suddenly entered the lumen. AOM+DSS/Tg comparewith AOM+DSS/WT, the weight loss was more obvious (7.00cm±0.97cm vs5.85 ± 0.78cm, P<0.05);(D)The AOM+DSS/Tg group. compared withAOM+DSS/ WT group, the dysplasia score was higher (P < 0.05).
图1-3 TL1A促进炎症相关结直肠癌的发生和发展Fig.1-3 TL1A promotes the development of inflammation related colorectcancer （A）tumor number in AOM+DSS/Tg group were obviously highthan that in AOM+DSS/WT group (3.50±1.19 vs 5.62±1.30, P<0.05), (Bcompared with the mice in control group, in AOM+DSS group the size of ceis different, the level of the cells is disordered, the polarity disappeared, thgoblet cells decreased, the nuclei increased, and the nuclear fission increaseThe normal structure disappears and the abnormal hyperplasia is obvious. (Ctumor formation rate of AOM+DSS/Tg group was obviously higher than thin AOM+DSS/WT group (88.9% vs 66.7%) (D). According to the degree intestinal mucosa cell dysplasia scores, the AOM+DSS/Tg group wsignificantly higher than AOM+DSS/WT group (2.75±0.5 vs 1.70±0.P<0.05).
【参考文献】：
期刊论文
[1]TL1A/DR3在炎症性肠病发病机制中的研究进展[J]. 贾楠,孙逊. 微生物学免疫学进展. 2017(01)
[2]中国炎症性肠病相关结直肠癌的风险评估和监测[J]. 吴开春,张琴. 中华消化杂志. 2016 (07)
[3]共聚焦激光显微内镜在炎症性肠病中的应用新进展[J]. 沈海燕,虞朝辉,陈春晓. 浙江医学. 2016(11)
[4]炎症性肠病患者结直肠癌前病变的内镜诊治——美国炎症性肠病不典型增生监测与管理国际专家共识解读[J]. 吴东,李景南,钱家鸣. 中国实用内科杂志. 2016(03)
[5]中国早期结直肠癌筛查及内镜诊治指南（2014年,北京）[J]. 柏愚,杨帆,马丹,邹文斌. 胃肠病学. 2015(06)
[6]溃疡性结肠炎大鼠结肠黏膜SOCS2、SOCS3的表达及意义[J]. 周婷婷,仝巧云,袁晋华. 华中科技大学学报(医学版). 2015(03)
[7]Wnt/β-catenin信号通路在结直肠癌中的研究进展[J]. 李悠然,侯毅,谷云飞,陈邑岐,竺平,王浩. 世界华人消化杂志. 2015(12)
[8]慢病毒载体及其研究进展[J]. 孟凡荣,陈琛,万海粟,周清华. 中国肺癌杂志. 2014(12)
[9]炎症在结直肠癌发生中的作用机制[J]. 徐春晓,张艳,朱益民. 第二军医大学学报. 2013(01)
[10]Regulatory T cells in inflammatory bowel diseases and colorectal cancer[J]. Gyrgyi Mzes,Béla Molnár,Ferenc Sipos. World Journal of Gastroenterology. 2012(40)
博士论文
[1]促炎因子和益生菌调控Wnt/β-catenin信号通路相关机制研究[D]. 徐天铭.北京协和医学院 2016
[2]维生素D3对急性结肠炎及炎症相关结直肠癌小鼠模型的干预研究及机制初探[D]. 周颖.北京协和医学院 2015
[3]溃疡性结肠炎相关性结肠癌发病机制初探[D]. 郑威扬.北京协和医学院 2009
硕士论文
[1]溃疡性结肠炎癌变机制的研究及结直肠息肉危险因素分析[D]. 李艳萍.北京协和医学院 2014
本文编号：3497455
【文章来源】：河北医科大学河北省
【文章页数】：116 页
【学位级别】：博士
【部分图文】：
淋系高表达TL1A小鼠的鉴定
图 1-2 淋系高表达TL1A小鼠在AOM+DSS模型中炎症程度较重Fig.1-2 TL1A overexpression mices are more susceptible to AOM+DSSinduced colitis，WT and Tg mice were injected with AOM and treated withfour rounds of DSS for 7days （A）Body weight changes of WT and Tg mice（B）DAI which is consisting of weight loss, stool consistency and FOB, wasmeasured daily. The AOM+DSS/Tg group displayed much severerinflammation compared with AOM+DSS/WT group (2.3±0.76 vs 1.28±0.47,P<0.05) （C）The colonic tissue became hard, poor elasticity, mucouscongestion and edema, localized stenosis, and the size of nodular eminencewas seen, and the lumen suddenly entered the lumen. AOM+DSS/Tg comparewith AOM+DSS/WT, the weight loss was more obvious (7.00cm±0.97cm vs5.85 ± 0.78cm, P<0.05);(D)The AOM+DSS/Tg group. compared withAOM+DSS/ WT group, the dysplasia score was higher (P < 0.05).
图1-3 TL1A促进炎症相关结直肠癌的发生和发展Fig.1-3 TL1A promotes the development of inflammation related colorectcancer （A）tumor number in AOM+DSS/Tg group were obviously highthan that in AOM+DSS/WT group (3.50±1.19 vs 5.62±1.30, P<0.05), (Bcompared with the mice in control group, in AOM+DSS group the size of ceis different, the level of the cells is disordered, the polarity disappeared, thgoblet cells decreased, the nuclei increased, and the nuclear fission increaseThe normal structure disappears and the abnormal hyperplasia is obvious. (Ctumor formation rate of AOM+DSS/Tg group was obviously higher than thin AOM+DSS/WT group (88.9% vs 66.7%) (D). According to the degree intestinal mucosa cell dysplasia scores, the AOM+DSS/Tg group wsignificantly higher than AOM+DSS/WT group (2.75±0.5 vs 1.70±0.P<0.05).
【参考文献】：
期刊论文
[1]TL1A/DR3在炎症性肠病发病机制中的研究进展[J]. 贾楠,孙逊. 微生物学免疫学进展. 2017(01)
[2]中国炎症性肠病相关结直肠癌的风险评估和监测[J]. 吴开春,张琴. 中华消化杂志. 2016 (07)
[3]共聚焦激光显微内镜在炎症性肠病中的应用新进展[J]. 沈海燕,虞朝辉,陈春晓. 浙江医学. 2016(11)
[4]炎症性肠病患者结直肠癌前病变的内镜诊治——美国炎症性肠病不典型增生监测与管理国际专家共识解读[J]. 吴东,李景南,钱家鸣. 中国实用内科杂志. 2016(03)
[5]中国早期结直肠癌筛查及内镜诊治指南（2014年,北京）[J]. 柏愚,杨帆,马丹,邹文斌. 胃肠病学. 2015(06)
[6]溃疡性结肠炎大鼠结肠黏膜SOCS2、SOCS3的表达及意义[J]. 周婷婷,仝巧云,袁晋华. 华中科技大学学报(医学版). 2015(03)
[7]Wnt/β-catenin信号通路在结直肠癌中的研究进展[J]. 李悠然,侯毅,谷云飞,陈邑岐,竺平,王浩. 世界华人消化杂志. 2015(12)
[8]慢病毒载体及其研究进展[J]. 孟凡荣,陈琛,万海粟,周清华. 中国肺癌杂志. 2014(12)
[9]炎症在结直肠癌发生中的作用机制[J]. 徐春晓,张艳,朱益民. 第二军医大学学报. 2013(01)
[10]Regulatory T cells in inflammatory bowel diseases and colorectal cancer[J]. Gyrgyi Mzes,Béla Molnár,Ferenc Sipos. World Journal of Gastroenterology. 2012(40)
博士论文
[1]促炎因子和益生菌调控Wnt/β-catenin信号通路相关机制研究[D]. 徐天铭.北京协和医学院 2016
[2]维生素D3对急性结肠炎及炎症相关结直肠癌小鼠模型的干预研究及机制初探[D]. 周颖.北京协和医学院 2015
[3]溃疡性结肠炎相关性结肠癌发病机制初探[D]. 郑威扬.北京协和医学院 2009
硕士论文
[1]溃疡性结肠炎癌变机制的研究及结直肠息肉危险因素分析[D]. 李艳萍.北京协和医学院 2014
本文编号：3497455
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