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胆囊癌淋巴转移分子机制研究进展

中国临床药理学与治疗学 2012年第8期17卷 919-923页

作者：张林李茂岚李松岗吴文广刘颖斌上海交通大学医学院附属新华医院普外科上海200092

胆囊癌是胆道系统常见的恶性肿瘤。影响胆囊癌手术预后的因素包括:侵袭深度,组织学分级,淋巴及周围神经浸润和淋巴结转移。淋巴转移是胆囊癌常见的转移方式,其分子机制目前仍不甚清楚。血管内皮生长因子-C(VEGF-C)/VEGF-D及其受体VEGFR-... 详细信息

胆囊癌是胆道系统常见的恶性肿瘤。影响胆囊癌手术预后的因素包括:侵袭深度,组织学分级,淋巴及周围神经浸润和淋巴结转移。淋巴转移是胆囊癌常见的转移方式,其分子机制目前仍不甚清楚。血管内皮生长因子-C(VEGF-C)/VEGF-D及其受体VEGFR-3能够促进淋巴管生成,在淋巴转移中起到重要作用;p16基因通过突变和甲基化,可能使肿瘤细胞恶性程度增加,与肿瘤的侵袭及淋巴结转移密切相关;缺氧诱导因子-1α(hypoxia inducible factor 1α,HIF-1α)可能通过诱导VEGF-C/-D的表达而调节肿瘤淋巴管生成,促进肿瘤淋巴结转移;细胞外基质(extracel-lular matrix,ECM)的降解是肿瘤细胞进入淋巴管的必要条件,基质金属蛋白酶(matrix metallo-proteinase,MMPs)家族中MMP-2与MMP-9通过降解细胞外基质,为肿瘤细胞进入淋巴管提供必要条件,可能与胆囊癌淋巴转移有关。

关键词：胆囊癌淋巴转移分子机制

胞内氯离子通道蛋白1表达与胆囊癌侵袭转移的相关性研究

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中华普通外科杂志 2013年第2期28卷 112-115页

作者：陆建华李茂岚李松岗董平顾钧吴文广饶龙华张林丁琦晨杨佳华吴向嵩穆嘉盛翁昊丁倩刘颖斌上海交通大学医学院附属新华医院普外科上海200092

目的探讨胆囊癌组织胞内氯离子通道蛋白1（chloride intraeellular channel 1，CLICl）蛋白表达与胆囊癌侵袭转移的关系。方法应用免疫组织化学sP染色法及Westernblot技术，检测36例胆囊癌和相应癌旁组织中CLICl蛋白的表达。采用Spearma... 详细信息

目的探讨胆囊癌组织胞内氯离子通道蛋白1（chloride intraeellular channel 1，CLICl）蛋白表达与胆囊癌侵袭转移的关系。方法应用免疫组织化学sP染色法及Westernblot技术，检测36例胆囊癌和相应癌旁组织中CLICl蛋白的表达。采用Spearman等级相关分析、x。检验对结果进行分析。结果免疫组化结果提示，CLICl蛋白高表达于胆囊癌组织，癌旁组织中CLICl蛋白表达较少，阳性表达率分别为81％（29／36）和44％（16／36），差异有统计学意义（P〈0．05）。胆囊癌组织CLICl表达与患者性别和年龄无关（P〉0．05），而与肿瘤的淋巴转移、浸润深度、TNM分期和分化程度相关（P〈0．05）。Westernblot结果显示，CLICl的特异性条带出现在Marker标准相对分子质量27000左右，CLICl在胆囊癌的阳性率高于癌旁组织（P〈0．05）。结论CLICl可能在胆囊癌的发生发展过程中发挥重要的作用，CLICl蛋白的高表达与胆囊癌的侵袭转移密切相关。

关键词：胆囊肿瘤肿瘤侵润细胞凋亡胞内氯离子通道蛋白1

Vimentin significantly promoted gallbladder carcinoma metastasis

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Chinese Medical Journal 2011年第24期000卷 4236-4244页

作者： DONG Ping HE Xiao-wei GU Jun WU Wen-guang LI Mao-lan YANG Jia-hua ZHANG Ling DING Qi-chen LU Jian-hua MU Jia-sheng CHEN Lei LI Song-gan DING Liang-fu WANG Jian-wei LIU Ying-bin Department of General Surgery Xinhua Hospital affiliated toSchool of Medicine Shanghai Jiao Tong University Shanghai200092 China Department of General Surgery First Hospital Affiliated to JiaxingMedical School Jiaxing Zhejiang 314000 China Department of General Surgery Baozhen Hospital ChongmingShanghai 200092 China Department of Surgery Second Affiliated Hospital School ofMedicine Zhejiang University Hangzhou Zhejiang 310009China

Background The precise molecular mechanisms underlying the gallbladder carcinoma （GBC） metastasis has not been fully elucidated. Methods In the present study, metastasis-associated proteins were identified by comparative proteomic analysis. The functional study of the candidate protein vimentin was further investigated. First, a pair of higher and lower metastatic sublines （termed GBC-SD/M3 and GBC-SD, respectively）, originated from the same parental cell line, was screened by spontaneous tumorigenicity and metastasis in vivo in animal study and further characterized by metastatic phenotypes analysis in vitro. Subsequently, a proteomic approach comprised two-dimensional gel electrophoresis analysis and mass spectroscopy was used to identify and compare the protein expression patterns between higher metastatic GBC-SD/M3 and lower metastatic GBC-SD cell lines. Then twenty-six proteins were identified. Results Among the 26 proteins identified, fourteen proteins were up-regulated and 12 proteins were down-regulated in GBC-SD/M3. Vimentin was identified and found to be overexpressed in GBC-SD/M3 as compared with GBC-SD. This result was further confirmed by quantitative PCR and Western blotting analysis. Furthermore, the cell migration and invasion potency of GBC-SD/M3 in vitro was remarkably suppressed after small interference RNA-mediated knockdown of vimentin. Moreover, immunoblot and immunohistochemical analysis on 12 human GBC specimens showed consistently increased vimentin expression in metastases compared with primary tumors. Conclusion Tumor vimentin level may reflect the pathological progression in some GBC and may be a useful marker for predicting tumor metastasis and a therapeutic target for the treatment of GBC patients with metastases.

关键词： gallbladder neoplasm hepatic metastasis vimentin proteomics

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胰腺癌十二指肠切除术

中华普外科手术学杂志(电子版) 2019年第4期13卷 344-344页

作者：刘颖斌上海交通大学医学院附属新华医院普通外科

目的采用kocher手法,分离十二指肠降部与下腔静脉之间间隙;分离胃结肠韧带,不保留大网膜,进入小网膜囊,小网膜囊后壁下面即为胰腺前缘;分离横结肠系膜前叶及胰腺背膜,于胰腺下缘找到肠系膜上静脉,分离钳顺着肠系膜上静脉在胰腺后侧打洞... 详细信息

目的采用kocher手法,分离十二指肠降部与下腔静脉之间间隙;分离胃结肠韧带,不保留大网膜,进入小网膜囊,小网膜囊后壁下面即为胰腺前缘;分离横结肠系膜前叶及胰腺背膜,于胰腺下缘找到肠系膜上静脉,分离钳顺着肠系膜上静脉在胰腺后侧打洞分离,直至门静脉;解剖肝十二指肠韧带,游离肝门三管;分别于胃大弯和胃小弯游离韧带,于固定处用直线切割闭合器切断胃;于预定切除处断胰;仔细分离钩突与SMV之间的小静脉、以及可能出现的胃结肠干、胃网膜右静脉等血管;施行胰肠吻合、胆肠吻合、胃肠吻合。

关键词：胰腺肿瘤胰十二指肠切除术