吃主食护大肠

英国剑桥大学最近在一项研究中,分析了10多个国家的人的饮食习惯和癌症之间的关系,结果发现,食用淀粉类食物越多,小肠、结肠和直肠癌的发病率越低.比如,以肉类食物为主食的澳大利亚人,结肠癌发病率是以淀粉类食物为主食的中国人的4倍.     

凉菜拌出夏日风情

不知不觉又进入了夏季,南方的潮湿,北方的燥热,常常使人食欲不振,精神委靡,尤其是对于康复期的病友来说,怎一个"热"字了得.夏季的饮食调养,应选择清凉爽口、少油腻、易消化的食物.这时从配角一跃成为主角的凉菜就闪亮登场了,不论生拌、热炝,每道菜都做足了开胃功夫,它们少油,少盐,对我们的健康大有裨益;省时省力,让我们减轻在厨房的劳动强度.只要掌握烹饪技巧,制作起来还是很简单的.     

过敏体质,怎么吃?

什么是过敏呢?过敏反应又称作变态反应,是患者身体对一种或多种物质的过强反应.其主要机制是由于过敏性素质患者的体内产生了过多的过敏抗体——免疫球蛋白E,它和环境中的过敏原相互作用,刺激机体产生和释放某些过敏介质,导致不同组织的损伤,继而产生各种症状.     

文艺汇演群星璀璨

2006年1月8日,中国抗癌协会癌症康复会在"北京展览馆剧场"圆满成功地举办了"阿斯利康首届全国癌症康复者文艺汇演--生命恋歌".这次文艺汇演有26个省、市上报节目50多个,经筹备组认真筛选,选出正式参加演出的节目16个,特邀节目3个,出演的癌症患者近300人.     

钻石之光--山药

"每个人都能在自家的后院找到钻石",有人借用此言,把山药比做养生的钻石. 山药是一种薯科植物,它的根茎垂直而颀长,往往盈尺,生长在坚硬的山冈的土质中,旋转攀缘.阳光下,山药的叶子很美,颜色从浓到浅,绿得缤纷,但被我们称之为钻石的是它营养丰富的块状根茎.山药的外观看上去粗糙,细小密布的根须如刺如须,但削了皮,却洁白得如水生荸荠,分泌一些透明的黏液,柔滑得抓它不住,仿佛泥鳅从手中挣脱.     

Benefit of adjuvant chemoradiotherapy in patients with pathologically lymph node-positive and locally advanced gastric cancer

Objective This study aimed to compare the effectiveness of adjuvant chemoradiotherapy(CRT)and adjuvant chemotherapy(ChT)for T3–4/N+gastric cancer(GC)following D2/R0 dissection,and identify the specific subgroups that could benefit from adjuvant CRT.Methods All eligible patients were divided into the CRT group and ChT group.We assessed the survival outcomes and patterns of recurrence for each group,and determined the prognostic factors for survival by performing Cox proportional risk regression analyses.Results A total of 192 gastric cancer patients were included in the study.The estimated 3-year and 5-year disease-free survival(DFS)probabilities in the CRT and ChT groups were 52.9%vs.36.7%(P=0.024)and 41.2%vs.31.1%(P=0.148),respectively,and the estimated 3-year and 5-year overall survival(OS)probabilities were 82.4%vs.70.0%(P=0.044)and 52.0%vs.35.6%(P=0.022).Patients in the CRT group had a lower risk of locoregional recurrence than those in the ChT group(20.6%vs.34.4%;P=0.031).The subset analyses revealed that patients with stage N1–2 disease were more likely to benefit from adjuvant CRT than from adjuvant ChT(DFS:53.1%vs.36.4%;P=0.039;OS:53.1%vs.38.6%;P=0.036).Conclusion For locally advanced gastric cancer patients with LN+,adjuvant CRT showed superior survival benefits compared with adjuvant ChT alone.Patients with N1–2 achieved better survival from adjuvant CRT.     

苦参碱对HepG2细胞杀伤作用及机制研究

Objective:To investigate the death mode of human hepatoma cells exposed to matrine and the role of glutathione (GSH) and cytochrome c.Methods:The MTT test and Cell Death Detection ELISA were used to identify cell death mode and viability of cells exposed to matrine.The volume of intracellular GSH was detected by GSH reductase.Finally Western blotting was chosen to analyze the expression of cytochrome c and Caspase-9 in HepG2 cells treated by matrine.Results:The apoptotic cell death induced by matrine in Hep G2 cells dramatically increased in the time-,dose-dependent manner.Matrine can exhaust intracellular GSH effectively to change the redox state in cells.Furthermore it affect the cytotoxicity of matrine.Results of Western blotting showed that matrine induced the release of cytochrome c from mitochondria to cytoplasm,and then stimulate the cleavage of Cespese-9 in a time-dependent manner.Conclusion:Matrine induced apoptosis in Hep G2 cells through the mitochondrial pathway,and oxidative stress via depletion of GSH is directly involved in the apoptotic process.     

熏烤煎炸不安全

据说人类发现用火是由于森林起火烧焦了动物而引起的,从那时起,便尝到了烧烤味道的鲜美.时至今日,熏烤煎炸食品气味香,味道美,仍不免会令人垂涎三尺,颇受嘴馋的人或一些儿童、少女青睐,从而造就许多中国人有喜食这类食品的习惯.这类食品如在聚餐酒桌上品尝助兴,少量吃点在所难免,如果大量贪食则可能会对健康不利.化学家在研究癌症病因时,发现一种很强的致癌物质苯并芘,它属于多环芳烃类化合物,与熏烤煎炸食物有关,并引起人们的关注.     

肺癌放疗新技术

肺癌是危害人类生命的最主要的癌肿,是名副其实的"癌王",特别是在发达国家更是如此.简单地说美国男性死于恶性肿瘤患者中约每3人中有1例是肺癌,女性中每4人中有1人是肺癌.中国随着城市化进度的加快和吸烟人群的增多,肺癌患者会越来越多.笔者在美国最著名的癌症医院--德州安德森肿瘤中心做客座教授期间接触了来自世界各地的放疗科医生,他们都在努力研究如何延长肺癌患者的生存期,提高生存质量.下面介绍一下这方面的最新技术.     

lncRNA NORAD促进食管鳞状细胞癌EC9706 细胞的增殖和迁移

目的：探讨长链非编码RNA（long non-coding RNA,lncRNA）DNA损伤激活的非编码RNA（non-coding RNA-activated by DNA damage,NORAD）对食管鳞状细胞癌（esophageal squamous cell carcinoma,ESCC）细胞株EC9706 增殖和迁移能力的影响及其机制。方法：采用RT-PCR 法检测不同ESCC细胞（EC9706、TE1、YES-2、KYSE150）中NORAD mRNA表达水平,通过RNA干扰技术将NORAD的小干扰RNA（siRNA）转染到EC9706 细胞（si-NORAD组）以建立NORAD低表达细胞,另设置空白对照组（Ctrl 组,不转染任何序列）及阴性对照组（NC组,转染siRNA 阴性对照序列）,qPCR验证其转染效果。用MTT、平板克隆形成和划痕愈合实验检测敲低NORAD前后EC9706 细胞增殖和迁移能力的变化,Western blotting 检测敲低NORAD前后EC9706 细胞中上皮钙黏蛋白（E-cadherin）、神经钙黏蛋白（N-cadherin）和锌指转录因子Snail 的表达变化。结果：在4 种ESCC 细胞中NORAD mRNA 均呈高表达状态,同时与TE1、YES-2、KYSE150 细胞相比,EC9706 细胞中NORAD mRNA 呈显著高表达（P<0.01）。与Ctrl 组和NC 组比较,转染NORAD-siRNA 后,si-NORAD 组EC9706 细胞中NORAD 表达水平显著降低（均P<0.01）,EC9706 细胞的增殖和迁移能力显著降低（均P<0.05）;敲低NORAD 表达后,EC9706 细胞中E-cadherin 表达升高而N-cadherin 和Snail 表达降低（均P<0.05）。结论：NORAD 在EC9706 细胞中呈高表达状态,敲低NORAD 表达可通过上调E-cadherin、下调N-cadherin 和Snail表达而抑制EC9706 细胞的增殖和迁移能力。     

Effects of Down-regulation of HDAC6 Expression on Proliferation,Cell Cycling and Migration of Esophageal Squamous CellCarcinoma Cells and Related Molecular Mechanisms

Objective: To study the effects of down-regulation of HDAC6 expression on proliferation, cell cycling andmigration of esophageal squamous cell carcinoma (ESCC) cells and related molecular mechanisms. Methods:ESCC cell line EC9706 cells were randomly divided into untreated (with no transfection), control siRNA(transfected with control siRNA) and HDAC6 siRNA (transfected with HDAC6 small interfering RNA) groups.Effects of HDAC6 siRNA interference on expression of HDAC6 mRNA and protein in EC9706 cells wereinvestigated by semi-quantitative RT-PCR, Western blotting and immunocytochemistry methods. Effects ofdown-regulation of HDAC6 expression on cell proliferation, cell cycle, and cell migration were studied usinga CCK-8 kit, flow cytometry and Boyden chambers, respectively. Changes of mRNA and protein expressionlevels of cell cycle related factor (p21) and cell migration related factor (E-cadherin) were investigated by semiquantitativeRT-PCR and Western blotting methods. Results: After transfection of HDAC6 siRNA, the expressionof HDAC6 mRNA and protein in EC9706 cells was significantly downregulated. In the HDAC6 siRNA group,cell proliferation was markedly inhibited, the percentage of cells in G0/G1 phase evidently increased and thepercentage of cells in S phase decreased, and the number of migrating cells significantly and obviously decreased.The mRNA and protein expression levels of p21 and E-cadherin in the HDAC6 siRNA group were significantlyhigher than those in the untreated group and the control siRNA group, respectively. Conclusions: HDAC6 siRNAcan effectively downregulate the expression of HDAC6 mRNA and protein in EC9706 cells. Down-regulation ofHDAC6 expression can obviously inhibit cell proliferation, arrest cell cycling in the G0/G1 phase and reduce cellmigration. The latter two functions may be closely related with the elevation of mRNA and protein expressionof p21 and E-cadherin.     

组蛋白去乙酰化酶在食管鳞癌中的表达及其表达下调对EC9706细胞生物特性的影响

目的:探讨组蛋白去乙酰化酶(histone deacetylase2,HDAC2)在食管鳞癌组织中的表达,并研究其表达下调对食管鳞癌EC9706细胞增殖、细胞周期和细胞凋亡的影响,以及分析其相关的分子机制。方法:采用免疫组织化学法检测食管鳞癌组织中HDAC2蛋白的表达。将特异性针对HDAC2基因的小分子干扰RNA(small interfering RNA,siRNA)和对照siRNA分别转染食管鳞癌EC9706细胞,实验分3组:未处理组、对照siRNA组和HDAC2siRNA组。蛋白质印迹法检测各组EC9706细胞中HDAC2蛋白的表达。CCK-8计数法检测转染前后细胞的增殖情况。FCM法检测细胞周期和细胞凋亡的变化。蛋白质印迹法检测与细胞增殖、细胞周期和细胞凋亡相关蛋白的表达变化。结果:HDAC2蛋白在食管鳞癌组织中表达的阳性率为79.71%,显著高于癌旁不典型增生组织的51.11%和正常食管黏膜组织的23.19%,3者之间差异具有统计学意义(χ2=44.121,P=0.000);此外,HDAC2蛋白表达与患者的年龄和性别无关(P均>0.05),但是与组织学分级、浸润深度、TNM分期和淋巴结转移均显著相关(P均<0.05)。HDAC2siRNA能有效下调食管鳞癌EC9706细胞中HDAC2蛋白的表达,明显抑制食管鳞癌EC9706细胞的增殖,促使细胞周期静止在G0/G1期,并诱导细胞凋亡。蛋白质印迹法检测结果显示,HDAC2表达下调能明显提高p21和凋亡相关蛋白bax的表达量,同时降低细胞周期蛋白cyclin D1和bcl-2的表达量。结论:HDAC2可能在食管鳞癌的发生、发展中具有重要作用,其表达下调介导的食管鳞癌细胞增殖抑制、细胞周期静止以及细胞凋亡可能与p21、bax的表达升高和cyclin D1、bcl-2表达降低密切相关。     

下调HDAC6表达对食管鳞癌细胞周期、细胞迁移的影响及其分子机制探讨

目的:探讨组蛋白去乙酰化酶6（HDAC6）表达的下调对食管鳞癌细胞周期、细胞迁移的影响及其分子机制。方法:将食管鳞癌EC9706细胞分为三组,即未处理组、对照siRNA组和HDAC6 siRNA组,后两组分别转染对照siRNA和HDAC6 siRNA。采用半定量反转录-聚合酶链反应、蛋白印迹方法检测各组细胞中细胞增殖和周期相关因子p21 mRNA和蛋白以及细胞迁移相关因子E-cadherin mRNA和蛋白的表达水平的变化。结果:HDAC6 siRNA组中p21及E-cadherin mRNA和蛋白的表达水平分别是0.440±0.120、0.840±0.070和0.580±0.090、0.450±0.080,且均明显高于未处理组（0.165±0.090、0.090±0.020;0.088±0.009、0.054±0.011）和对照siRNA组（0.163±0.021、0.070±0.040;0.820±0.070、0.066±0.007）中p21及E-cadherin mRNA和蛋白的表达水平,其表达差异均具有统计学意义（P均<0.05）,而未处理组和对照siRNA组之间p21及E-cadherin mRNA和蛋白的表达无差异（P＞0.05）。结论:HDAC6表达下调对食管鳞癌细胞周期的影响可能与p21表达的升高相关;对细胞迁移的影响可能与E-cadherin表达的上调有关。     

Notch1基因在食管鳞癌细胞株EC9706中的表达及其对细胞凋亡的影响

背景与目的:早期的研究显示,Notch1信号途径与肿瘤的发生密切相关,在细胞的生长、增殖、分化和凋亡中起着十分重要的作用.本研究旨在研究Notch1基因在食管鳞癌EC9706细胞中的表达及其对EC9706细胞凋亡的影响.方法:通过免疫细胞化学方法检测Notch1基因在EC9706细胞中的表达.采用RT-PCR技术扩增Notch1基因,构建真核表达载体pcDNA3.1-Notch1(命名为pcNICD),转染EC9706细胞,利用RT-PCR及Western blot检测稳定转染pcNICD 载体、转染pcDNA3.1空载体及未处理的EC9706细胞中Notch1的表达,另通过流式细胞仪检测未处理、转染pcDNA3.1和转染pcNICD的EC9706细胞的凋亡.结果:EC9706细胞中发现Notch1基因的表达.与未处理的和转染pcDNA3.1的EC9706细胞相比,转染pcNICD的EC9706细胞中Notch1基因的mRNA和蛋白表达水平均明显增加,大约增加3倍(P＜0.05);但未处理的和转染pcDNA3.1的EC9706细胞中Notch1的表达差异无统计学意义(P＞0.05).流式细胞检测结果显示,在未处理的和转染pcDNA3.1的EC9706细胞中,细胞凋亡率差异无统计学意义(P＞0.05);但与与未处理的和转染pcDNA3.1的EC9706细胞相比.转染pcNICD的EC9706细胞转染后24 h、48 h和72 h时细胞凋亡率明显增加(P＜0.01).结论:Notch信号途径的激活引起食管鳞癌EC9706 细胞的凋亡.提示Notch1基因有可能成为治疗食管鳞癌的新靶点.     

RNAi-induced K-Ras Gene Silencing Suppresses Growth of EC9706 Cells and Enhances Chemotherapy Sensitivity of Esophageal Cancer

To analyze the growth, proliferation, apoptosis, invasiveness and chemotherapy sensitivity of EC9706 cellsafter K-Ras gene silencing, an expression carrier pSilencer-siK-Ras was constructed, and the EC9706 cell linewas transfected using a liposome technique. Six groups were established: Control, siRNA NC (transfected withempty vector pSilencer2.1); Ras siRNA (transfected with pSilencer-siK-Ras2); Paclitaxel; Paclitaxel + siRNANC; and Ras siRNA + Paclitaxel. After the treatment, RT-PCR, Western blotting, MTT assay, flow cytometryand the Transwell technique were used to assess expression of K-Ras mRNA and protein in EC9706 cells, aswell as cell growth, proliferation, apoptosis and invasiveness. The effect of Paclitaxel chemotherapy was alsotested. pSilencer-siK-Ras2 effectively down-regulated expression of K-Ras mRNA and protein in EC9706 cells,growth being significantly inhibited. Flow cytometry indicated obvious apoptosis of cells in the experimentalgroup, with arrest in the G1 phase; cell migration ability was also reduced. After pSilencer-siK-Ras2 transfectionor the addition of Paclitaxel, EC9706 cells were suppressed to different extents; the suppressive effect wasstrengthened by combined treatment. The results suggested that RNAi-induced K-Ras gene silencing couldenhance chemotherapy sensitivity of esophageal cancer.     

siRNA靶向沉默MALAT-1基因对人食管癌EC9706细胞体外侵袭迁移的影响

目的:研究长链非编码RNA MALAT-1对食管癌EC9706细胞系迁移、侵袭能力的影响。方法:化学合成针对MALAT-1的siRNA,脂质体法转染EC9706细胞,转染48h后RT-PCR和Western blot检测各细胞MALAT-1在mRNA和蛋白质水平的表达。Transwell实验检测迁移、侵袭能力改变。结果:小干扰RNA下调MALAT-1表达后,RT-PCR和Western blot证实食管癌EC9706细胞中MALAT-1的表达在mRNA水平和蛋白质水平均明显下调,Transwell实验证实食管癌EC9706细胞迁移、侵袭能力下降。结论:抑制MALAT-1表达能够使食管鳞癌细胞的侵袭转移能力明显降低。     

LNC01852通过调控Bcl-2对食管癌EC9706细胞增殖和凋亡的影响及作用机制

目的:探究长链非编码RNA LNC01852对食管癌EC9706细胞增殖和凋亡的影响及其作用机制。方法:选取人食管癌细胞系EC9706、KYSE30、TE-13和人食管黏膜上皮细胞系HET-1A为研究对象,分别采用siRNA基因敲减技术、实时荧光定量聚合酶链反应（qRT-PCR）、蛋白质免疫印迹（Western blot）、MTS细胞增殖实验、克隆形成实验和流式细胞术细胞凋亡实验观察LNC01852对食管癌EC9706细胞增殖和凋亡能力以及对p53-Bcl-2/Bax凋亡信号通路标志分子mRNA和蛋白表达的影响。结果:qRT-PCR结果表明,人食管癌细胞系中LNC01852的表达较食管黏膜上皮细胞系HET-1A明显升高,差异有统计学意义（P＜0.05）;MTS细胞增殖实验、克隆形成实验和流式细胞术细胞凋亡实验结果表明,转染siLNC01852能够明显抑制人食管癌EC9706细胞中LNC01852的表达,同时抑制细胞的增殖能力和菌落形成能力,并促进细胞发生凋亡;此外,qRT-PCR和Western blot结果进一步证实,敲减LNC01852能够明显上调人食管癌EC9706细胞中促凋亡分子p53和Bax的mRNA和蛋白表达,同时明显抑制抗凋亡分子Bcl-2的mRNA和蛋白表达,差异有统计学意义（P＜0.05）。结论:LNC01852通过介导p53-Bcl-2/Bax凋亡信号影响人食管癌细胞增殖和凋亡,提示靶向LNC01852及其下游p53-Bcl-2/Bax凋亡信号,有望为临床食管癌治疗提供新的靶点和理论依据。     

胰岛素样生长因子1受体在食管鳞癌组织中的表达及RNA干扰沉默其表达对EC9706细胞增殖能力的影响

目的 探讨胰岛素样生长因子1受体(IGF-1R)在食管鳞癌组织中的表达及其与患者临床特征之间的关系,以及RNA干扰沉默其表达对人食管癌EC-9706细胞体外增殖能力的影响.方法 采用免疫组化法,检测80例食管鳞癌组织和18例正常食管上皮组织中IGF-1R的表达,通过RNA干扰技术沉默EC9706细胞中IGF-1R的表达,通过绘制生长曲线、四甲基偶氮唑蓝(MTT)实验和平板克隆形成试验,观察IGF-1R对细胞体外增殖能力的影响.结果 食管鳞癌组织中IGF-1R表达的总阳性率为86.3%,强阳性率为51.3%;正常食管上皮组织中IGF-1R表达的总阳性率为61.1%,强阳性率为11.1%.食管鳞癌组织中IGF-1R表达的总阳性率和强阳性率均高于正常食管组织(P＜0.01).有淋巴结转移患者组织中IGF-1R表达的总阳性率和强阳性率均高于无淋巴结转移患者(P＜0.01).IGF-1R的表达随肿瘤组织分化程度的增高而降低,差异均有统计学意义(均P＜0.05).不同年龄组间IGF-1R表达差异无统计学意义(均P＞0.05).Ⅲ～Ⅳ期患者组织中IGF-IR表达的总阳性率和强阳性率均高于Ⅰ～Ⅱ期患者(P＜0.01).稳定干扰后的EC9706细胞IGF-1R蛋白表达下降,生长缓慢,细胞倍增时间较实验对照组和空白对照组延长.培养48 h后,稳定转染细胞抑制率为17.3%,高于实验对照组(2.7%,P＜0.01).稳定转染细胞较实验对照组和空白对照组细胞克隆形成能力减弱(P＜0.05).结论 IGF-1R在食管鳞癌组织中呈高表达,与食管鳞癌的发生、转移、分化程度和临床分期相关;RNA干扰沉默IGF-IR的表达,可以使EC9706细胞的体外增殖能力降低.

Abstract：

Objective To explore the correlation of IGF-1R expression with clinical features of esophageal squamous cell carcinoma (ESCC) and to investigate the effect of silencing IGF-1R by siRNA on the proliferation of esophageal cancer cell line EC9706 cells. Methods Immunohistochemistry was used to detect the expresion of IGF-1R in 80 specimens of ESCC and 18 specimens of normal esophageal mucosa.IGF-I R siRNA was transfected into esophageal squamous cell carcinoma EC9706 cells, and the effect of RNAi was assessed by Western blot. The proliferation of EC9706 cells was determined by drawing growth curve, MTT assay and plate colony-forming assay. Results The total and strong positive rates of IGF-1R expression were 86.3% and 51.3% in ESCC, and 61.1% and 11.1% in normal esophageal epithelium,respectively. The total and strong positive rates of IGF-1 R expression in patients with lymph node metastasis were 94.4% and 74.1%, significantly higher than 69.2% and 3.9%, respectively, in those without lymph node metastasis (P ＜ 0. 01 ). A significantly higher IGF-1 R expression was associated with lower histological grade ( P ＜ 0.05 ). The total and strong rates of IGF-1 R expression in 39 patients of stages Ⅲ and Ⅳ were 97.4% and 71.8%, significantly higher than the 75.6% and 31.7%, respectively, in 41 cases of stages Ⅰ and Ⅱ (P ＜ 0. 01 ). IGF-1 R RNAi significantly inhibited IGF-1R expression and the growth of EC9706cells. The clone formation rate of RNAi-IGF-1R transfected cells was 19.1%, significantly lower than that of 52. 3% in non-transfected cells and 49.0% in empty vector-transfected EC9706 cells ( P ＜ 0.05 ).Conclusions The overexpression of IGF-1R is colerated with lymph node metastasis, differentiation and clinical stage. Down-regulation of IGF-1R can inhibit the proliferation of esophageal cancer EC9706 cells in vitro.