共查询到20条相似文献,搜索用时 156 毫秒
1.
2.
BEL-7402、HLE及HuH-7细胞p53基因突变检测 总被引:5,自引:0,他引:5
3.
4.
实验性大鼠肝纤维化进程中TNF-α、IL-6与IL-10的作用 总被引:7,自引:0,他引:7
5.
6.
大鼠免疫性肝纤维化形成中MMP-1和TIMP-1表达的动态变化 总被引:2,自引:0,他引:2
7.
8.
9.
11.
Sang Gyune Kim Su Jin Hong Kye Won Kwon Sung Won Jung Whan Yeol Kim In Seop Jung Bong Min Ko Chang Beom Ryu Young Seok Kim Jong Ho Moon Jin Oh Kim Joo Young Cho Joon Seong Lee Moon Sung Lee Chan Sup Shim Boo Sung Kim 《Taehan Sohwagi Hakhoe chi》2006,48(4):269-276
BACKGROUNDS/AIMS: p53 is known to play a central role in sensing and signaling for the growth arrest and apoptosis in cells with DNA damage. Mutation of p53 is a frequent event in esophageal squamous cell carcinoma (ESCC). p16 protein binds to cyclin dependent kinase 4 (CDK4) inhibiting the ability of CDK4 to interact with cyclin D1, and stimulates the passage through the G1 phase of cell cycle. We observed the expression patterns and frequencies of p53, p16, and cyclin D1 in esophageal dysplasia and in esophageal squamous cell carcinomas. METHODS: In 15 patients of ESCC, 5 patients of esophageal dysplasia and 5 volunteers with normal esophagus, tissue specimens were taken from esophageal lesions during the operation or endoscopic examination. We used specific monoclonal antibodies for p53 protein, p16(INK4 ) protein and cyclin D1. Immunoreactivity was scored. RESULTS: Mean age of all groups was 66 years old (range 47-93) and men to women ratio was 19:1. p53 mutation was observed in 87% (13/15) of ESCC, in 80% (4/5) of esophageal dysplasia, in 0% (0/5) of normal mucosa (p=0.001). p16 expression was seen in 40% (2/5) of esophageal dysplasia, 27% (4/15) of ESCC and 100% (5/5) of normal mucosa (p=0.016). Cyclin D1 expression was not significantly different among 20% (1/5) of esophageal dysplasia, 53% (8/15) of ESCC and 20% (1/5) of normal mucosa. Either the expression of p53 mutation or the loss of p16 occurred in 80% (4/5) of esophageal dysplasia and in 93% (14/15) of ESCC. CONCLUSIONS: The expression of p53 mutation and the loss of p16 might play a central role in the pathogenesis of esophageal squamous cell carcinoma (ESCC), and contribute to the development of precancerous lesion such as dysplasia. In addition, there is a possibility that the mutations of p53 and p16 silencing would be the early events in ESCC development. 相似文献
12.
目的探讨食管黏膜增殖凋亡和p53表达的增龄变化以及这些变化与食管鳞癌的关系。方法按年龄分层选择连续胃镜检查对象818例,男414例,女404例。分为青中年组(258例)、老年前期组(296例)和老年组(264例),进行食管活组织检查,应用TUNEL法检测凋亡指数(AI),免疫组化法检测增殖指数(PI)和p53表达。结果食管正常上皮→单纯增生→轻中重度异型增生→鳞癌的发展过程中,AI等级逐渐下降,PI等级和p53表达逐渐增高。在食管正常上皮中,AI等级青中年组〉老年前期组〉老年组;PI等级比较,老年前期组分别高于青中年组和老年组(P〈0.01);p53表达在老年前期组和老年组均高于青中年组(P〈0.01)。非条件logistic回归分析,食管鳞癌独立危险因素为增龄、PI等级和p53表达。当食管黏膜PI等级明显增高伴p53阳性时,鳞癌检出率明显增高,轻中重度异型增生有增高趋势,老年人尤为突出。结论食管黏膜正常上皮随增龄出现增殖凋亡和p53表达变化,与食管黏膜癌变过程变化相似,老年人食管黏膜PI明显增高伴p53阳性可作为食管鳞癌和癌前病变进一步随访和筛查的线索。 相似文献
13.
食管鳞癌组织p16基因调控区甲基化及其蛋白表达研究 总被引:2,自引:0,他引:2
目的探讨p16基因在食管癌变过程中表达缺失与其启动子区甲基化的关系。方法采用MSP免疫组化方法,检测环太行山地区45例食管鳞癌患者癌组织p16基因启动子区甲基化状态及蛋白表达情况。结果p16基因在癌组织中表达异常41例(91.1%),间变组织中表达异常38例(84.4%),发生纯合型甲基化的组织分别为33例(73.3%)(癌组织)和32例(71.1%)(间变组织),而其周围正常组织26例(57.8%)均发生了p16启动子区的杂合型甲基化。p16基因纯合型甲基化与癌组织、间变组织、p16蛋白表达缺失相关(P〈0.05)。结论该地区食管癌组织p16基因在癌前病变中p16启动子区即发生了纯合型甲基化、食管癌变的早期事件。p16基因启动子区甲基化可单独影响p16蛋白的正常表达。 相似文献
14.
Taghavi N Biramijamal F Sotoudeh M Moaven O Khademi H Abbaszadegan MR Malekzadeh R 《World journal of gastroenterology : WJG》2010,16(39):4958-4967
15.
16.
胃癌及癌前病变中p53蛋白的检测及意义 总被引:3,自引:0,他引:3
探讨p53蛋白表达与胃癌及癌病变的相互关系,方法:用免疫组化染色示检测33例肠化,26例异型增生和26例胃癌组织中p53蛋白的表达。结果:p53蛋白在胃癌组织中表达率最高(61.5%),在异型增生和肠化组织中的表达率分别为34.6%和12.1%,组间有显著差异,各期胃癌组织中p53蛋白的表达无显著差异,结论:p53蛋白在胃癌前病变中已有阳性表达,在肠化、异型增生及胃癌组织中,其表达率依次增高,p53蛋白积累主要发生在癌前病变晚期及胃癌早期,其表达与胃癌发生密切相关。 相似文献
17.
Yu LIU Hui-Xin Wang Ning Lu You-Sheng Mao Fang Liu Ying Wang Hai-Rong Zhang Kun Wang Min Wu Xiao-Hang Zhao 《World journal of gastroenterology : WJG》2003,9(4)
AIM: To investigate the alteration of the annexin I subcellular localization in esophageal squamous cell carcinoma (ESCC)and the correlation between the translocation and the tumorigenesis of ESCC.METHODS: The protein localization of annexin I was detected in both human ESCC tissues and cell line via the indirect immunofiuorescence strategy.RESULTS: In the normal esophageal epithelia the annexin I was mainly located on the plasma membrane and formed a consecutive typical trammels net. Annexin I protein also expressed dispersively in cytoplasm and the nuclei without specific localization on the nuclear membrane. In esophageal cancer annexin I decreased very sharply with scattered disappearance on the cellular membrane, however it translocated and highly expressed on the nuclear membrane,which was never found in normal esophageal epithelia. In cultured esophageal cancer cell line annexin I protein was also focused on the nuclear membrane, which was consistent with the result from esophageal cancer tissues.CONCLUSION: This observation suggests that the translocation of annexin I protein in ESCC may correlate with the tumorigenesis of the esophageal cancer. 相似文献
18.
Translocation of annexin I from cellular membrane to the nuclear membrane in human esophageal squamous cell carcinoma 总被引:5,自引:0,他引:5
Liu Y Wang HX Lu N Mao YS Liu F Wang Y Zhang HR Wang K Wu M Zhao XH 《World journal of gastroenterology : WJG》2003,9(4):645-649
AIM: To investigate the alteration of the annexin I subcellular localization in esophageal squamous cell carcinoma (ESCC) and the correlation between the translocation and the tumorigenesis of ESCC. METHODS: The protein localization of annexin I was detected in both human ESCC tissues and cell line via the indirect immunofluorescence strategy. RESULTS: In the normal esophageal epithelia the annexin I was mainly located on the plasma membrane and formed a consecutive typical trammels net. Annexin I protein also expressed dispersively in cytoplasm and the nuclei without specific localization on the nuclear membrane. In esophageal cancer annexin I decreased very sharply with scattered disappearance on the cellular membrane, however it translocated and highly expressed on the nuclear membrane, which was never found in normal esophageal epithelia. In cultured esophageal cancer cell line annexin I protein was also focused on the nuclear membrane, which was consistent with the result from esophageal cancer tissues. CONCLUSION: This observation suggests that the translocation of annexin I protein in ESCC may correlate with the tumorigenesis of the esophageal cancer. 相似文献
19.
胃癌前病变不同转归中p53,bcl—2基因的表达以及细胞增?… 总被引:5,自引:0,他引:5
目的 探讨p53、bcl-2基因和增殖细胞核抗原(PCNA)等生物学指标在胃癌前病变不同转归中的作用。方法 采用免疫组化(LSAB)法检测52例胃癌患者胃癌及癌的病变组织标本及56例非胃癌患者有病变「胃黏膜中度以上肠上皮化生和(或)异型增生」组织标本的p53、bcl-2和PCNA的表达。结果 ⑴在癌前病变中,p53、bcl-2在癌组与非癌组之间的表达差异无显著性(p〉0.05),PCNA标记指数( 相似文献
20.
S. L. Zhou W. B. Yue Z. M. Fan F. Du B. C. Liu B. Li X. N. Han J. W. Ku X. K. Zhao P. Zhang J. Cui F. Y. Zhou L. Q. Zhang X. P. Fan Y. F. Zhou L. L. Zhu H. Y. Liu L. D. Wang 《Diseases of the esophagus》2014,27(8):790-797
The aim of this study was to evaluate the diagnostic values by detecting sera autoantibodies to eight tumor‐associated antigens (TAAs) of P53, IMP1, P16, cyclin B1, P62, C‐myc, Survivn and Koc full‐length recombinant proteins for the screening of high‐risk subjects and early detection of esophageal squamous cell carcinoma (ESCC). Enzyme‐linked immunosorbent assay was used to detect autoantibodies against the eight selected TAAs in 567 sera samples from four groups, including 200 individuals with normal esophageal epithelia (NOR), 214 patients with esophageal basal cell hyperplasia (BCH), 65 patients with esophageal dysplasia (DYS), and 88 patients with ESCC. In addition, the expression of the eight antigens in esophageal tissues was analyzed by immunohistochemistry. Statistically significant distribution differences were identified among the four groups for each of the individual autoantibodies to six TAAs (P53, IMP1, P16, cyclin B1, P62, and C‐myc); the detection rates of antoantibodies were positively correlated with the progression of ESCC. When autoantibody assay successively accumulated to six TAAs (P53, IMP1, P16, cyclin B1, P62, and C‐myc), a stepwise increased detection frequency of autoantibodies was found in the four sera groups (6% in NOR, 18% in BCH, 38% in DYS, and 64% in ESCC, respectively), the risks to BHC, DYS, and ESCC steadily increased about 3‐, 9‐, and 27‐folds. The sensitivity and the specificity for autoantibodies against the six TAAs in diagnosing ESCC reached up to 64% and 94%, respectively. The area under the receiver operating characteristic curve for the six anti‐TAA autoantibodies was 0.78 (95% confidence interval 0.74–0.83). No more increasing in sensitivity was found with the addition of new anti‐TAA autoantibodies. A combination detection of autoantibodies to TAAs might distinguish ESCC patients from normal individuals and the patients with esophageal precancerous lesions. 相似文献