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TRAIL在食道鳞癌及癌旁组织中的表达 被引量:1

Expression of TRAIL in esophageal squamous cell cancer and the surrounding tissues
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摘要 目的 研究人肿瘤坏死因子相关凋亡诱导配体 (TNF relatedapoptosisinducingligand ,TRAIL)在食道鳞癌及癌旁组织中的表达及意义。方法 采用免疫组化S -P法 ,检测 42例食道鳞状细胞癌及其癌旁组织中TRAIL蛋白表达水平。结果 TRAIL在正常食道粘膜上皮、单纯增生、不典型增生、鳞癌组织中其阳性表达呈递减趋势 (P <0 .0 1) ;在Ⅰ、Ⅱ级鳞癌明显高于Ⅲ级和未分化鳞癌 (P <0 .0 1)。而在早期鳞癌和晚期鳞癌中的表达无差异 (P >0 .0 5 )。伴有淋巴结转移组和无转移组之间无差异 (P >0 .0 5 )。结论 TRAIL的表达可能与食道鳞癌的发生、发展密切相关 ;与食道鳞癌的分级呈负相关 ;与癌组织浸润深度和淋巴结转移无关。 Objective To study the expression and significance of TNF-related apoptosis inducing ligand (TRAIL) in esophageal squamous cell cancer and the surrounding tissues. Methods S-P immunohistochemical technique was used to examine the expression of TRAIL in 42 cases of esophageal squamous cell cancer and the surrounding tissues.Results TRAIL immunoreactivity decreased progressively from normal esophageal mucosa, simple hyperplasia, atypical hyperplasia to squamous carcinoma tissues (P<0.01). The TRAIL expression levels in esophageal squamous cell cancer of grade Ⅰ and Ⅱ were higher than those in esophageal squamous cell cancer of grade Ⅲ and undifferentiation tumor (P<0.01). There were no significant differences between early cancer and advanced cancer. Meanwhile, we found no differences in expression of TRAIL between lymph node metastasis group and non-lymph node metastasis group (P>0.05). Conclusion TRAIL may be related to the occurrence and development of esophageal squamous cell cancer. The expression of TRAIL in esophageal cancer has negative correlation with the cancer tissue differentiation grade, and has no relationship with neither cancer invasion nor lymph node metastasis.
出处 《西安交通大学学报(医学版)》 CAS CSCD 北大核心 2002年第5期447-449,共3页 Journal of Xi’an Jiaotong University(Medical Sciences)
关键词 TRAIL 食道鳞癌 癌旁组织 细胞凋亡 免疫组化 肿瘤坏死因子 esophagus squamous carcinoma TRAIL apoptosis immunohistochemistry
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  • 1李秀林,苏宝山.39例早期胃癌的免疫组化及粘液组化观察[J].西安医科大学学报,1993,14(4):327-330. 被引量:2
  • 2黄晓明.Bcl-2及其相关蛋白与细胞凋亡的调节[J].国外医学(分子生物学分册),1997,19(1):16-19. 被引量:18
  • 3[2]Park JR, Robertson K, Hickstein DD ,et al. Dysregulated Bcl-2 expression inhibits apoptosis but not differentiation of retinoic acid-induced HL-60 granulocytes [J], Blood,1994,84(2): 440.
  • 4[3]Oltvai ZN, Milliman CL and Korsmeyer SL. Bcl-2 heterodimerizes in vivo with a conserved homology, bax ,that accelerates programmed cell death[J]. Cell , 1993,74: 609.
  • 5[5]Krajewski S,Blomqvist C, franssila K ,et al. Reduced expression of proapoptotie gene bax is associated with poor response rates to combination chemotherapy and shorter survival in woman with metastatic breast adenoearcinoma [J].Caneer Res, 1995,55(19): 4471.
  • 6Griffith T S,J Immunol,1998年,161卷,10期,2833页
  • 7Bedi A, Pasricha PJ, Akhtar AJ, et al. Inhibition of apoptosis during development of colorectal cancer. Cancer Res, 1995, 55:1811-1816.
  • 8Oltval ZN, Milliman CL, Korsmeyer SJ. Bcl-2 heterodimerizes in vivo with a conserved homolog, bax, that accelerates programed cell death. Cell, 1993,74:609-619.
  • 9Yin XM, Oltval ZN, Korsmeyer SJ. BH1 and BH2 domains of bcl-2 are reqired for inhibition of apoptosis and heterodimerization with bax, Nature, 1994,369:321-327.
  • 10King ED, Matteson J, Jacobs SC, et al. Incidence of apoptosis cell proilferation and bcl-2 expression in transitional cell carcinoma of the bladder: Association with tumor progression, J Urol,1996,155(1):316-320.

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