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食管鳞癌中PTEN和Ki-67蛋白的表达
作者:李俐1 卜晓东2 樊克武1 
单位:1.南京医科大学附属南京第一医院,病理科,江苏,南京,210006; 2.东南大学基础医学院,病理学与病理生理学系,江苏,南京,210009
关键词:食管肿瘤 基因 抑制 肿瘤 Ki-67抗原/生物合成 免疫组织化学/方法 
分类号:R392.11, R392.31, R735.1, Q343
出版年·卷·期(页码):2003·22·第四期(264-265)
摘要:

目的:探讨食管鳞癌中PTEN和Ki-67蛋白表达情况及其临床意义.方法:采用SP免疫组织化学法对65例食管鳞癌标本进行了检测.结果:65例食管鳞癌中PTEN蛋白的阳性率为58.46%(38/65),高、中分化组与低分化组相比,有显著性差异(P<0.05).并且,食管鳞癌中PTEN与Ki-67蛋白表达之间存在显著的负相关关系(P<0.05).结论:PTEN基因的缺失或突变在食管鳞癌的发生发展中可能起重要作用,且与肿瘤恶性分化程度及细胞增殖情况密切相关.

Objective  To investigate the expression of PTEN and Ki?67 protein in esophageal squamous cancer and their clinical significance.Methods  Sixty-five cases of esophageal squamous cancer were examined by S?P immunohistochemical method.Results  The expression of PTEN in 58.46% esophageal squamous cancer (38/65) was positive.The level of PTEN expression increased in well and moderately differentiated groups compared with the poorly differentiated group(P&lt;0.05).An inverse correlation was observed between the expression of PTEN and Ki?67 protein in esophageal squamous cancer (P&lt;0.05).Conclusion  Deletion or mutation of PTEN may play an important role in the development of esophageal squamous cancer,and may be closely related to the differentiation and cellular proliferation of carcinoma.

参考文献:

[1] Li J, YEN C, LIAN D. PTEN,aputive protein tyrosine phosphatase gene mutated in human brain,breast and prostate cancer. 1997(5308). doi:10.1126/science.275.5308.1943
[2] Steck P A, PERSHOUS M A, JASSER S A. Identification of a candidate tumor suppressor gene,MMAC1 at chromosome 10q23.3 that is mutated in multiple advanced cancers. 1997(4). doi:10.1038/ng0497-356
[3] Li D M, SUN H. PTEN/NNAC1/TEP1suppresses the tunorigenicity and induces G1 cell cycle arrest in hunan glioblastoma cells, 1998(95)
[4] FURNARI F B, HUANG H J, CAVENEE W K. The phosphoinositol phosphatase activity of PTEN mediates a serum sensitive G1 growth arrest in glioma cells. 1998(22)
[5] Maehama T, DIXON J E. PTEN:a tumor suppressor that functions as a phospholipid phosphatase. 1999(4). doi:10.1016/S0962-8924(99)01519-6 

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