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鼻咽癌p16蛋白和VEGF表达及与临床的相关性 被引量:2

Expression of p16 Protein and VEGF in Nasopharyngeal Carcinoma and its Clinical Significance
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摘要 目的 探讨p16蛋白和VEGF在鼻咽癌组织中的表达及与鼻咽癌生物学行为的关系。方法 采用免疫组化S P法 ,检测 p16蛋白和VEGF在 70例鼻咽癌和 31例鼻咽粘膜炎性组织中的表达。 结果 鼻咽癌组织 p16蛋白阳性表达率明显低于鼻咽粘膜炎组织 (P <0 .0 5 ) ;Ⅰ和Ⅱ期患者 p16蛋白阳性表达率稍高于Ⅲ和Ⅳ期患者 ,但无统计学意义 (P >0 .0 5 ) ;p16蛋白表达与颈淋巴结转移及放疗后复发和转移无关 (P >0 .0 5 )。鼻咽癌和鼻咽粘膜炎组织中VEGF的表达无显著差异 (P >0 .0 5 ) ;VEGF表达与鼻咽癌临床分期、颈淋巴结转移及放疗后复发和转移无关 (P >0 .0 5 )。结论 p16蛋白的低表达可能涉及鼻咽癌的发生和发展过程。 Objective To investigate the expression of p16 protein and VEGF and its correlation to clinic biological behavior of nasopharyngeal carcinoma (NPC). Methods Expression of p16 protein and VEGF were examined by immunohistochemical staining S-P in 70 cases of NPC and 31 cases of inflammatory nasopharyngeal mucosa. Results The positive expression rate of p16 protein in NPC was significantly lower than it in inflammatory nasopharyngeal mucosa (P< 0.05). The positive expression rate of p16 protein of stageⅠand Ⅱ patients was higher than that of stage Ⅲ and Ⅳ patients, but no statistic significance was observed (P> 0.05). There was no significant relationship between the expression of p16 protein and lymph node metastasis and post-radiotherapy tumor recurrence and metastasis (P> 0.05). No significant difference in the positive expression rate of VEGF was observed between NPC and inflammatory nasopharyngeal mucosa (P> 0.05) and there was no significant correlation between the expression of VEGF and clinical staging, lymph node metastasis as well as post-radiotherapy tumor recurrence and metastasis in NPC. Conclusion Reduced expression of p16 protein may be associated with the carcinogenesis and development of NPC.
出处 《肿瘤防治研究》 CAS CSCD 2004年第3期142-144,共3页 Cancer Research on Prevention and Treatment
基金 深圳市卫生科技计划项目 (2 0 0 0 0 4 0 5 5 )
关键词 鼻咽癌 P16蛋白 VEGF 病理特点 肿瘤生物学 免疫组化SP法 炎性组织 肿瘤转移 Nasopharyngeal carcinoma p16 protein VEGF
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  • 1傅松滨.多重肿瘤抑制基因MTS1/p16CDK4I与细胞周期调节[J].国外医学(遗传学分册),1996,19(1):7-13. 被引量:30
  • 2[1]Diaz MO, Rubin CM, Harden A, et al. Deletions of interferon genes in acute lymphoblastic leukemia. N Engl J Med, 1990, 322(2): 77
  • 3[2]James CD, He J, Collins VP, et al. Localization of chromosome 9p homozygous in glioma cell lines with markers constituting a continuous linkage group. Cancer Res, 1993, 53(16): 3674
  • 4[3]Cheng Jinquan, Jhanwar SC, Lu Youyong, et al. Homozygous deletions within 9p21-p22 identify a small critical region of chromosomal loss in human malignant mesotheliomas. Cancer Res, 1993, 53(20): 4761
  • 5[4]Kamb A, Gruis N, Weaner-Feldhaus J, et al. A cell cycle regulator potentially involved in genesis of many tumor types. Science, 1994,15(264): 436
  • 6[5]Noborl T, Miura K, Wu DJ, et al. Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers. Nature, 1994,368(6473): 753
  • 7[6]Hirama T, Koeffler HP. Role of the cyclin-dependent kinase inhibitors in the development of cancer. Blood, 1995, 88 (3): 841
  • 8[7]Serrano M, Hannon GT, Beach D. A new regulation motif in cell cycle control causing special inhibition of cyclinD/CDK4. Nature,1993, 366(6456): 704
  • 9[8]Lew DJ, Dulic V, Reed SI. Isolation of three novel human cyclins by rescue of G1 cyclin function in yeast. Cell, 1991,66(165):1197
  • 10[9]Yang Rong, Gombart AF, Serrano M, et al. Mutational effects on the p16INK4a tumor suppression protein. Cancer Res, 1995, 55(15):2503

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