期刊文献+

胰腺良恶性组织p16基因缺失突变和蛋白表达

Study in the Deletion or Mutation and Expression of P16 Gene in Benign and Malignant Pancreatic Tissues
在线阅读 下载PDF
导出
摘要 目的:旨在从分子水平探讨p16基因在胰腺组织中缺失突变和蛋白表达情况及其与临床病理的联系。方法:利用免疫组织化学染色ABC法及聚合酶链反应-单链构象多态性(PCR-SSCP)分析技术分别检测29例胰腺良性组织和54例胰腺癌组织中p16蛋白表达和基因缺失突变情况。结果:正常胰腺及良性病变组织中p16蛋白表达率为75.86%,显著高于胰腺癌组织p16蛋白表达率(40.74%)(P<0.005),临床分期中Ⅰ、Ⅱ期p16蛋白表达率(68.18%)高于Ⅲ、Ⅳ期病例(21.88%)(P<0.05)。p16基因缺失突变率良性组织(10.34%)低于胰腺癌组织(42.59%)(P<0.005)。Ⅰ、Ⅱ期癌组织(18.18%)低于Ⅲ、Ⅳ期癌组织(59.38%)(P<0.05)。在胰腺癌不同病理类型及不同组织学分化程度中p16蛋白表达和基因缺失突变无明显差别。结论:p16基因缺失突变和蛋白表达的检测可作为胰腺癌预后评定的一个分子生物学指标。 Objective: To investigate the deletions or mutations and protein ex pression of p16 antioncogene and its relationship with clinical pathology at molecular level in pancreatic tissue. Methods:29 cases of benign pancreatic tissue and 54 cases of pancreatic carcinoma were analyzed for genetic deletions or mutations and protein expression of p16 by immunohistochemical staining and polymerase chain reaction-single stranded co nformation polymorphism (PCR-SSCP) respectively. Results:The frequency of p16 prot ein expression in normal and benign tissue(75.86% )was markedly high- er than that in pancreatic carcinoma(40.74% ) (P<0.005). The expression o f p16 protein in Ⅰ and Ⅱ stages (68.18%) in pancreatic carcinoma was higher than that in Ⅲ and Ⅳ stages(21.88%) (P<0. 05). The deletion or mut ation rate of p16 in benign tissue (10.34%) was lower than that in pancreatic car cinoma(42.59% ) (P<0.005). In pancreatic cancer, the frequency of deletions and mutations of p16 in Ⅰ and Ⅱ stages (18.18%)was lower than that in Ⅲ and Ⅳ stages (59.38%) (P<0.05). In addition,no correlati on was found between the deletions or mutations and expression of p16 and variou s pathological types or histodifferentiation. Conclusion:The detection of the d eletions or mutations and ex- pression of p16 could be regarded as a molecular biolo gical parameter for the prognosis of patients with pancreatic carci- noma.
出处 《中国误诊学杂志》 CAS 2004年第6期827-829,共3页 Chinese Journal of Misdiagnostics
关键词 胰腺肿瘤 遗传学 基因 p16 蛋白质p16/遗传学 免疫组织化学 聚合酶链反应 基因缺失 突变 Pancreatic neoplasms/genetics Gene,p16 Protein p16/genetics Immunohistochemistry Polymerase reaction Gene defection Mutation
  • 相关文献

参考文献12

  • 1冉瑞琼,傅晓颖,曹晓运,周决,曹世龙.P^(16)抑癌基因产物在肺癌中的表达及临床意义[J].上海医科大学学报,1997,24(2):83-86. 被引量:14
  • 2Kamb A,Gruis NA,Weaver-Feldhaus J,et al. A cell cycle regulator potentially involved in genesis of many tumor types[J]. Science, 1994,264 (5157): 436-440.
  • 3Spruck I CH,Gonzalez-Zulueta M,Shibata A,et al. p16 gene in uncultured tumors[J]. Nature, 1994,370(6486): 183-184.
  • 4Marx J. A challenge to p16 gene as a major tumor suppressor[J]. Science, 1994,264 (5167): 1846.
  • 5Marx J. New tumor suppressor may rival p53[J]. Science,1994,264 (5157): 344-345.
  • 6Naumann M,Savitskaia N,Eilert C,et al. Frequent codeletion of p16/MTS1 and p15/MTS2 and genetic alterations in p16/MTS1 in pancreatic tumors [J]. Gastroenterology, 1996,110 (4): 1215-1224.
  • 7Hirama T,Koeffler HP. Review article:Role of the cyclin-dependent kinase inhibitors in the development of cancer [J].Blood, 1995,86(3): 841-854.
  • 8Hahn SA, Kern SE. Molecular genetics of exocrine pancreatic neoplasms[J]. Pancreatic neoplasms ,1995,75(5) :857-869.
  • 9Marchini S,Codegoni AM,Bonazzi C,et al. Absence of deletions but frequent loss of expression of p16INK4 in human ovarian tumours[J]. Br J Cancer, 1997,76(2): 146-149.
  • 10Serrano M,Hannon GJ,Beach D. A New regulatory motif in cell cycle control causing specific inhibition of cyclin D/CDK4[J]. Nature, 1993,366 (6456): 704-707.

二级参考文献17

  • 1Herman JG, Merlo A, Mao L, et al. Inactivation of the CDKN2/P16/MTS1 gene is frequently associated with aberrant DNA methylation in all human cancer. Cancer Res, 1995,55 (20) : 4525-453O.
  • 2Nobori T, Miura K, Wu DJ, et al. Deletion of the eyelin-dependent kinase-4 inhibitor gene in multiple human cancer. Nature,1994,368(6473) : 753-756.
  • 3Kamb A,Gruis N, Weaver-Feldhaus J, et al. A cell cycle regulatorpotentially: involved in genesis of many tumor types. Science,1994,264(5157) :436-440.
  • 4Zhou X,Tarmin L,Yin J, et al. The MTS1 gene is frequently mutated in primary human esophageal tumor. Oncogen, 1994,9(12):3737-3741.
  • 5Liu L,Lassam NJ ,Slingerlang JM, et al. Germlin p16INK4a mutation and protein dysfunction in a family with inherited melanoma. Oncogene ,1995,11 (2) :405-412.
  • 6Bookstein R,Rio R,Mareperla SA, et al. Promoter deletion and loss of retinoblastoma gene expresion in human prostate carcinoma. Pro Natl Acad Sci USA,1990,87(19):7762-7766.
  • 7Yokote J, Akiyama T, Fung YK,et al. Altered expression of the retinoblastoma (RB) gene in small-cell carcinoma of the lung.Oncogene, 1988,3(4) :471-475.
  • 8Tam SW, Shay JW, Pagano M. Differential expression and cell cycle regulation of the cyclin-dependent kinase 4 inhibitor p16INK4. Cancer Res,1994,54(17) :5816-5820.
  • 9Li Yan. Nichols MA,Shay JW,et al. Transcriptional repression of the D-type cyclin-dependent Kinase inhibitor p16 by the retinoblastoma susceptibility gene product pRB. Cancer Res,1994,54 (23) : 6078-6082.
  • 10Shapiro GI,Edwards CD,Kobzik L, et al. Reciprocal RB inactivation and p16INK4 expression in primary lung cancers and cell lines. Cancer Res,1995,55(3):505-509.

共引文献16

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部