期刊文献+

肺癌纤维支气管镜刷落细胞中p16基因外显子2丢失的研究 被引量:1

Deletion of p16 gene exon 2 in bronchofibroscopic brush-off cells of human lung carcinoma
下载PDF
导出
摘要 目的 :探讨 p16基因外显子 2丢失与原发性肺癌发生发展之间的相关性 ,以及纤维支气管镜刷落细胞中检测 p16基因外显子 2丢失代替手术标本检测的可行性。方法 :在纤维支气管镜毛刷脱落细胞中采用 PCR-电泳-紫外成像条带密度扫描法 ,以β- actin基因为内对照 ,检测及分析病理证实的原发性肺癌患者病灶侧与其相对正常侧 p16基因外显子 2丢失的情况。结果 :p16基因外显子 2丢失率在肺癌患者相对正常侧毛刷脱落细胞中为 0 ( 0 /19 ) ,在病灶侧毛刷脱落细胞中为 35.5% ( 11/31) ,两者比较有统计学显著差异 ( P<0 .0 1)。小细胞肺癌 ( SCLC)标本中丢失率为 0 ( 0 /7) ,非小细胞肺癌 ( N SCLC)标本中丢失率为 50 % ( 11/2 2 ) ,两者比较有统计学显著差异 ( P<0 .0 5)。结论 :p16基因外显子 2丢失可能与 N SCLC的发生发展相关。纤维支气管镜直视下病灶处毛刷脱落细胞检测 p16基因外显子 2丢失率可代替手术标本以协助术前诊断与治疗。 Objective: To analyze the relationship between deletion of p16 gene exon 2 and lung cancer and to evaluate the possibility of detecting p16 gene exon 2 deletion in brush off cell instead of resected lung cancer mass. Methods: p16 gene exon 2 deletion in bronchofibroscopic brush off cells of lesion side and corresponding normal side was detected through PCR electrophoresis Image. Image value of p16 Vs β actin ≤0.5 was considered as p16 gene exon 2 deletion. Results: The rate of p16 gene exon 2 deletion in normal side was 0(0/19), whereas in lesion side was 35.5%(11/31), there is a significant statistical difference( P <0.01). In SCLC(small cell lung carcinoma) samples, the rate of p16 gene exon 2 deletion was 0(0/7), whereas in NSCLC(non small cell lung carcinoma) samples, that was 50%(11/12)( P <0.05). Conclusions: p16 gene exon 2 deletion might be related to the oncogenesis and development of lung carcinoma, especially NSCLC. Brush off cell specimens may replace surgical specimens in Detecting p16 gene exon 2 deletion.
出处 《浙江大学学报(医学版)》 CAS CSCD 2002年第4期250-253,共4页 Journal of Zhejiang University(Medical Sciences)
关键词 肺癌 纤维支气管镜 刷落细胞 P16基因 外显子2丢失 基因缺失 Lung neoplasma/pathol Gene, p16 Gene deletion Exons Bronchofibroscope
  • 相关文献

参考文献9

  • 1LV Gui-quan, CHEN Xu-feng, CAO Wei(吕桂泉,陈旭峰,曹巍). Clinical significance and district difference of P16 gene aberration in esophageal squamous cell carcinoma [J].Chinese Journal of Oncology(中华肿瘤杂志),1999,21(5):359-362. (in Chinese)
  • 2Kelly M J, Nakagawa K, Steinberg S M, et al. Differational Inactivation of CDKN2 and Rb protein in non-small-cell and small-cell lung cancer cell lines [J]. J Natl Cancer Inst,1995,87(10):756-761.
  • 3Shapiro G I, Edwards C D, Kobzik L, et al. Reciprocal Rb inactivation and P16INK4 expression in primary lung cancers and cell lines [J]. Cancer Res,1995,55(3):505-509.
  • 4Taga S, Osaki T, Ohgami A, et al. Prognostic value of the immunohistochemical detection of p16 INK4 expression in Non small cell lung carcinoma [J]. Cancer,1997,80(3):389-395.
  • 5Washimi O, Nagatake M, Osada H, et al. In vivo occurrence of p16(MTS1) and P15(MTS2) alterations preferentially in non small cell lung cancer [J]. Cancer Res,1995,55(1):514-517.
  • 6Spanakis N E, Gorgoulis V, Mariatos G, et al. Aberrant p16 expression is correlated with hemizygous deletions at 9P21-22 chromosome region in non-small cell lung carcinomas [J]. Anticancer Res, 1999,19(3A):1893-1899.
  • 7钟晓松,许凯黎,廖美琳,丁嘉安,关赛芳,周瑾.原发性非小细胞肺癌p16基因的丢失研究[J].肿瘤,1997,17(2):81-83. 被引量:10
  • 8Jin X, Nguyen D, Zhang W, et al. Cell cycle arrest and inhibition of tumor cell proliferation by the p16 INK4 gene mediated by an adenovirus vector [J]. Cancer Res,1995,55(15):3250-3253.
  • 9付晓颖,张颂文,冉瑞琼,申宗候,顾建新,曹世龙.外源性p16基因对wtp53型人肺腺癌细胞生长的影响[J].中华肿瘤杂志,1999,21(2):102-104. 被引量:5

二级参考文献5

共引文献13

同被引文献26

  • 1KAMB A, GRUIS N A, WEAVER - FELDHAUS J,et al. A cell cycle regulator potentially involved in genesis of many tumor types [J]. Science, 1994, 264(5157): 436.
  • 2MOTOKURA T, BLOOM T, KIM H G, et al. A novel cyclin encoded by a bcl1-linked candidate oncogene[J]. Nature, 1991, 350 (6318): 512.
  • 3WEINBERG R A. The retinoblastoma protein and cell cycle control[J]. Cell, 1995,81(3):323.
  • 4JIN X, NGUYEN D, ZHANG W W, et al. Cell cycle arrest and inhibition of tumor cell proliferation by the p16INK4 gene mediated by an adenovirus vector[J]. Cancer Res, 1995, 55(15): 3250.
  • 5WELCKER M, LUKAS J, STRAUSS M, et al. Enhanced protein stability: a novel mechanism of D-type cydin over - abundance identified in human sarcoma calls [J]. Oncogene, 1996, 13(2): 419.
  • 6ZHOU P, JIANG W, ZHANG Y J, et al. Antisense to cyclin D1 inhibits growth and reverses the transformed phenotype of human esophageal cancer cells[J]. Oncogene, 1995, 11(3): 571.
  • 7REED A L, CALIFANO J, CAIRNS P, et al. High frequency of p16 (CDKN2/MTS - 1/INK4A) inactivation in head and neck squamous cell carcinoma [J].Cancer Res, 1996, 56(16): 3630.
  • 8WASHIMI O, NAGATAKE M, OSADA H, et al.In vivo occurrence of p16 (MTS1) and p15 (MTS2)alterations preferentially in non - small cell lung cancers [J]. Cancer Res, 1995, 55(3): 514.
  • 9NAKAGAWA K, CONRAD N K, WILLIAMS J P,et al. Mechanism of inactivation of CDKN2 and MTS2 in non - small cell lung cancer and association with advanced stage [J]. Oncogene, 1995, 11(9):1843.
  • 10TAGA S, OSAKI T, OHGAMI A, et al. Prognostic value of the immuno-histochemical detection of p16INK4 expression in nonsmall cell lung carcinoma[J]. Cancer, 1997, 80(3): 389.

引证文献1

二级引证文献1

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