期刊文献+

乳腺良恶性病变组织端粒长度和端粒酶活性检测 被引量:2

Telomere length and telomerase activity in benign and malignant breast tumor
下载PDF
导出
摘要 目的 比较乳腺良恶性病变端粒长度改变及其在肿瘤发生发展中的意义 ;探讨端粒酶活性与临床病理参数的关系及其在乳腺癌诊断中的价值。方法 Southern印迹杂交检测TRF长度 ,端粒重复扩增分析 (TRAP)方法检测端粒酶活性。结果 乳腺癌组织平均TRF为 (5 2± 2 8)kb ,与正常组织比较明显缩短 (P <0 0 0 1) ,从正常乳腺组织到乳腺良性病变、乳腺原位癌及浸润性癌平均TRF呈递减趋势。 5 8例乳腺癌中 4 9例端粒酶阳性 (84 7% ) ,端粒酶活性与临床病理参数无相关性 ;癌旁组织端粒酶为阴性 ,而 7例乳腺增生症和 6例乳腺纤维腺瘤中分别有 1例端粒酶阳性 ,与乳腺癌比其差异有显著性 (P <0 0 0 1)。结论 端粒长度在肿瘤发生发展过程中渐进性缩短 ,并最终触发端粒酶的激活 ; Purpose To study the significance of telomere length alteration in carcinogenesis and the relationship of telomerase activity with clinicopathological parameters and it's value in diagnsis of breast cancer. Methods Telomeric restriction fragment (TRF) length were measured by Southern blot analysis. Telomerase activity were detected by telomeric repeat amplification protocol (TRAP) method. Results The mean TRF length of breast cancer was (5.2±2.8) kb, and was significantly shortened comparing to adjacent noncancerous tissue (P<0.001). The mean TRF length showed tendency of decreasing progressively from normal tissue to benign breast lesions to in situ carcinoma to invasive carcinoma. Telomerase activity was detected in 49 of 58 (84.7%) cases of breast cancer by TRAP method. There was no correlation between telomerase activity and clinical pathology parameters. The telomerase activity of adjacent noncancerous tissue was absent, while the activity was detected in 1 of 6 (16.7%) fibroadenomas and 1 of 7 (14.3%) fibrocystic disease., they all exhibited significant differences comparing with breast carcinomas (P<0.001) . Conclusions Telomere shortened gradually in the development of tumors and triggered the activation of telomerase. Detection of telomerase activity by TRAP method is useful in the diagnosis of malignant tumors.
出处 《临床与实验病理学杂志》 CAS CSCD 2004年第2期206-209,共4页 Chinese Journal of Clinical and Experimental Pathology
关键词 乳腺良恶性病变 端粒长度 端粒酶活性 检测 诊断 breast neoplasms telomere telomerase
  • 相关文献

参考文献8

  • 1Blackburn EH. Structure and function of telomeres. Nature,1991, 350(6319): 569-73.
  • 2Greider CW, Blackburn EH. Telomeres, telomerase and cancer.SciAm, 1996, 274(2): 92~7.
  • 3Ducray C, Pommier JP, Martins L, et al. Telomere dynamics,end-to-end fusions and telomerase activation during the human fibroblast immortalization process. Oncogene, 1999, 18 (29):4211~23.
  • 4Kim NW, Piatyszek MA, Prowse KR, etal. Specific association of human telomerase activity with immortal cells and cancers.Science, 1994 ,266: 2011~5.
  • 5Hiyama k, Ishioka S, Shay JW, et al. Telomerase activity as a marker of lung cancer and immune-associated lung diseases. Int J Mol Med, 1998, 1(3): 545~9.
  • 6Kyo S, Takakura M, Tanaka M, etal. Quantitative differences in telomerase activity among malignant, premalignant, and benign ovarian lesions. Clin Cancer Res, 1998, 4(2):399~405.
  • 7Sakabe H, Yahata N, Kimura T, et al. Human cord blood-derived primitive progenitors are enriched in CD34+c-kit-cells:correlation between long-term culture-initiating cells andtelomerase expression. Leukemia, 1998 ,12(5):728~34.
  • 8Nawaz S, Hashizumi TL, Markham NE, et al. Telomerase expression in human breast cancer with and without lymph node metastasis. Anatomic Pathol, 1997 ,107(5): 542~7.

同被引文献8

引证文献2

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