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癌前及肿瘤性胃和结肠病变中的端粒酶活性

Telomerase activity in preneoplastic and neoplastic gastric and colorectal lesions.

作者信息

Tahara H, Kuniyasu H, Yokozaki H, Yasui W, Shay J W, Ide T, Tahara E

机构信息

Department of Cellular and Molecular Biology and First Department of Pathology, Hiroshima University School of Medicine, 1-2-3 Kasumi, Minami-Ku, Hiroshima 734, Japan.

出版信息

Clin Cancer Res. 1995 Nov;1(11):1245-51.

PMID:9815918
Abstract

Recent evidence indicates that telomerase activity may be necessary for cell immortality, which is required for the sustained and indefinite growth of most malignant cells. We analyzed telomerase activity in gastric and colorectal cancers and in gastric and colorectal precancerous lesions to determine whether malignant progression depends on the activation of telomerase and at what stage of carcinogenesis cells have detectable telomerase activity. Telomerase activity was measured by the telomeric repeat amplification protocol assay and was detected in 17 (85%) of 20 primary gastric carcinoma tissues and in 19 (95%) of 20 primary colorectal carcinomas, regardless of tumor staging and histological types. All nodal metastases, peritoneal metastases, and a recurrent gastric cancer tumor were positive. All cell lines established from gastric and colorectal cancers contained telomerase activity. In precancerous lesions, 10 (100%) of 10 colorectal tubular adenomas were telomerase positive, in addition to 3 (23%) of 13 gastric intestinal metaplasias and 1 (50%) of 2 gastric adenomas, whereas the corresponding gastric normal mucosas as well as colorectal mucosas were negative. These results indicate overall that reactivation of telomerase may occur at an early stage of carcinogenesis and may correlate well with malignant progression of gastric cancer. Telomerase activity thus may serve as a powerful additional tool for cancer diagnosis.

摘要

最近的证据表明,端粒酶活性可能是细胞永生化所必需的,而细胞永生化是大多数恶性细胞持续和无限生长所需要的。我们分析了胃癌和结直肠癌以及胃癌和结直肠癌癌前病变中的端粒酶活性,以确定恶性进展是否依赖于端粒酶的激活,以及在致癌过程的哪个阶段细胞具有可检测到的端粒酶活性。通过端粒重复序列扩增法检测端粒酶活性,在20例原发性胃癌组织中的17例(85%)以及20例原发性结直肠癌中的19例(95%)检测到端粒酶活性,无论肿瘤分期和组织学类型如何。所有的淋巴结转移、腹膜转移以及一例复发性胃癌肿瘤均呈阳性。所有从胃癌和结直肠癌建立的细胞系都含有端粒酶活性。在癌前病变中,10例大肠管状腺瘤中的10例(100%)端粒酶呈阳性,此外,13例胃黏膜肠化生中的3例(23%)以及2例胃腺瘤中的1例(50%)端粒酶呈阳性,而相应的胃正常黏膜以及结肠黏膜均为阴性。这些结果总体表明,端粒酶的重新激活可能发生在致癌过程的早期,并且可能与胃癌的恶性进展密切相关。因此,端粒酶活性可能作为癌症诊断的一个有力辅助工具。

相似文献

1
Telomerase activity in preneoplastic and neoplastic gastric and colorectal lesions.癌前及肿瘤性胃和结肠病变中的端粒酶活性
Clin Cancer Res. 1995 Nov;1(11):1245-51.
2
Telomerase and telomere length in the development and progression of premalignant lesions to colorectal cancer.端粒酶与端粒长度在癌前病变发展为结直肠癌过程中的作用
Clin Cancer Res. 1997 Nov;3(11):1931-41.
3
Telomerase activity and hTERT mRNA in development and progression of adenoma to colorectal cancer.端粒酶活性及人端粒酶逆转录酶mRNA在腺瘤向结直肠癌发展及进展过程中的作用
Int J Mol Med. 2002 Aug;10(2):205-10.
4
Telomerase activation in colorectal carcinogenesis.端粒酶激活在结直肠癌发生过程中的作用
J Pathol. 1999 Oct;189(2):207-12. doi: 10.1002/(SICI)1096-9896(199910)189:2<207::AID-PATH424>3.0.CO;2-H.
5
Relative contribution of normal and neoplastic cells determines telomerase activity and telomere length in primary cancers of the prostate, colon, and sarcoma.正常细胞和肿瘤细胞的相对贡献决定了前列腺癌、结肠癌和肉瘤原发性肿瘤中的端粒酶活性和端粒长度。
Clin Cancer Res. 1997 Oct;3(10):1849-57.
6
[Telomerase activity in colorectal cancer--a semi-quantitative procedure].
Gan To Kagaku Ryoho. 1998 Apr;25 Suppl 3:469-74.
7
Gastric cancer with high telomerase activity shows rapid development and invasiveness.具有高端粒酶活性的胃癌表现出快速发展和侵袭性。
Oncol Rep. 2001 Jan-Feb;8(1):107-10.
8
Telomerase activity could be used as a marker for neoplastic transformation in gastric adenocarcinoma: but it does not have a prognostic significance.端粒酶活性可作为胃腺癌肿瘤转化的标志物:但它没有预后意义。
Genet Mol Res. 2007 Feb 15;6(1):41-9.
9
Change in telomerase activity during human colorectal carcinogenesis.人类结直肠癌发生过程中端粒酶活性的变化。
Anticancer Res. 1999 May-Jun;19(3B):2167-72.
10
Demonstration of constant upregulation of the telomerase RNA component in human gastric carcinomas using in situ hybridization.利用原位杂交技术证实人胃癌中端粒酶RNA成分持续上调。
J Pathol. 1998 Jun;185(2):139-44. doi: 10.1002/(SICI)1096-9896(199806)185:2<139::AID-PATH79>3.0.CO;2-L.

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