脑胶质瘤中心体的异常扩增及其与疾病分期的相关性
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摘要
目的:探讨脑胶质瘤中心体扩增情况及其与疾病分期的相关性。方法:对40例胶质瘤标本和10例正常脑组织标本进行HE染色的检测;免疫组织化学检测Ki67和γ-微管蛋白的表达;使用免疫荧光染色技术检测中心体扩增情况。结果:不同标本中,HE染色呈现不同的细胞形态特征;Ki67在正常脑组织中没有表达,但在Ⅰ/Ⅱ、Ⅲ和Ⅳ级胶质瘤中的阳性表达率分别为65%、80%和100%,各组间差异具有统计学意义(P<0.01),说明Ki67的表达与胶质瘤级别相关。γ-微管蛋白在正常脑组织和Ⅰ/Ⅱ、Ⅲ、Ⅳ级胶质瘤中的表达率分别为30%、50%、80%和100%,各组间差异具有统计学意义(P<0.01),说明胶质瘤级别升高,中心体扩增率增加;免疫荧光检测显示,中心体扩增率和脑胶质瘤的级别呈正相关。结论:中心体扩增是脑胶质瘤的恶性程度的特征之一,并且与胶质瘤发病阶段有关,提示中心体扩增和脑胶质瘤的发展具有密切的相关性。
Objective:To investigate the level of centrosome amplification in glioma and its relationship with the clinical stage of the disease.Methods:40 glioma specimens and 10 normal brain tissue specimens was examined using HE staining. The protein expression levels of Ki67 and γ-tubulin were detected by immunohistochemistry. Centrosome amplification was evaluated using immunofluorescence analysis.Results:HE staining showed different morphological characteristics in different samples. Compared with normal brain tissue, the glioma samples had significantly higher positive rates of Ki67 and γ-tubulin(P<0.01). Immunofluorescence results showed that the rate of centrosome amplification was increased with the increasing grade of glioma.Conclusion:Centrosome amplification occurs in glioma and correlates with the disease stage, which suggests that centrosome amplification contributes to the development of glioma.
Objective:To investigate the level of centrosome amplification in glioma and its relationship with the clinical stage of the disease.Methods:40 glioma specimens and 10 normal brain tissue specimens was examined using HE staining. The protein expression levels of Ki67 and γ-tubulin were detected by immunohistochemistry. Centrosome amplification was evaluated using immunofluorescence analysis.Results:HE staining showed different morphological characteristics in different samples. Compared with normal brain tissue, the glioma samples had significantly higher positive rates of Ki67 and γ-tubulin(P<0.01). Immunofluorescence results showed that the rate of centrosome amplification was increased with the increasing grade of glioma.Conclusion:Centrosome amplification occurs in glioma and correlates with the disease stage, which suggests that centrosome amplification contributes to the development of glioma.
引文
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[14] Yamamoto Y, Matsuyama H, Furuya T, et al. Centrosome hyperamplification predicts progression and tumor recurrence in bladder cancer[J]. Clin Cancer Res,2004,10(19):6449-6455.
[2] Lu Y C, Wang P, Wang J, et al. PCNA and JNK1-Stat3 pathways respectively promotes and inhibits diabetes-associated centrosome amplification by targeting at the ROCK1/14-3-3sigma complex in human colon cancer HCT116 cells[J]. J Cell Physiol, 2019,234(7):11511-11523.
[3] Van Westrhenen A, Senders J T, Martin E, et al. Clinical challenges of glioma and pregnancy:a systematic review[J]. J Neurooncol, 2018,139(1):1-11.
[4] Levine M S, Bakker B, Boeckx B, et al. Centrosome amplification is sufficient to promote spontaneous tumorigenesis in mammals[J]. Dev Cell, 2017,40(3):313-322.e5.
[5] Raynaud-Messina B, Merdes A. Gamma-tubulin complexes and microtubule organization[J]. Curr Opin Cell Biol, 2007,19(1):24-30.
[6] Li W, Zhang G, Wang H L, et al. Analysis of expression of cyclin E, p27kip1 and Ki67 protein in colorectal cancer tissues and its value for diagnosis, treatment and prognosis of disease[J]. Eur Rev Med Pharmacol Sci, 2016,20(23):4874-4879.
[7] Smith D L, Soria J C, Morat L, et al. Human telomerase reverse transcriptase(hTERT)and Ki-67 are better predictors of survival than established clinical indicators in patients undergoing curative hepatic resection for colorectal metastases[J]. Ann Surg Oncol, 2004,11(1):45-51.
[8] Wayne S, Robinson R A. Upper aerodigestive tract squamous dysplasia:correlation with p16, p53, pRb,and Ki-67 expression[J]. Arch Pathol Lab Med, 2006,130(9):1309-1314.
[9] Okumura Y, Nishimura R, Nakatsukasa K, et al.Change in estrogen receptor, HER2, and Ki-67 status between primary breast cancer and ipsilateral breast cancer tumor recurrence[J]. Eur J Surg Oncol, 2015,41(4):548-552.
[10] Godinho S A, Picone R, Burute M, et al. Oncogenelike induction of cellular invasion from centrosome amplification[J]. Nature, 2014,510(7503):167-171.
[11] Chan J Y. A clinical overview of centrosome amplification in human cancers[J]. Int J Biol Sci, 2011,7(8):1122-1144.
[12] Pihan G A, Wallace J, Zhou Y, et al. Centrosome abnormalities and chromosome instability occur together in pre-invasive carcinomas[J]. Cancer Res, 2003,63(6):1398-1404.
[13] Mahathre M M, Rida P C, Aneja R. The more the messier:centrosome amplification as a novel biomarker for personalized treatment of colorectal cancers[J].J Biomed Res, 2016,30(6):441-451.
[14] Yamamoto Y, Matsuyama H, Furuya T, et al. Centrosome hyperamplification predicts progression and tumor recurrence in bladder cancer[J]. Clin Cancer Res,2004,10(19):6449-6455.
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