期刊文献+

MSI和HPV16在鼻腔鼻窦肿瘤组织中的作用 被引量:4

Detection of MSI and HPV16 in tumor tissue of nasal cavity and sinus
下载PDF
导出
摘要 目的初步探讨微卫星不稳定性(MSI)和16型人乳头状瘤病毒(HPV16)在鼻腔鼻窦肿瘤发生过程中的作用。方法应用聚合酶链式反应、变性聚丙烯酰胺凝胶电泳、银染等方法,检测57例鼻窦鼻腔肿瘤组织MSI的情况,采用免疫组织化学对HPV16进行检测。结果HPV16抗原表达的阳性细胞在凹空细胞处分布较多,恶性肿瘤组HPV16感染率(28.0%)低于IP组(58.3%)和IP伴鳞状上皮不典型增生(62.5%)组(P<0.05);IP伴鳞状上皮不典型增生组HPV16感染率与IP组比较无显著差异(P>0.05);空白对照组无阳性表达。恶性肿瘤组MSI的阳性表现率(36.0%)高于内翻性乳头状瘤组(0),差异有显著性(P<0.01);IP伴鳞状上皮不典型增生组MSI的阳性表现率(12.5%)低于恶性肿瘤组(36.0%),差异有显著性(P<0.05);IP伴鳞状上皮不典型增生组MSI的阳性表现率高于内翻性乳头状瘤组(P<0.05)。结论HPV16可能是鼻窦鼻腔肿瘤的重要致病因素,MSI亦可能与鼻窦鼻腔恶性肿瘤的发生密切相关,但HPV16可能不是通过MSI诱发鼻窦鼻腔恶性肿瘤的发生。 Objective To determine whether there is a relationship between the microsatellite instability(MSI) and human papilloma virus 16(HPV16) infection in tumors of nasal cavity and sinus. Methods All of 57 cases of tumors tissues of nasal cavity and sinus were studied. MSI were examined by using polymerize chain reaction(PCR), denatured-polyac-rylamidenel-electrophoresis and silver staininn. HPV16 were detected by using immunohistochemistry method. Results The positive cells are more placed on the concave of cell. The rates of HPV16 infection in inverting papilloma(58.3% )and precancerous lesions (62.5 % ) of nasal cavity and sinus were markedly higher than those in carcinoma (28.0 % ). The incidences of MSI in carcinoma(36.0% )and precancerous lesions( 12.5% ) of nasal cavity and sinus were markedly higher than those in inverting papilloma(0). The patients with HPV16 infection had not markedly different incidence of MSI from that of noninfected patients(P〉0.05). Conclusion HPV16 is perhaps the important fact of causing the tumors of nasal cavity and sinus. MSI is highly related to it. However MSI does not induce the tumors of nasal cavity and sinus through HPV16.
出处 《新乡医学院学报》 CAS 2006年第1期40-42,共3页 Journal of Xinxiang Medical University
关键词 鼻腔鼻窦肿瘤 人乳头状瘤病毒 内翻性乳头状瘤 微卫星不稳定性 nasal cavity and sinus carcinoma inverting papilloma human papilloma virus microsatellite instability
  • 相关文献

参考文献8

  • 1Lo KW, Huang DP, Lee CK. Genetic changes in Nasopharyngeal carcinomal [J]. Chin Mied J, 1997,110 : 5482-5591.
  • 2Vander Riet P, Nawroz H, Hruban RH, et al. Frequent loss of chromosome 9p21-21 early in head and neck cancer progression.Phenotype and genotype of advanced premalignant head and neck lesions after chemopreventive therapy[J]. Cancer Res, 1994,54 :1156-1158.
  • 3Mutirangura A, Tanunyutthawongese C, Pornthanakasem W, et al. Genomic alterations in nasopharyngeal carcinoma: loss of heterozygosity and Epstein - Barr virus infection [J]. Br J Cancer,1997,76: 770-776.
  • 4Nawroz H, Vander Riet P, Hruban RH, et al. Allelicloss of head and neck squamous cell carcinoma [J]. Cancer Res, 1994, 54 :1152-1155.
  • 5Huang DP,Lo KW, van Hasselt A, et al. A region of homozygous deletion on chromosome 9p21-22 in Humanprimary nasopharyngeal carcinoma[J]. Cancer Res, 1994,54 : 4003-4006.
  • 6Howley PM. Role of the human papilloma virus in human cancer [J]. Cancer Res, 1991,51 : 5019-5025.
  • 7Furuta Y, Shinhara T, San K, et al. Molecular pathologic study of Human Papilloma virus in fection in puilloma and squarnous cell Carcinoma of the nasal cavities and paranasal sinuses[J]. Laryngoscope, 1991,101 : 79-85.
  • 8Weber RS, Shillitoe EJ, Robbins T, et al. Prevalence Of human papilloma Virus in inverted nasal papillomas[J]. Arch Otolaryngol Head Neck Surg, 1988,114:23-26.

同被引文献50

引证文献4

二级引证文献6

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