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Does HPV play a role in the etiopathogenesis of ameloblastoma? An immunohistochemical, in situ hybridization and polymerase chain reaction study of 18 cases using laser capture microdissection

机译:HPV是否在Ameloblastoma的病原体发生中发挥作用?一种免疫组织化学,原位杂交和聚合酶链反应研究18例使用激光捕获微散

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Ameloblastomas are epithelial tumors of odontogenic origin, biologically characterized by local recurrence. Among different etiologic factors, HPV infection has been recently postulated to be somehow involved in ameloblastoma etiopathogenesis. To address this issue, we studied 18 ameloblastomas by means of immunohistochemistry, in situ hybridization (conventional and amplified), polymerase chain reaction and nested-polymerase chain reaction analyses using laser capture microdissection in order to detect the occurrence of HPV in this setting. No evidence of HPV infection was detected by morphological examination, immunohistochemistry, in situ hybridization and conventional polymerase chain reaction, while nested-polymerase chain reaction showed a weak positive band in two cases. However, the subsequent restriction enzyme analysis carried out from the nested-polymerase chain reaction amplification products of these two samples excluded the presence of HPV subtypes 16, 18, 31, 33, 35, 52, and 58. The search for HPV 6 and 11 in the same specimens was also negative. In conclusion, our data do not support an etiopathogenetic evidence for HPV in ameloblastoma.
机译:Ameloblastomas是异常源性起源的上皮肿瘤,通过局部复发的生物学表征。在不同的病因因素中,最近已经假定了HPV感染,以某种方式参与了Ameloblastoma病因发生。为了解决这一问题,我们通过免疫组织化学研究了18例Ameloblastomas,原位杂交(常规和扩增),聚合酶链反应和巢式聚合酶链反应分析使用激光捕获微粉切除,以检测该设置中HPV的发生。没有通过形态学检查,免疫组织化学,原位杂交和常规聚合酶链反应检测HPV感染的证据,而巢式聚合酶链反应在两种情况下显示出弱阳性带。然而,从这两个样品的巢式聚合酶链反应扩增产物中进行的随后的限制酶分析排除了HPV亚型16,18,31,33,35,52和58的存在。搜索HPV 6和11在相同的标本中也是阴性的。总之,我们的数据不支持Ameloblastoma中HPV的病因源性证据。

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