作者: Roland Coras , Klaus Korn , Christian G. Bien , Thilo Kalbhenn , Karl Rössler
DOI: 10.1002/ANA.24328
关键词: Epitope 、 Biology 、 Cell 、 Epithelium 、 Mucocutaneous zone 、 Carcinogenesis 、 Cortical dysplasia 、 Antibody 、 Primer (molecular biology) 、 Pathology
摘要: Objective The etiology of focal cortical dysplasia type IIb (FCDIIb) remains enigmatic in patients suffering from drug-resistant epilepsy, and an aberrant activation the mammalian target rapamycin complex 1 signaling pathway (mTORC1) was detected this developmental brain malformation. Recently, human papillomavirus (HPV) oncoprotein E6 has been identified as a potent activator mTORC1, HPV16 described to persist balloon cells obtained surgical FCDIIb specimens. Although observation replicated by independent second report, it contradicts current knowledge HPV biology. infects squamous or mucocutaneous epithelium; hematogenic spread into other tissues not observed. In addition, carcinogenesis never reported patients. Herein, we have tried confirm 2 previous reports infection using series 14 specimens with histopathologically confirmed FCDIIb. Methods Snap-frozen were tested for DNA primer set amplification complete reading frame 3 sets primers (2 consensus detecting multiple genotypes, another specifically used HPV16). Furthermore, formalin-fixed paraffin-embedded histopathological preparations immunohistochemically analyzed previously antibodies directed against oncoprotein. Results All negative all 4 sets. Antibodies epitope showed weak labeling cytoplasm cells, FCDIIb, but also cell populations. Interpretation Our data did evidence detection FCDIIb. Ann Neurol 2015;77:312–319