作者: Núbia Braga Pereira , Victor Coutinho Bastos , Juliana Cristina De Souza , Marina Gonçalves Diniz , Jéssica Gardone Vitório
DOI: 10.1007/S00784-019-03107-4
关键词: Cancer research 、 Odontogenic myxoma 、 MAPK/ERK pathway 、 Cell culture 、 Fold change 、 In vivo 、 In vitro 、 Targeted therapy 、 MEK inhibitor 、 Medicine
摘要: Odontogenic myxoma (OM) occasionally responds poorly to surgical treatment. The MAPK pathway is constitutively activated in several neoplasms and we aimed test if the OM, order pave way for an alternative therapy aggressive recurrent cases. immunoexpression of phosphorylated ERK1/2 (pERK1/2) was assessed OM. We established a 3D organotypic culture model vitro study patient-derived xenografts (PDX) mice vivo study. MEK inhibitor U0126 used inhibit phosphorylation models. All OM showed strong pERK1/2 immunoexpression, consistent with activation. Treatment resulted reduced pERK1/2/ERK1/2 ratio. Consistent results, all PDX animals treated decreased volume fold change compared controls. its inhibition leads tumor shrinkage cell Our results offer pre-clinical frame OM-targeted therapy. Further work needed determine this initial finding holds clinical promise.