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Cytomegalovirus-induced salivary gland pathology: resistance to kinase inhibitors of the upregulated host cell EGFR/ERK pathway is associated with CMV-dependent stromal overexpression of IL-6 and fibronectin

机译:巨细胞病毒诱导的唾液腺病理:对上调的宿主细胞EGFR / ERK途径激酶抑制剂的抗性与CMV依赖的IL-6和纤连蛋白的基质过度表达有关

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Background Recently we identified a relationship between human cytomegalovirus (hCMV) and human salivary gland (SG) mucoepidermoid carcinoma (MEC) in over 90% of cases; tumorigenesis in these cases uniformly correlated with active hCMV protein expression and an upregulation of the EGFR → ERK pathway. Our previously characterized, novel mouse organ culture model of mouse CMV (mCMV)-induced tumorigenesis displays a number of histologic and molecular characteristics similar to human MEC.
机译:背景技术最近,我们在超过90%的病例中发现了人类巨细胞病毒(hCMV)与人类唾液腺(SG)粘液表皮样癌(MEC)之间的关系。在这些情况下,肿瘤发生与活跃的hCMV蛋白表达和EGFR→ERK通路的上调一致相关。我们以前表征的新型小鼠CMV(mCMV)诱导的肿瘤发生的小鼠器官培养模型显示出许多类似于人MEC的组织学和分子特征。

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