作者: Oliver R. Mikse , Jeremy H. Tchaicha , Esra A. Akbay , Liang Chen , Roderick T. Bronson
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摘要: Recurrent fusion of the v-myb avian myelobastosis viral oncogene homolog (MYB) and nuclear factor I/B (NFIB) generates MYB-NFIB transcription factor, which has been detected in a high percentage individuals with adenoid cystic carcinoma (ACC). To understand functional role this protein carcinogenesis, we generated conditional mutant transgenic mouse that expresses along p53 mutation tissues give rise to ACC: mammary tissue, salivary glands, or systemically whole body. Expression tissue resulted hyperplastic glands developed into adenocarcinoma 27.3% animals. Systemic expression caused more rapid development breast phenotype, but mice died due abnormal proliferation glomerular compartment kidney, led glomerulonephritis. These findings suggest is oncogenic treatments targeting may lead therapeutic responses ACC patients.