the human splice variant δ16her2 induces rapid tumor onset in a reporter transgenic mouse人类的剪接变体δ16her2诱发快速记者转基因小鼠肿瘤发病.pdfVIP

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the human splice variant δ16her2 induces rapid tumor onset in a reporter transgenic mouse人类的剪接变体δ16her2诱发快速记者转基因小鼠肿瘤发病.pdf

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the human splice variant δ16her2 induces rapid tumor onset in a reporter transgenic mouse人类的剪接变体δ16her2诱发快速记者转基因小鼠肿瘤发病

The Human Splice Variant D16HER2 Induces Rapid Tumor Onset in a Reporter Transgenic Mouse 1. 1. 2 1 1 Cristina Marchini , Federico Gabrielli , Manuela Iezzi , Santa Zenobi , Maura Montani , Lucia 1 1 3 3 3 3 Pietrella , Cristina Kalogris , Anna Rossini , Valentina Ciravolo , Lorenzo Castagnoli , Elda Tagliabue , 3 2 1 3 1 Serenella M. Pupa , Piero Musiani , Paolo Monaci , Sylvie Menard , Augusto Amici * 1 Department of Bioscience and Biotechnology, University of Camerino, Camerino, Italy, 2 Aging Research Centre, G. d’Annunzio University, Chieti, Italy, 3 Molecular Targeting Unit, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS, Istituto Nazionale dei Tumori, AmadeoLab, Milan, Italy Abstract Several transgenic mice models solidly support the hypothesis that HER2 (ERBB2) overexpression or mutation promotes tumorigenesis. Recently, a HER2 splice variant lacking exon-16 (D16HER2) has been detected in human breast carcinomas. This alternative protein, a normal byproduct of HER2, has an increased transforming potency compared to wild-type (wt) HER2 receptors. To examine the ability of D16HER2 to transform mammary epithelium in vivo and to monitor D16HER2- driven tumorigenesis in live mice, we generated and characterized a mouse line that transgenically expresses both human D16HER2 and firefly luciferase under the transcriptional control of the MMTV promoter. All the transgenic females develo