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  • 标题:Pancreatic tumor pathogenesis reflects the causative genetic lesion
  • 本地全文:下载
  • 作者:E P Sandgren ; C J Quaife ; A G Paulovich
  • 期刊名称:Proceedings of the National Academy of Sciences
  • 印刷版ISSN:0027-8424
  • 电子版ISSN:1091-6490
  • 出版年度:1991
  • 卷号:88
  • 期号:1
  • 页码:93-97
  • DOI:10.1073/pnas.88.1.93
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:Transgenic mice in which c-myc expression is targeted to pancreatic acinar cells develop mixed acinar/ductal pancreatic adenocarcinomas between 2 and 7 months of age. This contrasts with the effect on pancreas of the simian virus 40 tumor antigen or activated ras, which in adult mice causes lesions composed exclusively of acinar-like cells. Furthermore, during an early stage of myc-induced pathology, transformed acinar-derived cells appear within islets, suggesting that islet hormones may influence the progression of these exocrine pancreatic tumors. These findings demonstrate that the initial oncogenic alteration can influence the pattern of subsequent tumor pathogenesis and, given that human exocrine pancreatic tumors are predominantly ductal adenocarcinomas, support the suggestion that transformed acinar cells may contribute to the genesis of this serious disease in man.
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