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首页> 外文期刊>Cancer Cell >EGF Receptor Signaling Is Essential for K-Ras Oncogene-Driven Pancreatic Ductal Adenocarcinoma
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EGF Receptor Signaling Is Essential for K-Ras Oncogene-Driven Pancreatic Ductal Adenocarcinoma

机译：EGF受体信号对于K-Ras癌基因驱动的胰管腺癌必不可少

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摘要

Clinical evidence indicates that mutation/activation of EGF receptors (EGFRs) is mutually exclusive with the presence of K-RAS oncogenes in lung and colon tumors. We have validated these observations using genetically engineered mouse models. However, development of pancreatic ductal adenocarcinomas driven by K-Ras oncogenes are totally dependent on EGFR signaling. Similar results were obtained using human pancreatic tumor cell lines. EGFRs were also essential even in the context of pancreatic injury and absence of p16Ink4a/p19Arf. Only loss of p53 made pancreatic tumors independent of EGFR signaling. Additional inhibition of PI3K and STAT3 effectively prevented proliferation of explants derived from these p53-defective pancreatic tumors. These findings may provide the bases for more rational approaches to treat pancreatic tumors in the clinic.
机译：临床证据表明，EGF受体（EGFR）的突变/激活与肺和结肠肿瘤中存在K-RAS癌基因互斥。我们已经使用基因工程小鼠模型验证了这些观察结果。然而，由K-Ras癌基因驱动的胰腺导管腺癌的发展完全依赖于EGFR信号传导。使用人胰腺肿瘤细胞系获得了相似的结果。即使在胰腺损伤和缺乏p16Ink4a / p19Arf的情况下，EGFR也是必不可少的。仅p53的丧失使胰腺肿瘤独立于EGFR信号传导。对PI3K和STAT3的其他抑制作用有效地阻止了源自这些p53缺陷型胰腺肿瘤的外植体的增殖。这些发现可能为临床上更合理地治疗胰腺肿瘤提供基础。

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