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首页> 外文期刊>Cancer Cell >Oncogenic Kras-Induced GM-CSF Production Promotes the Development of Pancreatic Neoplasia
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Oncogenic Kras-Induced GM-CSF Production Promotes the Development of Pancreatic Neoplasia

机译：致癌性Kras诱导的GM-CSF生产促进胰腺肿瘤的发展

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摘要

Stromal responses elicited by early stage neoplastic lesions can promote tumor growth. However, the molecular mechanisms that underlie the early recruitment of stromal cells to sites of neoplasia remain poorly understood. Here, we demonstrate an oncogenic Kras G12D-dependent upregulation of GM-CSF in mouse pancreatic ductal epithelial cells (PDECs). An enhanced GM-CSF production is also observed in human PanIN lesions. Kras G12D-dependent production of GM-CSF in vivo is required for the recruitment of Gr1 +CD11b + myeloid cells. The suppression of GM-CSF production inhibits the in vivo growth of Kras G12D-PDECs, and, consistent with the role of GM-CSF in Gr1 +CD11b + mobilization, this effect is mediated by CD8 + T cells. These results identify a pathway that links oncogenic activation to the evasion of antitumor immunity.
机译：早期肿瘤性病变引起的基质反应可促进肿瘤生长。然而，对基质细胞早期募集到瘤形成部位的分子机制仍知之甚少。在这里，我们证明了小鼠胰腺导管上皮细胞（PDECs）中GM-CSF的致癌性Kras G12D依赖性上调。在人类PanIN病变中还观察到GM-CSF产生增强。募集Gr1 + CD11b +骨髓细胞需要体内Kras G12D依赖的GM-CSF生产。抑制GM-CSF的产生会抑制Kras G12D-PDEC的体内生长，并且与GM-CSF在Gr1 + CD11b +动员中的作用一致，这种作用是由CD8 + T细胞介导的。这些结果确定了将致癌激活与逃避抗肿瘤免疫联系起来的途径。

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