New avenue for molecular diagnosis of pancreatic and gynecological cancers

AURKA和S100A4基因的过度表达和DUSP6基因的表达抑制是胰腺癌发生的驱动因素。此外，AURKA基因被敲除后对紫杉烷具有协同化疗敏感性。DUSP6的修复通过抑制Ets-2抑制AURKA。此外，还发现PRDM2和VASH1与S100A4的表达有关联。MAPK和PI3K级联信号通路都是子宫内膜癌发生的关键，对这些级联信号通路的调控对临床治疗有潜在的帮助。

Overexpression of the AURKA and S100A4 genes and expressional suppression of the DUSP6 gene functions as the drivers of pancreatic carcinogenesis. In addition, knockdown of AURKA caused synergistic chemosensitivity with taxane. Restoration of DUSP6 caused suppression of AURKA via suppression of ETS-2. Further, expressional link of PRDM2 and VASH1 with S100A4 was found. Both MAPK and PI3K cascades are keys in endometrial carcinogenesis and regulation of these cascade are potentially useful for clinical managements.