Loss of Setd2 promotes Kras-induced acinar-to-ductal metaplasia and epithelia-mesenchymal transition during pancreatic carcinogenesis.

Ningning NiuPing LuYanlin YangRuizhe HeLi ZhangJuanjuan ShiJinghua WuMinwei YangZhi-Gang ZhangLi-Wei WangWei-Qiang GaoAida HabtezionGary Guishan XiaoYong-Wei SunLi LiJing Xue

Published in: Gut (2019)

Together, our findings highlight the function of SETD2 during pancreatic carcinogenesis, which would advance our understanding of epigenetic dysregulation in PDAC. Moreover, it may also pave the way for development of targeted, patients-tailored therapies for PDAC patients with SETD2 deficiency.

Keyphrases

end stage renal disease
ejection fraction
newly diagnosed
chronic kidney disease
stem cells
dna methylation
gene expression
peritoneal dialysis
prognostic factors
high glucose
cancer therapy
diabetic rats
smoking cessation
drug delivery
patient reported
wild type