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

ObjectiveSETD2, the sole histone H3K36 trimethyltransferase, is frequently mutated or deleted in human cancer, including pancreatic ductal adenocarcinoma (PDAC). However, whether SETD2/H3K36me3 alteration results in PDAC remains largely unknown.DesignTCGA(PAAD) public database and PDAC tissue array...

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Veröffentlicht in:	Gut 2020-04, Vol.69 (4), p.715-726
Hauptverfasser:	Niu, Ningning, Lu, Ping, Yang, Yanlin, He, Ruizhe, Zhang, Li, Shi, Juanjuan, Wu, Jinghua, Yang, Minwei, Zhang, Zhi-Gang, Wang, Li-Wei, Gao, Wei-Qiang, Habtezion, Aida, Xiao, Gary Guishan, Sun, Yongwei, Li, Li, Xue, Jing
Format:	Artikel
Sprache:	eng
Schlagworte:	Acinar cells Adenocarcinoma AKT protein cancer genetics Cancer therapies Carcinogenesis Cdc4 protein Deoxyribonucleic acid DNA DNA repair Epigenetics Extracellular matrix Gene expression Genomes Genotype & phenotype Homeostasis K-Ras protein Laboratories Medical prognosis Medical research Mesenchyme Metaplasia Metastases Metastasis Mutants Mutation Pancreas Pancreatic cancer Ribonucleic acid RNA Stem cells Tissue engineering Tumors Variance analysis
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