| Literature DB >> 31780287 |
Abakundanda Nsenga Ariston Gabriel1, Qinlian Jiao2, Umwali Yvette3, Xuemei Yang1, Samed A Al-Ameri1, Lutao Du1, Yun-Shan Wang4, Chuanxin Wang5.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is among the dangerous human cancers, is the 10th highly prevalent cancer, and the fourth sole cause of cancer-related mortality in the United States of America. Notwithstanding the significant commitment, the forecast for people with this burden continues to have a five-year survival rate of just 4-6%. The most critical altered genes within PDAC consist of K-ras the proto-oncogene which is usually mutationally activated above 90% cases and tumor suppressors likeTrp53 are altered at 55%. To face the burden of pancreatic ductal adenocarcinoma, a variety of genetically engineered pancreatic cancer mice models have been created over the last past years. These models have distinctive features and are not all appropriate for preclinical studies. In this review, we focus on differences between two mice models K-rasLSL.G12D/+;Pdx-1-Cre(KC) and K-rasLSL.G12D/+; Trp53R172H/+; Pdx-1-Cre(KPC) in terms of their modeling biology and their clinical relevance.Entities:
Keywords: Clinical relevance; Genetic engineered mouse model; KC and KPC; Modeling biology; Pancreatic ductal adenocarcinoma
Mesh:
Year: 2019 PMID: 31780287 DOI: 10.1016/j.pan.2019.11.006
Source DB: PubMed Journal: Pancreatology ISSN: 1424-3903 Impact factor: 3.996