Differences between KC and KPC pancreatic ductal adenocarcinoma mice models, in terms of their modeling biology and their clinical relevance

Abakundana Nsenga Ariston Gabriel; Qinlian Jiao; Umwali Yvette; Xuemei Yang; Samed A Al-Ameri; Lutao Du; Yun-Shan Wang; Chuanxin Wang

doi:10.1016/j.pan.2019.11.006

Differences between KC and KPC pancreatic ductal adenocarcinoma mice models, in terms of their modeling biology and their clinical relevance

Pancreatology. 2020 Jan;20(1):79-88. doi: 10.1016/j.pan.2019.11.006. Epub 2019 Nov 18.

Authors

Abakundana Nsenga Ariston Gabriel¹, Qinlian Jiao², Umwali Yvette³, Xuemei Yang¹, Samed A Al-Ameri¹, Lutao Du¹, Yun-Shan Wang⁴, Chuanxin Wang⁵

Affiliations

¹ Department of Clinical Laboratory, The Second Hospital of Shandong University, 247 Beiyuan Street, Jinan, 250033, Shandong, China.
² Department of Clinical Laboratory, The Second Hospital of Shandong University, 247 Beiyuan Street, Jinan, 250033, Shandong, China; International Biotechnology R&D Center, Shandong University School of Ocean, 180 Wenhua Xi Road, Weihai, Shandong, 264209, China.
³ Department of Clinical Laboratory, Qilu Hospital, Shandong University, 107 Wenhua Xi Road, Jinan, 250012, China.
⁴ Department of Clinical Laboratory, The Second Hospital of Shandong University, 247 Beiyuan Street, Jinan, 250033, Shandong, China. Electronic address: wangyunshan135@126.com.
⁵ Department of Clinical Laboratory, The Second Hospital of Shandong University, 247 Beiyuan Street, Jinan, 250033, Shandong, China. Electronic address: cxwang@sdu.edu.cn.

PMID: 31780287
DOI: 10.1016/j.pan.2019.11.006

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-ras^LSL.G12D/+;Pdx-1-Cre(KC) and K-ras^LSL.G12D/+; Trp53^R172H/+; Pdx-1-Cre(KPC) in terms of their modeling biology and their clinical relevance.

Keywords: Clinical relevance; Genetic engineered mouse model; KC and KPC; Modeling biology; Pancreatic ductal adenocarcinoma.

Publication types

Review

MeSH terms

Animals
Carcinoma, Pancreatic Ductal / genetics*
Disease Models, Animal*
Genetic Predisposition to Disease
Mice
Mice, Inbred Strains
Mutation
Pancreatic Neoplasms / genetics*
Proto-Oncogene Mas