scholarly journals Genetically Engineered Mouse Models of Pancreatic Cancer: The KPC Model ( LSL‐Kras G12D/+ ;LSL‐Trp53 R172H/+ ;Pdx‐1‐Cre ), Its Variants, and Their Application in Immuno‐oncology Drug Discovery

2016 ◽  
Vol 73 (1) ◽  
Author(s):  
Jae W. Lee ◽  
Chad A. Komar ◽  
Fee Bengsch ◽  
Kathleen Graham ◽  
Gregory L. Beatty
Nanoscale ◽  
2019 ◽  
Vol 11 (45) ◽  
pp. 22006-22018 ◽  
Author(s):  
Vijay Sagar Madamsetty ◽  
Krishnendu Pal ◽  
Sandeep Keshavan ◽  
Thomas R. Caulfield ◽  
Shamit Kumar Dutta ◽  
...  

Schematic representation demonstrating the fabrication and in vivo evaluation of an immune-modulatory nano-formulation consisting of irinotecan and curcumin in immune-competent mouse models of pancreatic adenocarcinoma.


2013 ◽  
Vol 6 (1) ◽  
pp. 67 ◽  
Author(s):  
Michela Capello ◽  
Paola Cappello ◽  
Federica Linty ◽  
Roberto Chiarle ◽  
Isabella Sperduti ◽  
...  

Cancers ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 71
Author(s):  
Yuriko Saiki ◽  
Can Jiang ◽  
Masaki Ohmuraya ◽  
Toru Furukawa

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy, and the seventh leading cause of cancer-related deaths worldwide. An improved understanding of tumor biology and novel therapeutic discoveries are needed to improve overall survival. Recent multi-gene analysis approaches such as next-generation sequencing have provided useful information on the molecular characterization of pancreatic tumors. Different types of pancreatic cancer and precursor lesions are characterized by specific molecular alterations. Genetically engineered mouse models (GEMMs) of PDAC are useful to understand the roles of altered genes. Most GEMMs are driven by oncogenic Kras, and can recapitulate the histological and molecular hallmarks of human PDAC and comparable precursor lesions. Advanced GEMMs permit the temporally and spatially controlled manipulation of multiple target genes using a dual-recombinase system or CRISPR/Cas9 gene editing. GEMMs that express fluorescent proteins allow cell lineage tracing to follow tumor growth and metastasis to understand the contribution of different cell types in cancer progression. GEMMs are widely used for therapeutic optimization. In this review, we summarize the main molecular alterations found in pancreatic neoplasms, developed GEMMs, and the contribution of GEMMs to the current understanding of PDAC pathobiology. Furthermore, we attempted to modify the categorization of altered driver genes according to the most updated findings.


2019 ◽  
Vol 8 (9) ◽  
pp. 1369 ◽  
Author(s):  
Weng ◽  
Lin ◽  
Cheng

Pancreatic cancer is often treatment-resistant, with the emerging standard of care, gemcitabine, affording only a few months of incrementally-deteriorating survival. Reflecting on the history of failed clinical trials, genetically engineered mouse models (GEMMs) in oncology research provides the inspiration to discover new treatments for pancreatic cancer that come from better knowledge of pathogenesis mechanisms, not only of the derangements in and consequently acquired capabilities of the cancer cells, but also in the aberrant microenvironment that becomes established to support, sustain, and enhance neoplastic progression. On the other hand, the existing mutational profile of pancreatic cancer guides our understanding of the disease, but leaves many important questions of pancreatic cancer biology unanswered. Over the past decade, a series of transgenic and gene knockout mouse modes have been produced that develop pancreatic cancers with features reflective of metastatic pancreatic ductal adenocarcinoma (PDAC) in humans. Animal models of PDAC are likely to be essential to understanding the genetics and biology of the disease and may provide the foundation for advances in early diagnosis and treatment.


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