Abstract
Pancreatic cancer is the fourth most common cause of cancer-related deaths in both men and women. The 5-year survival rate for metastatic pancreatic cancer is only 8%. There remains a need for improved early diagnosis and therapy for pancreatic cancer. Murine models are the current standard for preclinical study of pancreatic cancer. However, mice may not accurately reflect human biology because of a variety of differences between the two species. Remarkably, only 5-8% of anticancer drugs that have emerged from preclinical studies and entered clinical studies have ultimately been approved for clinical use. The cause of this poor approval rate is multi-factorial, but may in part be due to use of murine models that have limited accuracy with respect to human disease. Murine models also have limited utility in the development of diagnostic or interventional technology that require a human-sized model. So, at present, there remains a need for improved animal models of pancreatic cancer. The rationale for a porcine model of pancreatic cancer is (i) to enable development of diagnostic/therapeutic devices for which murine models have limited utility; and (ii) to have a highly predictive preclinical model in which anti-cancer therapies can be tested and optimized prior to a clinical trial. Recently, pancreatic tumors were induced in transgenic Oncopigs and porcine pancreatic ductal cells were transformed that contain oncogenic KRAS and p53-null mutations. Both techniques to induce pancreatic tumors in pigs are undergoing further refinement and expansion. The Oncopig currently is commercially available, and it is conceivable that other porcine models of pancreatic cancer may be available for general use in the near future.
| Original language | English (US) |
|---|---|
| Article number | 144 |
| Journal | Frontiers in Oncology |
| Volume | 9 |
| Issue number | MAR |
| DOIs | |
| State | Published - Jan 1 2019 |
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Keywords
- KRAS
- P53
- Pancreatic cancer
- Porcine
- Swine
- Transgenic
ASJC Scopus subject areas
- Oncology
- Cancer Research
Cite this
Porcine models of pancreatic cancer. / Bailey, Katie L.; Carlson, Mark A.
In: Frontiers in Oncology, Vol. 9, No. MAR, 144, 01.01.2019.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Porcine models of pancreatic cancer
AU - Bailey, Katie L.
AU - Carlson, Mark A.
PY - 2019/1/1
Y1 - 2019/1/1
N2 - Pancreatic cancer is the fourth most common cause of cancer-related deaths in both men and women. The 5-year survival rate for metastatic pancreatic cancer is only 8%. There remains a need for improved early diagnosis and therapy for pancreatic cancer. Murine models are the current standard for preclinical study of pancreatic cancer. However, mice may not accurately reflect human biology because of a variety of differences between the two species. Remarkably, only 5-8% of anticancer drugs that have emerged from preclinical studies and entered clinical studies have ultimately been approved for clinical use. The cause of this poor approval rate is multi-factorial, but may in part be due to use of murine models that have limited accuracy with respect to human disease. Murine models also have limited utility in the development of diagnostic or interventional technology that require a human-sized model. So, at present, there remains a need for improved animal models of pancreatic cancer. The rationale for a porcine model of pancreatic cancer is (i) to enable development of diagnostic/therapeutic devices for which murine models have limited utility; and (ii) to have a highly predictive preclinical model in which anti-cancer therapies can be tested and optimized prior to a clinical trial. Recently, pancreatic tumors were induced in transgenic Oncopigs and porcine pancreatic ductal cells were transformed that contain oncogenic KRAS and p53-null mutations. Both techniques to induce pancreatic tumors in pigs are undergoing further refinement and expansion. The Oncopig currently is commercially available, and it is conceivable that other porcine models of pancreatic cancer may be available for general use in the near future.
AB - Pancreatic cancer is the fourth most common cause of cancer-related deaths in both men and women. The 5-year survival rate for metastatic pancreatic cancer is only 8%. There remains a need for improved early diagnosis and therapy for pancreatic cancer. Murine models are the current standard for preclinical study of pancreatic cancer. However, mice may not accurately reflect human biology because of a variety of differences between the two species. Remarkably, only 5-8% of anticancer drugs that have emerged from preclinical studies and entered clinical studies have ultimately been approved for clinical use. The cause of this poor approval rate is multi-factorial, but may in part be due to use of murine models that have limited accuracy with respect to human disease. Murine models also have limited utility in the development of diagnostic or interventional technology that require a human-sized model. So, at present, there remains a need for improved animal models of pancreatic cancer. The rationale for a porcine model of pancreatic cancer is (i) to enable development of diagnostic/therapeutic devices for which murine models have limited utility; and (ii) to have a highly predictive preclinical model in which anti-cancer therapies can be tested and optimized prior to a clinical trial. Recently, pancreatic tumors were induced in transgenic Oncopigs and porcine pancreatic ductal cells were transformed that contain oncogenic KRAS and p53-null mutations. Both techniques to induce pancreatic tumors in pigs are undergoing further refinement and expansion. The Oncopig currently is commercially available, and it is conceivable that other porcine models of pancreatic cancer may be available for general use in the near future.
KW - KRAS
KW - P53
KW - Pancreatic cancer
KW - Porcine
KW - Swine
KW - Transgenic
UR - http://www.scopus.com/inward/record.url?scp=85063346444&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85063346444&partnerID=8YFLogxK
U2 - 10.3389/fonc.2019.00144
DO - 10.3389/fonc.2019.00144
M3 - Review article
C2 - 30915276
AN - SCOPUS:85063346444
VL - 9
JO - Frontiers in Oncology
JF - Frontiers in Oncology
SN - 2234-943X
IS - MAR
M1 - 144
ER -