Session 3F: MR Microscopic Phenotyping of the Pancreas in Mutant Kras Mouse Models of Pancreatic Cancer
Session Number
Session 3F: 3rd Presentation
Advisor(s)
Palamadai Venkatasubramanian, NorthShore University HealthSystem
Location
Room A115
Start Date
28-4-2017 1:15 PM
End Date
28-4-2017 2:30 PM
Abstract
There is a need to better understand the progression of pancreatic ductal adenocarcinoma (PDAC), commonly known as pancreatic cancer, in the early stages. The purpose of this investigation is to determine how MR microscopy, an advanced imaging technology, can be used to track the onset and development of pancreatic cancer. MR imaging was performed ex vivo at 14.1T on pancreas from ELKRAS (EK) and p48-Cre/LSL·Kras (KC) transgenic mouse models at different ages. Both EK and KC mice develop precancerous lesions and in KC mice lesions might advance to pancreatic cancer. Diffusion Trace and T2 maps were generated and diffusion coefficient and T2 relaxation time were calculated for four major cell structures: the acinar lobules, ducts, hyperintense lesions and hypointense lesions. These parameters, along with 3-D images, revealed different trajectories in precancerous lesion development for the two genotypes. In EK mice, changes in the acinar lobules began early, but progressed slowly, and lesions appeared to develop and spread slowly as well. In KC mice, acinar changes began much later, but more lesions were detected, suggesting rapid progression of the disease. Using these findings in future in vivo mouse or human imaging experiments will be valuable in providing early diagnosis of the disease.
Session 3F: MR Microscopic Phenotyping of the Pancreas in Mutant Kras Mouse Models of Pancreatic Cancer
Room A115
There is a need to better understand the progression of pancreatic ductal adenocarcinoma (PDAC), commonly known as pancreatic cancer, in the early stages. The purpose of this investigation is to determine how MR microscopy, an advanced imaging technology, can be used to track the onset and development of pancreatic cancer. MR imaging was performed ex vivo at 14.1T on pancreas from ELKRAS (EK) and p48-Cre/LSL·Kras (KC) transgenic mouse models at different ages. Both EK and KC mice develop precancerous lesions and in KC mice lesions might advance to pancreatic cancer. Diffusion Trace and T2 maps were generated and diffusion coefficient and T2 relaxation time were calculated for four major cell structures: the acinar lobules, ducts, hyperintense lesions and hypointense lesions. These parameters, along with 3-D images, revealed different trajectories in precancerous lesion development for the two genotypes. In EK mice, changes in the acinar lobules began early, but progressed slowly, and lesions appeared to develop and spread slowly as well. In KC mice, acinar changes began much later, but more lesions were detected, suggesting rapid progression of the disease. Using these findings in future in vivo mouse or human imaging experiments will be valuable in providing early diagnosis of the disease.