MRI has been appreciated in the clinical assessment of various pancreatic diseases such as pancreatitis and in the diagnosis of pancreatic cysts and tumors [1]. However, only few preclinical studies rely on MRI to assess and monitor pancreatic tissue changes in animal models [2], mostly due to the inherently low conspicuity of the murine pancreas, it’s more amorphous presentation and splayed out position within the retroperitoneum and abdominal cavity. Pancreatic inflammation is a risk factor for pancreatic ductal adenocarcinoma development in humans, and its initiation is linked to activating mutations in KRAS oncogene (p48+/Cre;Kras+/G12D, refered to as KC model here) with acinar cells undergoing ductal reprogramming through premalignant pancreatic intraepithelial neoplastic lesions, finally leading to tumor formation. Here we explore the potential of preclinical in vivo MRI to visualize the murine pancreas and assess changes associated with cellular transformations in this mouse model of pancreatic carcinogenesis.MR imaging was performed on a 4.7T/20 cm Bruker PharmaScan unit equipped with transmit/receive a 40 mm bird-cage resonator. Motion-gated T1-weighted FLASH sequences (TE/TR 5/410ms, FA 80°, NA 4, MTX 256x256) w/o fat suppression and Magnetization Transfer prepulses (1.5 kHz offset, 0.4 kHz bandwidth, 20, 40 and 60 uT pulse strength), and quantitative T2 images (MSME sequence, PD and T2 weighted, TE/TR 15 resp. 75/426ms, NA 4) were acquired in 11 image slices at a spatial resolution of 117x117x700um3. Four wildtype and two KC mice underwent two MRI examinations, without and with prior oral contrast (10ml/kg paramagentic ion rich blueberry fruit juice administered by oral gavage). During MRI mice were intubated, mechanically ventilated and maintained under 1.8-2% isoflurane anesthesia in a 1:5 oxygen:air mixture. High-resolution abdominal images were obtained consistently from all animals. The pancreas was identified and outlined anatomically by locating the head of the pancreas using the posterior border of the stomach, spleen and kidney as anatomical landmarks and tracing it through subsequent posterior slices (Fig. 1). Contrast-enhancement with oral contrast agent facilitated delineation of the pancreas by providing contrast to surrounding intestinal structures. In the KC mice the pancreas was found to be substantially enlarged and to extend laterally into the right side of the animal (Fig. 2), confirmed by autopsy after the MRI examination. Furthermore, KC pancreas presented as heterogenous in T2- and T1-weighted images, and such heterogeneity in the pancreatic mass is consistent with histological findings of acinar and ductal metaplasia in this animal model. Furthermore, conspicuous globular foci of <200-700 um diameter were found in KC mice, suggestive of small cystic masses or mucin-secreting lesions. However, quantitative analysis of MRI tissue parameters such as T2, fat and macromolecular content were inconclusive as yet, and need to be established with more animals.Robust imaging methods have been set up to visualize the murine pancreas on T1- and T2-weighted structural images. Conspicuity of the pancreas from surrounding organs is critical, in particular in the KC model, where the pancreas is pathologically enlarged and hence needs to be tracked beyond typical anatomical landmarks suggesting the use of target-specific contrast agents. Finally, more quantitative measures of tissue transformation beyond anatomical presentation need yet to be established.