Objectives: To assess the feasibility of 5.0 T magnetic resonance imaging (MRI) in characterizing pancreatic cystic lesions (PCLs), compared with 3.0 T MRI and multidetector computed tomography (MDCT). Methods: Thirty-five patients with PCLs underwent 5.0 T MR alongside 3.0 T MR or MDCT. Two observers measured subjective and objective image quality scores. The consistency of two observers between 5.0 T and 3.0 T was calculated by intraclass correlation coefficients. The characteristics of PCLs and their specific diagnosis, as well as benignity/malignancy, were evaluated across MDCT, 3.0 T, and 5.0 T MRI. Results: The 5.0 T MR demonstrated significantly higher subjective image quality and SNR on T1WI compared to that in 3.0 T MR (p < 0.05). The 5.0 T MRI identified more cyst lesions than the 3.0 T MRI (40 and 32) and MDCT (82 and 56). The sensitivity, specificity, and accuracy for differentiating benign from malignant lesions with 5.0 T MRI (75%, 100%, and 91.4%, respectively) surpassed those of 3.0 T MRI and MDCT. The accuracy of the specific diagnosis of PCLs at 5.0 T MRI (80%) was superior to 3.0 T MRI and MDCT. Conclusions: 5.0 T MRI exhibits certain superiority in delineating details of PCLs and in clinical diagnostic accuracy, outperforming MDCT and 3.0 T MRI while maintaining sufficient image quality.

Mutant KRAS activation occurs in most of pancreatic ductal adenocarcinoma (PDAC), which induce the sensitivity to ferroptosis of PDAC cells, but the underlying mechanism is still poorly understood. Here, we show how KRAS acts in signaling to activate transcription factor FOSL1, which promotes the expression of the iron uptake receptor TFRC. In PDAC cells, repression of TFRC by KRAS/FOSL1 signaling inhibited intracellular iron levels, thereby restricting the occurrence of ferroptosis. Furthermore, the KRAS/FOSL1/TFRC axis can make the PDAC cells vulnerable to alteration of the iron level in the tumor microenvironment. Our study highlights a pivotal mechanism of PDAC ferroptosis through iron metabolism and supports a new therapeutic strategy for PDAC with superior potential.