Chemical Exchange Saturation Transfer (CEST) MRI is emerging as a tool for the studies of human malignancy. However, the translation of CEST into a successful tool for renal cancer characterization has been slow and hampered by technical difficulties associated with body imaging, such as motion, contaminating lipid signals and increased B0 ingomogeneity. Here we optimize CEST protocol for characterization of renal masses and demonstrate CEST measurements are feasible in kidneys using combination of motion synchronization, post-processing registration and lipid artifact removal. In addition, first Renal Cell Carcinoma patient CEST-mDixon data is shown and imaging results are correlated with the pathology.
The role of MRI in the evaluation of kidney diseases, including renal cancer, continues to expand. The development of non-invasive quantitative MRI techniques aims to provide objective information about changes in tumor biology, especially prior to changes in size or morphology. This may be particularly advantageous in patients with renal masses, such as those undergoing active surveillance.
Chemical Exchange Saturation Transfer (CEST) MRI is emerging as a tool in the clinical and preclinical studies of malignancy1-2. However, the translation of CEST into a successful imaging tool for body, specifically for renal cancer has been slow and hampered by technical difficulties typically associated with body imaging. Specifically, the presence of contaminating fat signals, physiological motion, and large B0 inhomogeneities, that are more pronounced in the body, challenge the CEST data acquisition
Here we focus on optimizing the protocol for characterization of renal masses with CEST. First, we incorporate advances in motion synchronization and post-processing with effective fat separation. We combined guided breathing and post-processing motion correction with Turbo-Spin Echo (TSE) or multi-point Dixon Turbo-Field Echo (mDixon-TFE) acquisition3. The results of TSE and mDixon-TFE are compared. Next, we aim to use the optimized protocol in a group of Renal Cell Carcinoma (RCC) patients prior to nephrectomy and correlate the results of CEST with the gold standard pathology results. To the best of our knowledge this is the first application of CEST to RCC.
Figure 1 compares representative MTRasym(2ppm) maps and Z-spectra from the data acquired using TSE (A-D) and mDixon (E-H) at B1rms=1.2 μT. The TSE acquisition offered increased overall SNR, however Z-spectra were contaminated by the lipid presence (red arrows). The nature of the large peaks in CEST-TSE at +3.5ppm (blue arrows) is under investigation, as they do not appear in CEST-mDixon Z-spectra. Since they are too narrow for amide peaks lines (typical for this region), they could potentially be attributed to amide signals from protein molecules extracted in urine. Overall, CEST-mDixon generates smoother Z-spectra (Fig.1B-C vs Fig.1F-G), by successfully removing lipid artifacts. Moreover, embedded acquisition of B0 map saves time and removes uncertainties associated with separate B0 acquisition (due to motion or dynamic changes), leading to a more robust experiment.
Figure 2 shows MTRasym at different frequency ranges: 1ppm, 2ppm and 3.5ppm corresponding to weighting by –OH, -NH2 and –NH chemical groups, respectively. The highest CEST is observed at 1ppm and 2ppm, with 2ppm possibly assigned to contributions from urea7-8 (see also Fig.1F).
Figure 3 demonstrates the first in vivo renal cancer patient data (B-E) together with the post-surgery specimen (A). The average MTRasym values for the three frequency ranges for different areas are listed in Table 1. Although the results are preliminary in nature, necrosis demonstrated higher MTRasym in all the three frequency ranges. Tumor-kidney tissue difference is the largest for MTRasym(1ppm) (Fig.3B and Table 1). Work is in progress to compare the results using different B1 levels as well as applying more advanced analysis schemes, e.g. Lorentzian peak fitting. Larger patient study is also underway.
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