Glioma is a kind of malignant neoplasm of Central Nervous System (CNS). The conventional diagnosis approach such as T1 weighted imaging (T1WI), T2 weighted imaging (T2WI) and contrast enhanced T1WI (CE-T1) manifests as the oversimplified presentation of anatomical structures [1]. Chemical exchange saturation transfer (CEST) as a special type of magnetization transfer (MT) imaging presents a new way to detect small solute pools through indirect measurements of attenuated water signals, and makes the probing of semi-solid macromolecular protons possible [2, 3].To investigate the correlation between Nuclear Overhauser Enhancement (NOE) mediated CEST effect and the progression of glioma in a rat tumor model at 7.0 Tesla.We firstly build the rats glioma model with C6 glioma cells and then acquired NOE mediated CEST images (asymmetric magnetization transfer ratio (MTRasym) at -3.8 ppm, B1 = 0.6 μT), amide proton transfer (APT) mediated CEST images (MTRasym at 3.5 ppm, B1 = 1.6 μT) and T2 mediated images (T2WI) at the 8th day, 12th day, 16th day, 20th day after plantting tumor cells with a continuous wave pre-saturating echo planar imaging (EPI) acquisition sequence (CW-EPI sequence) at 7T. The EPI sequence parameters were set up as follows: flip angle = 90°, the repetition time (TR) = 6000 ms, the time of echo (TE) = 26.51 ms, matrix size = 64 × 64 mm2, field of view (FOV) = 30 × 30 mm2, number of acquisitions (NA) = 2, slice thickness = 2 mm, saturation duration time = 4 s. NOE mediated CEST effects decreased along with the growth of the tumor as shown in Fig. 1and Fig. 2. The NOE signal intension on the 8th day, 12th day, 16th day, 20th day is (3.84 +/- 0.114)%, (3.29 +/- 0.127)%, (2.22 +/- 0.105)%, (1.46 +/- 0.161)%, respectively (Fig. 2). A constant decrease trend of NOE effect was found in the tumor tissue, and its decrease extent continues with tumor growth (p < 0.01).In this study we observed a correlation between NOE-mediated CEST signal and the glioma progression at 7T in vivo.To our knowledge, this is the first study in which NOE effect changing with tumor progression was observed. Further research is needed to confirm the explicit origin of NOE mediated CEST and its clinical applications on the neoplasm stage estimate and the curative effect assessment.The contributors to the NOE peaks in brain are believed to include proteins/peptides, lipids, or restricted metabolites. The lipid content of brain tissue is low, so the contribution of lipids is generally not to be assessed in the brain NOE imaging. As we know many cellular activities including intercellular and intracellular communications are performed by proteins, and a lowered protein content in the C6 tumor tissues might explain why the NOE signal dropped. These in a molecular level provide pregnant information in tumor growth in vivo and are promising for clinical application.