DNA methylation is an epigenetic change to the genome that impacts gene activities without modification to the DNA sequence. Alteration in the methylation pattern is a naturally occurring event throughout the human life cycle which may result in the development of diseases such as cancer. In this study, we analyzed methylation data from The Cancer Genome Atlas, under the Lower-Grade Glioma (LGG) and Glioblastoma Multiforme (GBM) projects, to identify methylation markers that exhibit unique changes in DNA methylation pattern along with tumor grade progression, to predict patient survival. We found ten glioma grade-associated Cytosine-phosphate-Guanine (CpG) sites that targeted four genes (SMOC1, KCNA4, SLC25A21, and UPP1) and the methylation pattern is strongly associated with glioma specific molecular alterations, primarily isocitrate dehydrogenase (IDH) mutation and chromosome 1p/19q codeletion. The ten CpG sites collectively distinguished a cohort of diffuse glioma patients with remarkably poor survival probability. Our study highlights genes (KCNA4 and SLC25A21) that were not previously associated with gliomas to have contributed to the poorer patient outcome. These CpG sites can aid glioma tumor progression monitoring and serve as prognostic markers to identify patients diagnosed with less aggressive and malignant gliomas that exhibit similar survival probability to GBM patients.
Fluctuations in serum autofluorescence (AF) intensity have recently been widely used as markers of certain diseases such as cancer. To determine the diagnostic value of serum AF intensity for liver fibrosis in rats, we induced liver fibrosis by subcutaneous injection of carbon tetrachloride into rats. The rat serum AF intensities were detected at the excitation wavelength of 337 nm and the emission wavelength of 512 nm. The degree of liver fibrosis was evaluated by Van Gieson’s staining. The relationship between serum AF intensity and the degree of liver fibrosis was analyzed by Spearman and Pearson Correlation. The diagnostic sensitivity and specificity of the serum AF was determined by analyzing the receiver operating characteristic (ROC) curves. Our results show that the serum AF intensity in the rat liver fibrosis model increased when compared with control rats eight weeks and twelve weeks post induction of liver fibrosis. However, there was no significant difference in serum AF intensity between fibrotic and control rats at four week post induction. Furthermore, serum AF intensity correlated positively with the severity of the degree of hepatic fibrosis. ROC analysis further suggested that serum AF intensity is a valid marker for staging fibrosis. Therefore, it may potentially be developed as a novel diagnostic tool for hepatic fibrosis.
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