MATERIALS AND METHODS: We analyzed 46 histologically proven glioma (WHO grades II-IV) patients using standard 3T magnetic resonance imaging brain tumor protocol and IOP sequence. Lipid fraction was derived from the IOP sequence signal-loss ratio. The lipid fraction of solid nonenhancing region of glioma was analyzed, using a three-group analysis approach based on volume under surface of receiver-operating characteristics to stratify the prognostic factors into three groups of low, medium, and high lipid fraction. The survival outcome was evaluated, using Kaplan-Meier survival analysis and Cox regression model.
RESULTS: Significant differences were seen between the three groups (low, medium, and high lipid fraction groups) stratified by the optimal cut-off point for overall survival (OS) (p ≤ 0.01) and time to progression (p ≤ 0.01) for solid nonenhancing region. The group with high lipid fraction had five times higher risk of poor survival and earlier time to progression compared to the low lipid fraction group. The OS plot stratified by lipid fraction also had a strong correlation with OS plot stratified by WHO grade (R = 0.61, p < 0.01), implying association to underlying histopathological changes.
CONCLUSION: The lipid fraction of solid nonenhancing region showed potential for prognostication of glioma. This method will be a useful adjunct in imaging protocol for treatment stratification and as a prognostic tool in glioma patients.
METHODS: Oral cancer cell lines and a normal oral keratinocyte cell line were used together with tissue samples of normal oral mucosa (n = 21), oral epithelial dysplasia (n = 74) and early stage (Stages I and II) oral squamous cell carcinoma (n = 31). Immunocytochemical staining, immunoblotting and real-time quantitative polymerase chain reaction (PCR) were performed to assess protein as well as gene expression levels.
RESULTS: The expression levels of Epsin3 and Notch1 mRNA and protein are variable across different oral squamous cell carcinoma derived cell lines. Epsin3 was upregulated in oral epithelial dysplasia and oral squamous cell carcinoma tissues compared with normal epithelium. Overexpression of Epsin3 resulted in a significant reduction of Notch1 expression in oral squamous cell carcinoma. Notch1 was generally downregulated in the dysplasia and oral squamous cell carcinoma samples.
CONCLUSION: Epsin3 is upregulated in oral epithelial dysplasia and oral squamous cell carcinoma and has the potential to be used as a biomarker for oral epithelial dysplasia. Notch signalling is downregulated in oral squamous cell carcinoma, possibly through an Epsin3-induced de-activation pathway.
CASE REPORT: This case report is that of a 9-year-old male who presented with frontal headache of eight days, with associated photophobia, nausea and vomiting, and diplopia. Biopsy with intraoperative navigation was done and the specimen was referred for histopathologic evaluation. The biopsy showed findings consistent with a mature teratoma with no histologic findings of an immature component or secondary somatic malignancy. Comparison of the pre-operative and post-operative multiaxial cranial CT scan showed findings that was consistent with a residual lesion. This was correlated with the pre-operative serum tumour markers which showed alpha-fetoprotein of 22.5 ng/mL and beta-HCG of 1.0 mIU/mL(IU/L), and the post-operative tumour markers of the cerebrospinal fluid that showed alpha-fetoprotein of 3.28 ng/mL and beta-HCG of 18.9 mIU/mL (IU/L).
CONCLUSION: A review of the literature and comparison with current case in relation to the histopathologic, serum and CSF findings, and imaging studies was done to better understand the mechanism of this lesion.