Non-Hodgkin's lymphoma of T-cell types are rare neoplasms. Central nervous system metastasis is unusual. We are reporting a patient with peripheral T-cell lymphoma unspecified who had extra nodal metastasis into the brain that manifested with extrapyramidal dysfunction. The clinical presentation was exceptional in that the course was indolent and patient had no overt extra neural manifestations of malignancy for nearly 3 years after the onset of Parkinsonism. Striking brain imaging late in the disease supported by pathological findings enabled the diagnosis of this rare condition.

Background: Glioblastoma (GBM) is the most malignant and accounts for 60% of brain tumors in adults. Current therapy for GBM involves surgical removal of the tumor followed by radiotherapy with concomitant adjuvant therapy temozolomide. Despite improvements in therapy, patient survival remains low. The exact etiology of a brain tumor is uncertain, and numerous unknown genes are involved in the progression of GBM. The aim of the present study was to evaluate various genes involved in GBM through bioinformatic approach. Methods: In the present study, gene expression profile of GSE68424 was retrieved from the GEO database to explore the genes in GBM. Results: Analysis of expression profile data revealed that 33 genes were upregulated and 1189 genes were downregulated based on the log2 fold change cut-off criteria. The genes S-Phase kinase-associated protein 1 (SKP1) and Catenin beta-1 (CTNNB1) have been linked to GBM prognosis. Conclusion: SKP1 and CTNNB1 were identified as a candidate gene for GBM study as a result of these findings. Catenin beta-1 was the protein with the highest closeness centrality value and is the key component of canonical Wnt signaling downstream pathway. More study is needed to establish the molecular function of SKP1 and CTNNB1 in GBM development, as well as the biomarker's specificity and sensitivity.

Glioblastoma (GBM) is the primary brain tumor of the central nervous system which is most common and the most aggressive of all other types of tumors. Current therapy for GBM involves surgical removal (excision) of the tumor followed by radiotherapy with concomitant and adjuvant therapy with temozolomide. Despite the improvement in therapy for GBM, survival of the patients remains poor, only up to 1 year. Treatment for GBM is limited due to the presence of blood brain barrier which prevents the entry of molecules with molecular weight >500 Dalton. Various gene mutations or over expressions lead to GBM growth. Evidence from the earlier reports suggest that epidermal growth factor receptor is overexpressed in 60% of GBM. Interestingly, recent studies have suggested the involvement of sex hormones in the development and progression of GBM though the underlying mechanism of action of these hormones is poorly understood. In this review, we discuss the role of sex hormones and their receptors, a contributing factor in the development of GBM

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