Site specific hypermethylation of CpGs in Connexin genes 30, 26 and 43 in different grades of glioma and attenuated levels of their mRNAs.

Aim: Gliomas, the intracranial tumours are considered the deadliest malignancies. The gap junctional Connexins (Cxs) that maintain cellular homeostasis perform a unique function in glial tumour suppression. However, the differential methylation patterns of Cxs were not revealed in glioma so far.

Implication of connexin30 on the stemness of glioma: connexin30 reverses the malignant phenotype of glioma by modulating IGF-1R, CD133 and cMyc.

Gap-junctional intercellular communication (GJIC) plays a major role in the malignant growth of glioma. Although the mechanistic aspects of GJIC have been extensively studied, the role of connexins in the regulation of the malignant behavior of glioma stem cells (GSCs) remains unclear. In our previous studies, we have shown that connexin30 can interfere with the insulin-like growth factor 1 receptor (IGF-1R), which is known for self-renewal and pluripotency.

Connexin 30 downregulates Insulin-like growth factor receptor-1, abolishes Erk and potentiates effects of an IGF-R inhibitor in a glioma cell line.

Connexins (Cx) play a crucial role in cell communication though regulation of cell growth and proliferation. In recent decades, both suppressive and enhancing roles of gap junction proteins in malignancy have been proposed, though mechanisms remain unclear. We intend to evaluate the impact of Cx30 on dysregulated growth of glioma owing to an aberrant expression of Insulin-like growth factor-1 receptor (IGF-1R).

Pediatric gliosarcoma with fibrosarcomatous differentiation: report of a rare case.

Gliosarcoma is a rare variant of glioblastoma with a biphasic pattern showing glial and mesenchymal differentiation. It is seen in adults during their fifth to sixth decades of life and is extremely rare in children. We report a case of primary gliosarcoma with fibrosarcomatous differentiation in an 11-year-old boy presenting with headache and vomiting.