Therapeutic intervention of glioma with the novel antineoplastic agent T11TS: the story so far.

The disease relevance of novel therapeutic agent T11TS, established first by the authors' group, was shown to ameliorate experimental glioma through multimodal mechanistic activities. T11TS reverses immunosuppression in glioma, causing profound effects on immune potentiation via peripheral, intracranial and hematopoietic cells. T-cell signaling in glioma is reversed by T11TS, modulating cytokine levels and favoring apoptotic killing of glioma cells. T11TS arrests the glioma cell cycle at the G1 phase via activation of p21. VEGF downregulation hypophosphorylates the Akt pathway. T11TS hinders endothelial cell progression and metastasis by arresting matrix degradation, inhibiting the Ras-Raf and Akt-PTEN pathways and initiating inflammatory changes, causing apoptosis. T11TS is effective against Glioma is a fatal brain tumor, and conventional treatments with surgery, radiotherapy, and chemotherapy often cause cancer recurrence. Therefore, newer strategies of treatment are being developed. In the authors' laboratory, a novel molecular approach with the biomolecule T11TS has been successfully applied in the eradication of glioma in an experimental rat model and on human samples. T11TS ameliorates glioma by various means, including immune augmentation and cytokine modulation; causes glioma cell death (apoptotic); halts the glioma cell cycle; and retards glioma blood vessel growth (antiangiogenic). T11TS is nontoxic. The author's study points to novel glioma therapy.