Ghosalkar, J and Sonawane, V and Khan, M and Joshi, K and Shastry, P (2022) Prostate Apoptosis Response-4: a Therapeutic Target for Malignant Gliomas. In: Tumor Suppressor Par-4. : Role in Cancer and other Diseases. Springer, pp. 77-111.
Full text not available from this repository. (Request a copy)Abstract
Gliomas are the most common type of primary brain tumors and glioblastoma (GBM), the most lethal of gliomas accounts for more than 60% of all brain tumors in adults. Despite the advances in multimodal therapies over the last two decades, the prognosis is extremely poor. Various factors including glioma stem cells (GSC), genetic mutations, epigenetic modifications, and dysregulated pathways cumulatively render the GBM resistant to radiation and chemotherapies. While efforts are on to develop new drugs that can efficiently cross the blood–brain barrier (BBB), it has become important to identify novel strategies and molecular targets that reduce the tumor size, increase overall survival, progression-free survival and improve the quality of life. Prostate apoptosis response-4 (Par-4) is a unique tumor suppressor with the ability to selectively induce apoptosis in cancer cells but not kill the normal cells. The pro-apoptotic activity of Par-4 is exerted in an autocrine as well as paracrine manner. Furthermore, various inducers and secretagogues of Par-4 which have the ability to upregulate both intracellular and secretory Par-4 are being explored as strategies for cancer therapy. This chapter provides an overview of gliomas with a focus on GBM and the challenges in the development of drugs for the treatment of GBM. Also, we discuss the importance of microenvironment and the potential role of Par-4 in the highly interconnected signaling network thereby highlighting the importance of Par-4 as an exciting therapeutic target.
Item Type: | Book Section |
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Subjects: | Cancer Biology |
Depositing User: | Mr. Rameshwar Nema |
Date Deposited: | 12 Oct 2022 09:55 |
Last Modified: | 12 Oct 2022 09:55 |
URI: | http://nccs.sciencecentral.in/id/eprint/1155 |
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