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Hindi Editorial, J Spine Neurosurg Vol: 0 Issue: 0
Glioblastoma Multiforme(GBM) Therapy: Targeting Angiogenesis and Inflammation Pathways
| Andrew M. Albrecht, Jingxuan Yang and Min Li* |
| The Vivian L. Smith Department of Neurosurgery, The University of Texas Medical School at Houston, Houston, Texas 77030, USA |
| Corresponding author : Min Li, Ph.D The Vivian L. Smith Department of Neurosurgery, The University of Texas Medical School at Houston, 6431 Fannin Street, MSE R266, Houston, TX 77030 Tel: (713) 500-6491; Fax: (713) 500-6493 E-mail: Min.Li@uth.tmc.edu |
| Received: July 28, 2012 Accepted: July 29, 2012 Published: July 31, 2012 |
| Citation: Albrecht AM, Yang J, Li M (2012) Glioblastoma Multiforme (GBM) Therapy: Targeting Angiogenesis and Inflammation Pathways. J Spine Neurosurg 1:1. doi:10.4172/2325-9701.1000e103 |
Abstract
Glioblastoma Multiforme(GBM) Therapy: Targeting Angiogenesis and Inflammation Pathways
Glioblastoma multiforme (GBM) is the most common and deadly primary brain tumor due to its high rate of metastasis and aggressive infiltration into surrounding tissues. Because of the high resistance to standard therapy, the median survival time of GBM is only 15 months for a patient undergoing reductive surgical resection followed by chemotherapeutics such as temozolomide (TMZ) as well as adjuvant radiotherapy. The current therapies are ineffective largely due to the poor drug delivery and the incomplete knowledge of the signaling pathways controlling the malignant behavior, leading to an extremely high occurrence of relapse. As we learn more about the epigenetic factors and genetic mutations that drive GBM’s progression, we are left with the question: is it possible to develop a novel treatment which can effectively inhibit GBM cell growth and metastasis? Although the mechanisms of GBM pathogenesis and progression are not completely understood, recent advances in the understanding of the signaling pathways that underlie GBM progression and the interaction of the tumor cells with the microenvironment have led to new insights in development of novel therapeutic approaches targeting multiple oncogenic pathways associated with GBM.
