{"title":"Glioblastoma treatment: Where to now?","authors":"T. Ware, Hong-Jian Zhu","doi":"10.15761/icst.1000280","DOIUrl":null,"url":null,"abstract":"Glioblastoma (GBM) remains an incurable disease with a poor overall survival. Despite extensive research into clinical trials, temozolomide remains the only therapeutic agent to improve patient survival in the past 50 years. This is despite only providing a modest increase of 2.5 months to median survival. Resistance to traditional therapies has become a hallmark of GBM, owing to its complex and undetermined molecular landscape. Studies now suggest that GBM is a disease of genetic subtypes and require tailored approaches to therapeutic care. Further strategies for GBM treatment involve targeting tumour associated neovascularisation. While early attempts to attenuate the tumour vascularisation with anti-VEGF has not been successful, studies are now looking towards other angiogenic factors and novel mechanisms of neovascularisation that have yet to be explored. A shift towards understanding the molecular and biological mechanisms of GBM pathogenesis represents a promising new strategy for treatment. Here we highlight some of the major developments to genetic profiling and anti-neovascularisation therapy.","PeriodicalId":90850,"journal":{"name":"Integrative cancer science and therapeutics","volume":"5 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Integrative cancer science and therapeutics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15761/icst.1000280","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Glioblastoma (GBM) remains an incurable disease with a poor overall survival. Despite extensive research into clinical trials, temozolomide remains the only therapeutic agent to improve patient survival in the past 50 years. This is despite only providing a modest increase of 2.5 months to median survival. Resistance to traditional therapies has become a hallmark of GBM, owing to its complex and undetermined molecular landscape. Studies now suggest that GBM is a disease of genetic subtypes and require tailored approaches to therapeutic care. Further strategies for GBM treatment involve targeting tumour associated neovascularisation. While early attempts to attenuate the tumour vascularisation with anti-VEGF has not been successful, studies are now looking towards other angiogenic factors and novel mechanisms of neovascularisation that have yet to be explored. A shift towards understanding the molecular and biological mechanisms of GBM pathogenesis represents a promising new strategy for treatment. Here we highlight some of the major developments to genetic profiling and anti-neovascularisation therapy.