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This review summarizes targeted therapeutic strategies for glioblastoma using English-language literature from major research databases and emphasizes key search terms related to glioblastoma, molecular targets, and targeted therapeutic 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Targeted Therapeutic Drugs in Treatment of Glioblastoma: A Review Article  \nHimanshu Singh 1  \n1 Department of Oral and Maxillofacial Pathology and Oral Microbiology, Index Institute of Dental Sciences, Indore, Madhya Pradesh, India  \nGlob Med Genet 2023;10:42–47.  \nAddress for correspondence Himanshu Singh, MDS, Department of Oral and Maxillofacial Pathology and Oral Microbiology, Index Institute of Dental Sciences, Indore, Madhya Pradesh, 452016, India (e-mail: [himanshustar3g@gmail.com](himanshustar3g@gmail.com)).  \nAbstract  \nKeywords  \n► glioblastoma  \n► targeted therapy  \n► molecular targets  \n► therapeutic drugs  \nGlioblastoma is remarkably periodic primary brain tumor, characterizing an eminently heterogeneous pattern of neoplasms that are utmost destructive and threatening cancers.  \nAn enhanced and upgraded knowledge of the various molecular pathways that cause malignant changes in glioblastoma has resulted in advancement of numerous biomarkers and the interpretation of various agents that pointedly target tumor cells and microenvironment. In this review, literature or information on various targeted therapy for glioblastoma is discussed. English language articles were scrutinized in plentiful directory or databases like PubMed, ScienceDirect, Web of Sciences, Google Scholar, and Scopus. The important keywords used for searching databases are “Glioblastoma,”“Targeted therapy in glioblastoma,” “Therapeutic drugs in glioblastoma,” and “Molecular targets in glioblastoma.”  \nIntroduction  \nGlioblastoma is the utmost common and destructive primary malignant brain tumor seen in adults including average overall survival (OS) of 10 to 20 months.1–4 Glioblastoma comprises an eminently heterogeneous collection of protruding malignant tumors of the brain.5  \nIn a nutshell, the abovementioned research demonstrated that nearly all tumors suppress periodic molecular modifi cations eradicating core pathways engaged in the control of growth and deoxyribonucleic acid repair. It is acknowledged that glioblastomas are described by considerable intratumor and intertumor genomic heterogeneity.6–10 Depending upon the findings of the Cancer Genome Atlas, there are four distinctive subdivisions of glioblastomas. These are the neural, proneural, mesenchymal, and classical subtypes. The neural subdivision illustrates 16% of glioblastoma. The  \nDOI [https://doi.org/](https://doi.org/)[ ](https://doi.org/)[10.1055/s-0043-57028.](10.1055/s-0043-57028.)[ ](10.1055/s-0043-57028.)[ISSN](ISSN 2699-9404.)[ 2699-9404.](ISSN 2699-9404.)  \nneural subdivision is represented by the expression of various neuron markers like GABRA1, SLC1A5, and NEFL. The proneural subdivision demonstrates mutation in plateletderived growth factor receptor A (PDGFRA). The classical subdivision demonstrated CDKN2A deletion and epidermal growth factor receptor (EGFR) amplification. The mesenchymal subdivision demonstrates mutations in phosphatase and tensin homolog (PTEN) and NF1 (neurofibromatosis type 1).11  \nIn this review, literature or information on various targeted therapy for glioblastoma is discussed. English language articles were scrutinized in plentiful directory or databases like PubMed, ScienceDirect, Web of Sciences, Google Scholar, and Scopus. The important keywords used for searching databases are “Glioblastoma,” “Targeted therapy in glioblastoma,” “Therapeutic drugs in glioblastoma,” and “Molecular targets in glioblastoma.”  \n© 2023 . The Author(s) .  \nThis is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited.([https://creativecommons.org/licenses/by/4.0/](https://creativecommons.org/licenses/by/4.0/))  \nGeorg Thieme Verlag KG, Rüdigerstraße 14, 70469 Stuttgart, Germany  \nMolecular Targeted Drugs and Glioblastoma Singh ","cbCaiiWR66vfIsx9","https://ap.wps.com/l/cbCaiiWR66vfIsx9","pdf",180077,"English","# Abstract and Keywords\n# Introduction\n# Various Molecular Targeted Therapeutics for Glioblastoma\n## Receptor Tyrosine Kinases\n## Epidermal Growth Factor Receptor","[{\"question\":\"What is the main focus of this review article on glioblastoma?\",\"answer\":\"It discusses targeted therapeutic drugs and strategies that point toward molecular targets in glioblastoma, including how knowledge of molecular pathways supports these therapies.\"},{\"question\":\"How are glioblastoma subtypes described in the introduction?\",\"answer\":\"Four subdivisions are referenced—neural, proneural, mesenchymal, and classical—with representative molecular marker and alteration patterns for each subtype.\"},{\"question\":\"Which molecular target class is discussed first under targeted therapeutics?\",\"answer\":\"Receptor tyrosine kinases are introduced as transmembrane proteins involved in cellular processes, and their dysregulation is linked to glioblastoma initiation and progression.\"}]","Role of Molecular Targeted Therapeutic Drugs in Treatment of Glioblastoma - A Review Article | PDF",1790560515,15]