Glioblastoma multiforme (GBM): An overview of current therapies and mechanisms of resistance

Glioblastoma multiforme (GBM) is a WHO grade IV glioma and the most common malignant, primary brain tumor with a 5-year survival of 7.2%. Its highly infiltrative nature, genetic heterogeneity, and protection by the blood brain barrier (BBB) have posed great treatment challenges. The standard treatme...

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Published in	Pharmacological research Vol. 171; p. 105780
Main Authors	Wu, Wei, Klockow, Jessica L., Zhang, Michael, Lafortune, Famyrah, Chang, Edwin, Jin, Linchun, Wu, Yang, Daldrup-Link, Heike E.
Format	Journal Article
Language	English
Published	Netherlands Elsevier Ltd 01.09.2021
Subjects	Animals Antineoplastic Agents - therapeutic use Brain Neoplasms - drug therapy Chemotherapy Drug Resistance, Neoplasm Glioblastoma Glioblastoma - drug therapy Humans Immunotherapy Nanotherapy Radiotherapy Targeted therapy Lomustine (PubChem CID: 3950) Targeted therapy Glioblastoma Niraparib (PubChem CID: 24958200) Radiotherapy Nanotherapy Erlotinib (PubChem CID: 176870) Temozolomide (PubChem CID: 5394) Chemotherapy Veliparib (PubChem CID: 11960529) Carmustine (PubChem CID: 2578) Immunotherapy Irinotecan (PubChem CID: 60838) Cediranib (PubChem CID: 9933475) Gefitinib (PubChem CID: 123631) Olaparib (PubChem CID: 23725625)
Online Access	Get full text
ISSN	1043-6618 1096-1186 1096-1186
DOI	10.1016/j.phrs.2021.105780

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Abstract	Glioblastoma multiforme (GBM) is a WHO grade IV glioma and the most common malignant, primary brain tumor with a 5-year survival of 7.2%. Its highly infiltrative nature, genetic heterogeneity, and protection by the blood brain barrier (BBB) have posed great treatment challenges. The standard treatment for GBMs is surgical resection followed by chemoradiotherapy. The robust DNA repair and self-renewing capabilities of glioblastoma cells and glioma initiating cells (GICs), respectively, promote resistance against all current treatment modalities. Thus, durable GBM management will require the invention of innovative treatment strategies. In this review, we will describe biological and molecular targets for GBM therapy, the current status of pharmacologic therapy, prominent mechanisms of resistance, and new treatment approaches. To date, medical imaging is primarily used to determine the location, size and macroscopic morphology of GBM before, during, and after therapy. In the future, molecular and cellular imaging approaches will more dynamically monitor the expression of molecular targets and/or immune responses in the tumor, thereby enabling more immediate adaptation of tumor-tailored, targeted therapies. [Display omitted]
AbstractList	Glioblastoma multiforme (GBM) is a WHO grade IV glioma and the most common malignant, primary brain tumor with a 5-year survival of 7.2%. Its highly infiltrative nature, genetic heterogeneity, and protection by the blood brain barrier (BBB) have posed great treatment challenges. The standard treatment for GBMs is surgical resection followed by chemoradiotherapy. The robust DNA repair and self-renewing capabilities of glioblastoma cells and glioma initiating cells (GICs), respectively, promote resistance against all current treatment modalities. Thus, durable GBM management will require the invention of innovative treatment strategies. In this review, we will describe biological and molecular targets for GBM therapy, the current status of pharmacologic therapy, prominent mechanisms of resistance, and new treatment approaches. To date, medical imaging is primarily used to determine the location, size and macroscopic morphology of GBM before, during, and after therapy. In the future, molecular and cellular imaging approaches will more dynamically monitor the expression of molecular targets and/or immune responses in the tumor, thereby enabling more immediate adaptation of tumor-tailored, targeted therapies. Glioblastoma multiforme (GBM) is a WHO grade IV glioma and the most common malignant, primary brain tumor with a 5-year survival of 7.2%. Its highly infiltrative nature, genetic heterogeneity, and protection by the blood brain barrier (BBB) have posed great treatment challenges. The standard treatment for GBMs is surgical resection followed by chemoradiotherapy. The robust DNA repair and self-renewing capabilities of glioblastoma cells and glioma initiating cells (GICs), respectively, promote resistance against all current treatment modalities. Thus, durable GBM management will require the invention of innovative treatment strategies. In this review, we will describe biological and molecular targets for GBM therapy, the current status of pharmacologic therapy, prominent mechanisms of resistance, and new treatment approaches. To date, medical imaging is primarily used to determine the location, size and macroscopic morphology of GBM before, during, and after therapy. In the future, molecular and cellular imaging approaches will more dynamically monitor the expression of molecular targets and/or immune responses in the tumor, thereby enabling more immediate adaptation of tumor-tailored, targeted therapies. [Display omitted] Glioblastoma multiforme (GBM) is a WHO grade IV glioma and the most common malignant, primary brain tumor with a 5-year survival of 7.2%. Its highly infiltrative nature, genetic heterogeneity, and protection by the blood brain barrier (BBB) have posed great treatment challenges. The standard treatment for GBMs is surgical resection followed by chemoradiotherapy. The robust DNA repair and self-renewing capabilities of glioblastoma cells and glioma initiating cells (GICs), respectively, promote resistance against all current treatment modalities. Thus, durable GBM management will require the invention of innovative treatment strategies. In this review, we will describe biological and molecular targets for GBM therapy, the current status of pharmacologic therapy, prominent mechanisms of resistance, and new treatment approaches. To date, medical imaging is primarily used to determine the location, size and macroscopic morphology of GBM before, during, and after therapy. In the future, molecular and cellular imaging approaches will more dynamically monitor the expression of molecular targets and/or immune responses in the tumor, thereby enabling more immediate adaptation of tumor-tailored, targeted therapies.Glioblastoma multiforme (GBM) is a WHO grade IV glioma and the most common malignant, primary brain tumor with a 5-year survival of 7.2%. Its highly infiltrative nature, genetic heterogeneity, and protection by the blood brain barrier (BBB) have posed great treatment challenges. The standard treatment for GBMs is surgical resection followed by chemoradiotherapy. The robust DNA repair and self-renewing capabilities of glioblastoma cells and glioma initiating cells (GICs), respectively, promote resistance against all current treatment modalities. Thus, durable GBM management will require the invention of innovative treatment strategies. In this review, we will describe biological and molecular targets for GBM therapy, the current status of pharmacologic therapy, prominent mechanisms of resistance, and new treatment approaches. To date, medical imaging is primarily used to determine the location, size and macroscopic morphology of GBM before, during, and after therapy. In the future, molecular and cellular imaging approaches will more dynamically monitor the expression of molecular targets and/or immune responses in the tumor, thereby enabling more immediate adaptation of tumor-tailored, targeted therapies.
ArticleNumber	105780
Author	Chang, Edwin Wu, Yang Daldrup-Link, Heike E. Wu, Wei Lafortune, Famyrah Zhang, Michael Jin, Linchun Klockow, Jessica L.
AuthorAffiliation	5. Department of Neuropathology, Institute of Pathology, Technical University of Munich, Munich, Bayern, 81675, Germany 4. Lillian S. Wells Department of Neurosurgery, University of Florida, Gainesville, FL, 32611, USA 1. Department of Radiology, Molecular Imaging Program at Stanford, Stanford University, Stanford, CA, 94305, USA 2. Department of Radiation Oncology, Stanford University, Stanford, CA, 94305, USA 3. Department of Neurosurgery, Stanford University, Stanford, CA, 94305, USA
AuthorAffiliation_xml	– name: 3. Department of Neurosurgery, Stanford University, Stanford, CA, 94305, USA – name: 4. Lillian S. Wells Department of Neurosurgery, University of Florida, Gainesville, FL, 32611, USA – name: 5. Department of Neuropathology, Institute of Pathology, Technical University of Munich, Munich, Bayern, 81675, Germany – name: 1. Department of Radiology, Molecular Imaging Program at Stanford, Stanford University, Stanford, CA, 94305, USA – name: 2. Department of Radiation Oncology, Stanford University, Stanford, CA, 94305, USA
Author_xml	– sequence: 1 givenname: Wei orcidid: 0000-0002-0419-3466 surname: Wu fullname: Wu, Wei organization: Department of Radiology, Molecular Imaging Program at Stanford, Stanford University, Stanford, CA 94305, USA – sequence: 2 givenname: Jessica L. surname: Klockow fullname: Klockow, Jessica L. organization: Department of Radiation Oncology, Stanford University, Stanford, CA 94305, USA – sequence: 3 givenname: Michael orcidid: 0000-0002-7067-0689 surname: Zhang fullname: Zhang, Michael organization: Department of Radiology, Molecular Imaging Program at Stanford, Stanford University, Stanford, CA 94305, USA – sequence: 4 givenname: Famyrah orcidid: 0000-0001-5147-2102 surname: Lafortune fullname: Lafortune, Famyrah organization: Department of Radiology, Molecular Imaging Program at Stanford, Stanford University, Stanford, CA 94305, USA – sequence: 5 givenname: Edwin orcidid: 0000-0002-5672-0520 surname: Chang fullname: Chang, Edwin organization: Department of Radiology, Molecular Imaging Program at Stanford, Stanford University, Stanford, CA 94305, USA – sequence: 6 givenname: Linchun surname: Jin fullname: Jin, Linchun organization: Lillian S. Wells Department of Neurosurgery, University of Florida, Gainesville, FL 32611, USA – sequence: 7 givenname: Yang orcidid: 0000-0002-3104-153X surname: Wu fullname: Wu, Yang organization: Department of Neuropathology, Institute of Pathology, Technical University of Munich, Munich, Bayern 81675, Germany – sequence: 8 givenname: Heike E. surname: Daldrup-Link fullname: Daldrup-Link, Heike E. email: heiked@stanford.edu organization: Department of Radiology, Molecular Imaging Program at Stanford, Stanford University, Stanford, CA 94305, USA
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/34302977$$D View this record in MEDLINE/PubMed
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Keywords	Lomustine (PubChem CID: 3950) Targeted therapy Glioblastoma Niraparib (PubChem CID: 24958200) Radiotherapy Nanotherapy Erlotinib (PubChem CID: 176870) Temozolomide (PubChem CID: 5394) Chemotherapy Veliparib (PubChem CID: 11960529) Carmustine (PubChem CID: 2578) Immunotherapy Irinotecan (PubChem CID: 60838) Cediranib (PubChem CID: 9933475) Gefitinib (PubChem CID: 123631) Olaparib (PubChem CID: 23725625)
Language	English
License	Copyright © 2021 Elsevier Ltd. All rights reserved.
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Undefined-3 Credit Author Statement All authors are involved in the critical review and final acceptance of the submission. Co-first author
ORCID	0000-0002-0419-3466 0000-0001-5147-2102 0000-0002-5672-0520 0000-0002-3104-153X 0000-0002-7067-0689
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PublicationDate_xml	– month: 09 year: 2021 text: 2021-09-01 day: 01
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PublicationPlace_xml	– name: Netherlands
PublicationTitle	Pharmacological research
PublicationTitleAlternate	Pharmacol Res
PublicationYear	2021
Publisher	Elsevier Ltd
Publisher_xml	– name: Elsevier Ltd
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Snippet	Glioblastoma multiforme (GBM) is a WHO grade IV glioma and the most common malignant, primary brain tumor with a 5-year survival of 7.2%. Its highly...
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SubjectTerms	Animals Antineoplastic Agents - therapeutic use Brain Neoplasms - drug therapy Chemotherapy Drug Resistance, Neoplasm Glioblastoma Glioblastoma - drug therapy Humans Immunotherapy Nanotherapy Radiotherapy Targeted therapy
Title	Glioblastoma multiforme (GBM): An overview of current therapies and mechanisms of resistance
URI	https://dx.doi.org/10.1016/j.phrs.2021.105780 https://www.ncbi.nlm.nih.gov/pubmed/34302977 https://www.proquest.com/docview/2555110184 https://pubmed.ncbi.nlm.nih.gov/PMC8384724
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