For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
10
views
157
references
 Top references
cited by
34
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      397
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Mouse models of glioblastoma for the evaluation of novel therapeutic strategies

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Glioblastoma (GBM) is an incurable brain tumor with a median survival of approximately 15 months despite an aggressive standard of care that includes surgery, chemotherapy, and ionizing radiation. Mouse models have advanced our understanding of GBM biology and the development of novel therapeutic strategies for GBM patients. However, model selection is crucial when testing developmental therapeutics, and each mouse model of GBM has unique advantages and disadvantages that can influence the validity and translatability of experimental results. To shed light on this process, we discuss the strengths and limitations of 3 types of mouse GBM models in this review: syngeneic models, genetically engineered mouse models, and xenograft models, including traditional xenograft cell lines and patient-derived xenograft models.

          Related collections

          Most cited references157

          • Record: found
          • Abstract: found
          • Article: not found

          Tumor mutational load predicts survival after immunotherapy across multiple cancer types

          Robert M. Samstein, Chung-Han Lee, Alexander Shoushtari … (2019)
          Immune checkpoint inhibitor (ICI) treatments benefit some patients with metastatic cancers, but predictive biomarkers are needed. Findings in select cancer types suggest that tumor mutational burden (TMB) may predict clinical response to ICI.To examine this association more broadly, we analyzed the clinical and genomic data of 1662 advanced cancer patients treated with ICI, and 5371 non-ICI treated patients, whose tumors underwent targeted next-generation sequencing (MSK-IMPACT). Among all patients, higher somatic TMB (highest 20% in each histology) was associated with better OS (HR 0.52; p=1.6 ×10 −6 ). For most cancer histologies, an association between higher TMB and improved survival was observed. The TMB cutpoints associated with improved survival varied markedly between cancer types. These data indicate that TMB is associated with improved survival in patients receiving ICI across a wide variety of cancer types, but that there may not be one universal definition of high TMB.
          Article 0 comments Cited 1623 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found

            Comprehensive genomic characterization defines human glioblastoma genes and core pathways

            (2008)
            Human cancer cells typically harbor multiple chromosomal aberrations, nucleotide substitutions and epigenetic modifications that drive malignant transformation. The Cancer Genome Atlas (TCGA) pilot project aims to assess the value of large-scale multidimensional analysis of these molecular characteristics in human cancer and to provide the data rapidly to the research community. Here, we report the interim integrative analysis of DNA copy number, gene expression and DNA methylation aberrations in 206 glioblastomas (GBM), the most common type of adult brain cancer, and nucleotide sequence aberrations in 91 of the 206 GBMs. This analysis provides new insights into the roles of ERBB2, NF1 and TP53, uncovers frequent mutations of the PI3 kinase regulatory subunit gene PIK3R1, and provides a network view of the pathways altered in the development of GBM. Furthermore, integration of mutation, DNA methylation and clinical treatment data reveals a link between MGMT promoter methylation and a hypermutator phenotype consequent to mismatch repair deficiency in treated glioblastomas, an observation with potential clinical implications. Together, these findings establish the feasibility and power of TCGA, demonstrating that it can rapidly expand knowledge of the molecular basis of cancer.
            Article 0 comments Cited 916 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Glioma stem cells promote radioresistance by preferential activation of the DNA damage response.

              Shideng Bao, Qiulian Wu, Roger McLendon … (2006)
              Ionizing radiation represents the most effective therapy for glioblastoma (World Health Organization grade IV glioma), one of the most lethal human malignancies, but radiotherapy remains only palliative because of radioresistance. The mechanisms underlying tumour radioresistance have remained elusive. Here we show that cancer stem cells contribute to glioma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity. The fraction of tumour cells expressing CD133 (Prominin-1), a marker for both neural stem cells and brain cancer stem cells, is enriched after radiation in gliomas. In both cell culture and the brains of immunocompromised mice, CD133-expressing glioma cells survive ionizing radiation in increased proportions relative to most tumour cells, which lack CD133. CD133-expressing tumour cells isolated from both human glioma xenografts and primary patient glioblastoma specimens preferentially activate the DNA damage checkpoint in response to radiation, and repair radiation-induced DNA damage more effectively than CD133-negative tumour cells. In addition, the radioresistance of CD133-positive glioma stem cells can be reversed with a specific inhibitor of the Chk1 and Chk2 checkpoint kinases. Our results suggest that CD133-positive tumour cells represent the cellular population that confers glioma radioresistance and could be the source of tumour recurrence after radiation. Targeting DNA damage checkpoint response in cancer stem cells may overcome this radioresistance and provide a therapeutic model for malignant brain cancers.
              Article 0 comments Cited 705 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Neurooncol Adv
                Journal ID (iso-abbrev): Neurooncol Adv
                Journal ID (publisher-id): noa
                Title: Neuro-oncology Advances
                Publisher: Oxford University Press (US )
                ISSN (Electronic): 2632-2498
                Publication date Collection: Jan-Dec 2021
                Publication date (Electronic): 26 July 2021
                Publication date PMC-release: 26 July 2021
                Volume: 3
                Issue: 1
                Electronic Location Identifier: vdab100
                Affiliations
                [1 ]Department of Neurological Surgery, University of California , San Francisco, California, USA
                [2 ]Department of Radiation Oncology, University of California , San Francisco, San Francisco, California, USA
                Author notes
                Corresponding Author: Nicholas A. Butowski, MD, Department of Neurological Surgery, University of California, San Francisco, 400 Parnassus Ave Eighth Floor, San Francisco, CA, 94143, USA ( nicholas.butowski@ 123456ucsf.edu ).
                Author information
                https://orcid.org/0000-0003-1983-4892
                Article
                Publisher ID: vdab100
                DOI: 10.1093/noajnl/vdab100
                PMC ID: 8403483
                PubMed ID: 34466804
                SO-VID: cdfd5c4c-4cbc-4143-82f8-492920f12bce
                Copyright © © The Author(s) 2021. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date: 29 August 2021
                Page count
                Pages: 16
                Categories
                Subject: Reviews
                Subject: AcademicSubjects/MED00300
                Subject: AcademicSubjects/MED00310

                Keywords: murine models,glioblastoma,tumor,u87,gl261
                Data availability:
                Keywords: murine models, glioblastoma, tumor, u87, gl261

                Comments

                Comment on this article

                scite_

                Similar content397

                See all similar

                Cited by34

                See all cited by

                Most referenced authors2,926

                See all reference authors