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      Combined-therapeutic strategies synergistically potentiate glioblastoma multiforme treatment via nanotechnology

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          Abstract

          Glioblastoma multiforme (GBM) is a highly aggressive and devastating brain tumor characterized by poor prognosis and high rates of recurrence. Numerous therapeutic strategies and delivery systems are developed to prolong the survival time. They exhibit enhanced therapeutic effects in animal models, whereas few of them is applied in clinical trials. Taking into account the drug-resistance and high recurrence of GBM, combined-therapeutic strategies are exploited to maximize therapeutic efficacy. The combined therapies demonstrate superior results than those of single therapies against GBM. The co-therapeutic agents, the timing of therapeutic strategies and the delivery systems greatly affect the overall outcomes. Herein, the current advances in combined therapies for glioblastoma via systemic administration are exhibited in this review. And we will discuss the pros and cons of these combined-therapeutic strategies via nanotechnology, and provide the guidance for developing rational delivery systems to optimize treatments against GBM and other malignancies in central nervous system.

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          A restricted cell population propagates glioblastoma growth following chemotherapy

          Jian Chen, Yanjiao Li, Tzong-Shiue Yu … (2012)
          Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor, with a median survival of about one year 1 . This poor prognosis is due to therapeutic resistance and tumor recurrence following surgical removal. Precisely how recurrence occurs is unknown. Using a genetically-engineered mouse model of glioma, we identify a subset of endogenous tumor cells that are the source of new tumor cells after the drug, temozolomide (TMZ), is administered to transiently arrest tumor growth. A Nestin-ΔTK-IRES-GFP (Nes-ΔTK-GFP) transgene that labels quiescent subventricular zone adult neural stem cells also labels a subset of endogenous glioma tumor cells. Upon arrest of tumor cell proliferation with TMZ, pulse-chase experiments demonstrate a tumor re-growth cell hierarchy originating with the Nes-ΔTK-GFP transgene subpopulation. Ablation of the GFP+ cells with chronic ganciclovir administration significantly arrested tumor growth and combined TMZ-ganciclovir treatment impeded tumor development. These data indicate the existence of a relatively quiescent subset of endogenous glioma cells that are responsible for sustaining long-term tumor growth through the production of transient populations of highly proliferative cells.
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            Current state of immunotherapy for glioblastoma

            Chetan Bettegowda, Michael Lim, Yuanxuan Xia … (2018)
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              Combined antiangiogenic and anti–PD-L1 therapy stimulates tumor immunity through HEV formation

              Elizabeth Allen, Arnaud Jabouille, Lee B. Rivera … (2017)
              Inhibitors of VEGF (vascular endothelial growth factor)/VEGFR2 (vascular endothelial growth factor receptor 2) are commonly used in the clinic, but their beneficial effects are only observed in a subset of patients and limited by induction of diverse relapse mechanisms. We describe the up-regulation of an adaptive immunosuppressive pathway during antiangiogenic therapy, by which PD-L1 (programmed cell death ligand 1), the ligand of the negative immune checkpoint regulator PD-1 (programmed cell death protein 1), is enhanced by interferon-γ-expressing T cells in distinct intratumoral cell types in refractory pancreatic, breast, and brain tumor mouse models. Successful treatment with a combination of anti-VEGFR2 and anti-PD-L1 antibodies induced high endothelial venules (HEVs) in PyMT (polyoma middle T oncoprotein) breast cancer and RT2-PNET (Rip1-Tag2 pancreatic neuroendocrine tumors), but not in glioblastoma (GBM). These HEVs promoted lymphocyte infiltration and activity through activation of lymphotoxin β receptor (LTβR) signaling. Further activation of LTβR signaling in tumor vessels using an agonistic antibody enhanced HEV formation, immunity, and subsequent apoptosis and necrosis in pancreatic and mammary tumors. Finally, LTβR agonists induced HEVs in recalcitrant GBM, enhanced cytotoxic T cell (CTL) activity, and thereby sensitized tumors to antiangiogenic/anti-PD-L1 therapy. Together, our preclinical studies provide evidence that anti-PD-L1 therapy can sensitize tumors to antiangiogenic therapy and prolong its efficacy, and conversely, antiangiogenic therapy can improve anti-PD-L1 treatment specifically when it generates intratumoral HEVs that facilitate enhanced CTL infiltration, activity, and tumor cell destruction.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Theranostics
                Journal ID (iso-abbrev): Theranostics
                Journal ID (publisher-id): thno
                Title: Theranostics
                Publisher: Ivyspring International Publisher (Sydney )
                ISSN (Electronic): 1838-7640
                Publication date Collection: 2020
                Publication date (Electronic): 10 February 2020
                Volume: 10
                Issue: 7
                Pages: 3223-3239
                Affiliations
                [1 ]State Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Sciences, Beijing 100190, PR China
                [2 ]University of Chinese Academy of Sciences, Beijing 100049, PR China
                Author notes
                ✉ Corresponding author: Xin Zhang, State Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Sciences. Tel./fax: +86 10 82544853. Email: xzhang@ 123456ipe.ac.cn .

                *These authors contributed equally to this work.

                Competing Interests: The authors have declared that no competing interest exists.

                Article
                Publisher ID: thnov10p3223
                DOI: 10.7150/thno.40298
                PMC ID: 7053190
                PubMed ID: 32194864
                SO-VID: 2f6c5a29-4b3f-4b0f-950d-70383514254d
                Copyright © © The author(s)
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.

                History
                Date received : 14 September 2019
                Date accepted : 6 December 2019
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: glioblastoma,combined therapy,nanotechnology,drug delivery
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: glioblastoma, combined therapy, nanotechnology, drug delivery

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