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Cancers
Special Issues
Novel Experimental Therapeutic Targets and Strategies for Brain Tumors
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Novel Experimental Therapeutic Targets and Strategies for Brain Tumors

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: 31 May 2025 | Viewed by 6696

Special Issue Editors

Dr. Yunqing Li

E-Mail Website
Guest Editor
Hugo W. Moser Research Institute at Kennedy Krieger and Department of Neurology, The Johns Hopkins School of Medicine, Baltimore, MD, USA
Interests: glioblastoma; brain tumors
Prof. Dr. Roger Abounader

E-Mail Website
Guest Editor
Department of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, VA 22903, USA
Interests: basic and translational brain tumor research

Special Issue Information

Dear Colleagues,

Brain cancers are one of the most deadly tumors with poor prognoses. The 5-year survival rate for people with a cancerous brain or CNS tumor in the USA is about 36%, despite the advances in surgical resection and ionizing radiation +/− chemotherapy. Since treating malignant brain tumors is frustratingly ineffective, it is imperative to identify novel therapeutic targets and approaches, and develop more effective combinational therapies.

This Special Issue focuses on the identification of new experimental therapeutic targets and/or the development of new therapeutic strategies for adult and pediatric brain tumors. We are particularly (but not exclusively) interested in drugs and approaches that sensitize tumors to standard-of-care radiotherapy, chemotherapy, and immunotherapy, as well as clinical trials with small molecule inhibitors and other drugs. We are also seeking articles that describe novel combinational therapies and innovative drug delivery approaches. We are pleased to invite you to submit original research articles and reviews on the above areas of research. We hope that this Special Issue will enhance our understanding of brain tumors and the development and testing of new therapies. We look forward to receiving your contributions.

Dr. Yunqing Li
Prof. Dr. Roger Abounader
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • brain tumors
  • glioma
  • glioblastoma
  • medulloblastoma
  • radiotherapy
  • chemotherapy
  • immunotherapy
  • combination therapy
  • microRNAs
  • oncogene signaling pathways
  • epigenetic regulation
  • metabolic regulation
  • nanotechnology
  • drug delivery

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Published Papers (3 papers)

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Research

13 pages, 6624 KiB  
Article
Temozolomide and the PARP Inhibitor Niraparib Enhance Expression of Natural Killer Group 2D Ligand ULBP1 and Gamma-Delta T Cell Cytotoxicity in Glioblastoma
by Amber B. Jones, Kaysaw Tuy, Cyntanna C. Hawkins, Colin H. Quinn, Joelle Saad, Sam E. Gary, Elizabeth A. Beierle, Lei Ding, Kate M. Rochlin, Lawrence S. Lamb and Anita B. Hjelmeland
Cancers 2024, 16(16), 2852; https://doi.org/10.3390/cancers16162852 - 15 Aug 2024
Viewed by 1051
Abstract
Glioblastoma (GBM) is an immunologically cold tumor, but several immunotherapy-based strategies show promise, including the administration of ex vivo expanded and activated cytotoxic gamma delta T cells. Cytotoxicity is partially mediated through interactions with natural killer group 2D ligands (NKG2DL) on tumor cells. [...] Read more.
Glioblastoma (GBM) is an immunologically cold tumor, but several immunotherapy-based strategies show promise, including the administration of ex vivo expanded and activated cytotoxic gamma delta T cells. Cytotoxicity is partially mediated through interactions with natural killer group 2D ligands (NKG2DL) on tumor cells. We sought to determine whether the addition of the blood–brain barrier penetrant PARP inhibitor niraparib to the standard of care DNA alkylator temozolomide (TMZ) could upregulate NKG2DL, thereby improving immune cell recognition. Changes in viability were consistent with prior publications as there was a growth inhibitory effect of the combination of TMZ and niraparib. However, decreases in viability did not always correlate with changes in NKG2DL mRNA. ULBP1/Mult-1 mRNA was increased with the combination therapy in comparison to either drug alone in two of the three cell types tested, even though viability was consistently decreased. mRNA expression correlated with protein levels and ULBP1/MULT-1 cell surface protein was significantly increased with TMZ and niraparib treatment in four of the five cell types tested. Gamma delta T cell-mediated cytotoxicity at a 10:1 effector-to-target ratio was significantly increased upon pretreatment of cells derived from a GBM PDX with TMZ and niraparib in comparison to the control or either drug alone. Together, these data demonstrate that the combination of PARP inhibition, DNA alkylation, and gamma delta T cell therapy has the potential for the treatment of GBM. Full article
(This article belongs to the Special Issue Novel Experimental Therapeutic Targets and Strategies for Brain Tumors)
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16 pages, 9024 KiB  
Article
Phase I/II Trial of Urokinase Plasminogen Activator-Targeted Oncolytic Newcastle Disease Virus for Canine Intracranial Tumors
by John H. Rossmeisl, Jamie N. King, John L. Robertson, James Weger-Lucarelli and Subbiah Elankumaran
Cancers 2024, 16(3), 564; https://doi.org/10.3390/cancers16030564 - 29 Jan 2024
Cited by 1 | Viewed by 1595
Abstract
Neurotropic oncolytic viruses are appealing agents to treat brain tumors as they penetrate the blood–brain barrier and induce preferential cytolysis of neoplastic cells. The pathobiological similarities between human and canine brain tumors make immunocompetent dogs with naturally occurring tumors attractive models for the [...] Read more.
Neurotropic oncolytic viruses are appealing agents to treat brain tumors as they penetrate the blood–brain barrier and induce preferential cytolysis of neoplastic cells. The pathobiological similarities between human and canine brain tumors make immunocompetent dogs with naturally occurring tumors attractive models for the study of oncolytic virotherapies. In this dose-escalation/expansion study, an engineered Lasota NDV strain targeting the urokinase plasminogen activator system (rLAS-uPA) was administered by repetitive intravenous infusions to 20 dogs with intracranial tumors with the objectives of characterizing toxicities, immunologic responses, and neuroradiological anti-tumor effects of the virus for up to 6 months following treatment. Dose-limiting toxicities manifested as fever, hematologic, and neurological adverse events, and the maximum tolerated dose (MTD) of rLAS-uPA was 2 × 107 pfu/mL. Mild adverse events, including transient infusion reactions, diarrhea, and fever were observed in 16/18 of dogs treated at or below MTD. No infectious virus was recoverable from body fluids. Neutralizing antibodies to rLAS-uPA were present in all dogs by 2 weeks post-treatment, and viral genetic material was detected in post-treatment tumors from six dogs. Tumor volumetric reductions occurred in 2/11 dogs receiving the MTD. Systemically administered rLAS-uPA NDV was safe and induced anti-tumor effects in canine brain tumors, although modifications to evade host anti-viral immunity are needed to optimize this novel therapy. Full article
(This article belongs to the Special Issue Novel Experimental Therapeutic Targets and Strategies for Brain Tumors)
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22 pages, 2384 KiB  
Article
Repurposing Clemastine to Target Glioblastoma Cell Stemness
by Michael A. Sun, Rui Yang, Heng Liu, Wenzhe Wang, Xiao Song, Bo Hu, Nathan Reynolds, Kristen Roso, Lee H. Chen, Paula K. Greer, Stephen T. Keir, Roger E. McLendon, Shi-Yuan Cheng, Darell D. Bigner, David M. Ashley, Christopher J. Pirozzi and Yiping He
Cancers 2023, 15(18), 4619; https://doi.org/10.3390/cancers15184619 - 18 Sep 2023
Cited by 1 | Viewed by 3382
Abstract
Brain tumor-initiating cells (BTICs) and tumor cell plasticity promote glioblastoma (GBM) progression. Here, we demonstrate that clemastine, an over-the-counter drug for treating hay fever and allergy symptoms, effectively attenuated the stemness and suppressed the propagation of primary BTIC cultures bearing PDGFRA amplification. These [...] Read more.
Brain tumor-initiating cells (BTICs) and tumor cell plasticity promote glioblastoma (GBM) progression. Here, we demonstrate that clemastine, an over-the-counter drug for treating hay fever and allergy symptoms, effectively attenuated the stemness and suppressed the propagation of primary BTIC cultures bearing PDGFRA amplification. These effects on BTICs were accompanied by altered gene expression profiling indicative of their more differentiated states, resonating with the activity of clemastine in promoting the differentiation of normal oligodendrocyte progenitor cells (OPCs) into mature oligodendrocytes. Functional assays for pharmacological targets of clemastine revealed that the Emopamil Binding Protein (EBP), an enzyme in the cholesterol biosynthesis pathway, is essential for BTIC propagation and a target that mediates the suppressive effects of clemastine. Finally, we showed that a neural stem cell-derived mouse glioma model displaying predominantly proneural features was similarly susceptible to clemastine treatment. Collectively, these results identify pathways essential for maintaining the stemness and progenitor features of GBMs, uncover BTIC dependency on EBP, and suggest that non-oncology, low-toxicity drugs with OPC differentiation-promoting activity can be repurposed to target GBM stemness and aid in their treatment. Full article
(This article belongs to the Special Issue Novel Experimental Therapeutic Targets and Strategies for Brain Tumors)
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