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New Molecular Mechanisms in the Development of Brain Tumors and Metastases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 5732

Special Issue Editors

Dr. Raffaele Addeo

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Guest Editor
Medical Oncology Unit, San Giovanni di Dio Hospital, 80027 Frattamaggiore, Naples, Italy
Interests: cancer biology; treatment; tumors; oncology; neurology; cancer therapy; chemotherapy; neuro-oncology; glioblastoma
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Michele Caraglia

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Guest Editor
Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, Via L. De Crecchio 7, 80138 Naples, Italy
Interests: noncoding RNAs; micro-RNAs; prostate cancer; nanotechnological delivery of anticancer drugs and nucleic acids; diagnostic markers in cancer; urotensin II receptor; next-generation sequencing; predictive markers of response; circulating tumor cells
Special Issues, Collections and Topics in MDPI journals
Dr. Marianna Abate

E-Mail Website
Guest Editor
Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, Via L. De Crecchio 7, 80138 Naples, Italy
Interests: oncology; biochemistry; nanotechnologies; RNA interference
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain tumors and metastases are among the most lethal neoplasms. Enhanced understanding of the molecular biology of both primary and secondary central nervous system tumors has led to changes in their clinical approach. However, despite these advances, patients with brain tumors have a poor prognosis.

The aim of this Special Issue is to draw attention to the state of the art of scientific research in the study of brain tumors. Particular emphasis will be placed on the most common primary brain tumor of adult age: glioblastoma. Importantly, knowledge about the molecular changes and heterogeneity of glioblastoma together with advances in the understanding of the cellular and molecular characteristics of its physiological barriers (above all the blood–brain barrier) represent new challenges in the treatment of glioblastoma patients. Contributions that examine the genetic and epigenetic landscape of glioblastoma, which may provide insights into its known heterogeneity and resilience, are welcome to be submitted. Knowledge of the tumor microenvironment, the blood–brain barrier, and new gene mutations could help to achieve this objective. Particular emphasis will also be placed on non-coding RNAs (i.e., microRNAs and long non-coding RNAs) in the definition of the growth, spreading, and chemo-radio and immunological resistance of brain tumors. The goal of this Special Issue is to discuss new research opportunities that can lead to precise and personalized medicine for these tumors, with a clear improvement in both the quality of life and survival of patients.

This Special Issue is supervised by Dr. Raffaele Addeo and Dr. Michele Caraglia, assisted by our Topical Advisory Panel Member Dr. Marianna Abate (University of Campania “Luigi Vanvitelli”).

Dr. Raffaele Addeo
Prof. Dr. Michele Caraglia
Dr. Marianna Abate
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 short 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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 tumor
  • brain metastasis
  • blood–brain barrier
  • target therapy
  • cancer molecular biology
  • brain tumor microenvironment
  • molecular biomarkers

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Published Papers (2 papers)

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Research

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18 pages, 5641 KiB  
Article
The Large GTPase Guanylate-Binding Protein-1 (GBP-1) Promotes Mitochondrial Fission in Glioblastoma
by Ryan C. Kalb, Geoffrey O. Nyabuto, Michael P. Morran, Swagata Maity, Jacob S. Justinger, Andrea L. Nestor-Kalinoski and Deborah J. Vestal
Int. J. Mol. Sci. 2024, 25(20), 11236; https://doi.org/10.3390/ijms252011236 - 19 Oct 2024
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Abstract
Glioblastomas (aka Glioblastoma multiformes (GBMs)) are the most deadly of the adult brain tumors. Even with aggressive treatment, the prognosis is extremely poor. The large GTPase Guanylate-Binding Protein-1 (GBP-1) contributes to the poor prognosis of GBM by promoting migration and invasion. GBP-1 is [...] Read more.
Glioblastomas (aka Glioblastoma multiformes (GBMs)) are the most deadly of the adult brain tumors. Even with aggressive treatment, the prognosis is extremely poor. The large GTPase Guanylate-Binding Protein-1 (GBP-1) contributes to the poor prognosis of GBM by promoting migration and invasion. GBP-1 is substantially localized to the cytosolic side of the outer membrane of mitochondria in GBM cells. Because mitochondrial dynamics, particularly mitochondrial fission, can drive cell migration and invasion, the potential interactions between GBP-1 and mitochondrial dynamin-related protein 1 (Drp1) were explored. Drp1 is the major driver of mitochondrial fission. While GBP-1 and Drp1 both had punctate distributions within the cytoplasm and localized to regions of the cytoplasmic side of the plasma membrane of GBM cells, the proteins were only molecularly co-localized at the mitochondria. Subcellular fractionation showed that the presence of elevated GBP-1 promoted the movement of Drp1 from the cytosol to the mitochondria. The migration of U251 cells treated with the Drp1 inhibitor, Mdivi-1, was less inhibited in the cells with elevated GBP-1. Elevated GBP-1 in GBM cells resulted in shorter and wider mitochondria, most likely from mitochondrial fission. Mitochondrial fission can drive several important cellular processes, including cell migration, invasion, and metastasis. Full article
(This article belongs to the Special Issue New Molecular Mechanisms in the Development of Brain Tumors and Metastases)
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Review

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14 pages, 1154 KiB  
Review
Roles of CDR2 and CDR2L in Anti-Yo Paraneoplastic Cerebellar Degeneration: A Literature Review
by Pablo S. Martínez Lozada, Rafael Mancero Montalvo, Andrea Iturralde Carrillo, Maria Montesdeoca-Lozada, Jose A. Rodas and Jose E. Leon-Rojas
Int. J. Mol. Sci. 2025, 26(1), 70; https://doi.org/10.3390/ijms26010070 - 25 Dec 2024
Viewed by 1171
Abstract
Paraneoplastic cerebellar degeneration (PCD) is a rapidly progressive, immune-mediated syndrome characterized by the degeneration of Purkinje cells, often associated with the presence of antibodies targeting intracellular antigens within these cells. These autoantibodies are implicated in the induction of cytotoxicity, leading to Purkinje cell [...] Read more.
Paraneoplastic cerebellar degeneration (PCD) is a rapidly progressive, immune-mediated syndrome characterized by the degeneration of Purkinje cells, often associated with the presence of antibodies targeting intracellular antigens within these cells. These autoantibodies are implicated in the induction of cytotoxicity, leading to Purkinje cell death, as demonstrated in in vitro models. However, the precise roles of antibodies and T lymphocytes in mediating neuronal injury remain a subject of ongoing research, with T cells appearing to be the main effectors of cerebellar injury. Notably, at least 50% of PCD cases involve anti-Yo autoantibodies, also referred to as anti-PCA1 (Purkinje cell antigen 1) antibodies, which specifically target cerebellar degeneration-related protein 2 (CDR2) and its paralogue, CDR2-like (CDR2L). Another recognized antigen is CDR 34, a 34 kDa Purkinje cell antigen characterized by tandem repeats and a B-cell epitope; its detection in non-cerebellar tissues necessitates further in situ hybridization studies. Onconeural antigens are expressed in both Purkinje cells and tumour cells, where they localize in the cytoplasm and associate with membrane-bound and free ribosomes, playing critical roles in regulating transcription and calcium homeostasis. Recent studies suggest that the breakdown of immune tolerance is linked to genetic alterations in tumour cell antigens, leading to the formation of neoantigens that can elicit autoreactive T cells, which may underscore the function of Yo antibodies. In vitro studies indicate that anti-Yo antibodies can induce cell death independent of T lymphocytes. The disease progresses by initial lymphocytic infiltration, followed by a rapid loss of Purkinje cells without significant inflammation. However, in vivo models showcase that anti-Yo PCD is primarily T-cell mediated, with antibodies serving as biomarkers rather than direct effectors of neuronal death. This review examines the mechanisms underlying PCD, focusing on the roles of CDR2 and CDR2L in tumour development and their potential role in the degeneration of cerebellar Purkinje neurons. A comprehensive understanding of these processes is essential for advancing diagnostic, prognostic, and therapeutic strategies for PCD and associated malignancies. Full article
(This article belongs to the Special Issue New Molecular Mechanisms in the Development of Brain Tumors and Metastases)
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