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Cancer Neuroscience

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 31 July 2026 | Viewed by 1044

Editor


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Guest Editor
1. Cancer and Neurobiology Laboratory, Experimental Research Center, Clinical Hospital (CPE-HCPA), Federal University of Rio Grande do Sul, Porto Alegre 90035-003, Brazil
2. Department of Pharmacology, Institute for Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre 90035-003, Brazil
Interests: brain tumor; glioma; glioblastoma; neuroblastoma; medulloblastoma; growth factors; membrane receptors; epigenetics
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Special Issue Information

Dear Colleagues,

Cancer neuroscience has emerged as a rapidly expanding field at the interface of oncology and neurobiology. Accumulating evidence demonstrates that nervous-system-derived mechanisms actively contribute to cancer initiation, progression, and therapeutic response. This field encompasses at least four interconnected dimensions. First, tumor cells hijack molecular and cellular programs that are fundamental to normal nervous system development and synaptic plasticity. Second, cancers establish functional communication with neurons through paracrine signaling and, in some contexts, through direct neuro-tumoral synaptic structures, allowing neuronal activity to modulate tumor proliferation, invasion, and treatment resistance. Third, tumors actively remodel their microenvironment by promoting de novo innervation, a process increasingly recognized not only in primary brain tumors but also in peripheral malignancies such as pancreatic cancers. Finally, cancer neuroscience also encompasses the impact of cancer therapies on the nervous system, as many antineoplastic agents—particularly chemotherapeutics—induce cognitive, behavioral, and neurobiological alterations that affect the patient’s quality of life and long-term outcomes. Together, these advances redefine cancer as a disease shaped by dynamic, bidirectional interactions with the nervous system. The convergence of neuroscience, cancer biology, imaging, and translational research has positioned cancer neuroscience as one of the most active and conceptually transformative areas in contemporary oncology.

This Special Issue aims to capture the breadth, mechanistic depth, and clinical implications of this burgeoning field, highlighting emerging concepts, experimental models, and therapeutic opportunities arising from neuro-tumor interactions.

Dr. Rafael Roesler
Guest Editor

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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-anonymized 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 tumor
  • glioma
  • medulloblastoma
  • glioma-neuron crosstalk
  • cancer-neuron interaction
  • neuro-tumoral synapse
  • neurotransmitter signaling in cancer
  • tumor innervation
  • tumor microenvironment
  • chemobrain

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Published Papers (1 paper)

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Research

19 pages, 14335 KB  
Article
DLG2DLG4 Expression Is Associated with Improved Survival and a Synaptic Gene Signature in Lower-Grade Glioma
by Felipe Gaia, Henrique Ritter Dal-Pizzol, Osvaldo Malafaia, Rafael Roesler and Gustavo R. Isolan
Cancers 2026, 18(10), 1646; https://doi.org/10.3390/cancers18101646 - 20 May 2026
Viewed by 638
Abstract
Background/Objectives: Increasing evidence indicates that gliomas co-opt mechanisms of excitatory synaptic transmission and plasticity to support tumor progression, yet these processes remain poorly characterized in lower-grade gliomas (LGGs). Here, we investigated whether genes associated with excitatory synaptic function are linked to patient [...] Read more.
Background/Objectives: Increasing evidence indicates that gliomas co-opt mechanisms of excitatory synaptic transmission and plasticity to support tumor progression, yet these processes remain poorly characterized in lower-grade gliomas (LGGs). Here, we investigated whether genes associated with excitatory synaptic function are linked to patient prognosis in LGG. Methods: A curated panel of 36 synaptic genes was analyzed in LGG using RNA-sequencing and clinical data from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) datasets. Results: Among the genes investigated, DLG2, DLG3, and DLG4, which encode the postsynaptic scaffolding proteins PSD-93, SAP-102, and PSD-95, respectively, showed strong associations with patient overall survival (OS). Higher expression of each gene was consistently associated with longer OS across both datasets. Expression of DLG2DLG4 was higher in oligodendroglioma and IDH-mutant, 1p/19q co-deleted tumors, and lower in astrocytoma and IDH-wild-type tumors. Furthermore, expression of all three genes positively correlated with a broad gene signature associated with a synaptic gene program, including multiple components of glutamatergic signaling and postsynaptic organization. Conclusions: These findings suggest that elevated expression of DLG2DLG4 is associated with a transcriptional program resembling differentiated neuron-like features and favorable clinical outcome in LGG. Full article
(This article belongs to the Special Issue Cancer Neuroscience)
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