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Exploring Novel Molecular, Metabolic and Cellular Mechanisms for Developing New Therapeutic Targets Against Childhood Cancers, 2nd Edition

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 February 2026 | Viewed by 3347

Special Issue Editors

Dr. Alessandro Fanzani

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine (DMMT), University of Brescia, Viale Europa 11, 25123 Brescia, Italy
Interests: rhabdomyosarcoma; caveolins; cavins; oxidative stress; muscle
Special Issues, Collections and Topics in MDPI journals
Dr. Silvia Codenotti

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine (DMMT), University of Brescia, Brescia, Italy
Interests: rhabdomyosarcoma; metastasis; radioresistance; Caveolin-1; liposarcoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is dedicated to childhood cancers, in particular blood tumors (leukemias, lymphomas), embryonal tumors (retinoblastoma, neuroblastoma, Wilms tumor), central nervous system tumors (medulloblastoma, glioma, astrocytoma, oligodendroglioma, and ependymoma), and bone and soft tissue sarcomas (osteosarcoma, Ewing sarcoma, and rhabdomyosarcoma), which are the leading causes of pediatric death in developed countries. Unlike in adults, in whom the onset of cancer commonly occurs due to gene mutations in one or more somatic cells, pediatric tumors are often genetically inherited. Indeed, there are several examples of cancer syndromes that cause pediatric tumors, including Fanconi anemia and Xeroderma pigmentosum, retinoblastoma, Li–Fraumeni syndrome, DICER1 syndrome and neurofibromatosis, one RAS mosaic condition, and Down syndrome. Therefore, in this Special Issue, we will collect studies on pediatric tumors that focus on the molecular/cellular landscape, metabolic vulnerabilities, and new therapies for accelerating the development of combined anti-tumor strategies.

Dr. Alessandro Fanzani
Dr. Silvia Codenotti
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

  • childhood cancers
  • rhabdomyosarcoma
  • leukemias
  • lymphomas
  • central nervous system tumors
  • sarcomas of bone and soft tissue
  • neuroblastoma
  • retinoblastoma
  • rhabdoid tumors
  • rare cancers
  • genomic alterations
  • molecular drivers
  • tissue microenvironment
  • development of drugs
  • therapies

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Related Special Issue

Published Papers (2 papers)

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Research

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16 pages, 3071 KiB  
Article
Is Fluoride Blameless?—The Influence of Fluorine Compounds on the Invasiveness of the Human Glioma-like Cell Line U-87
by Wojciech Żwierełło, Agnieszka Maruszewska, Marta Skórka-Majewicz, Agata Wszołek and Izabela Gutowska
Int. J. Mol. Sci. 2024, 25(23), 12773; https://doi.org/10.3390/ijms252312773 - 27 Nov 2024
Cited by 1 | Viewed by 1029
Abstract
Glioblastoma remains one of the most treatment-resistant and malignant human cancers. Given the documented harmful effects of fluoride on the developing central nervous system and the rising incidence of brain tumors, especially among children, it is pertinent to explore the role of environmental [...] Read more.
Glioblastoma remains one of the most treatment-resistant and malignant human cancers. Given the documented harmful effects of fluoride on the developing central nervous system and the rising incidence of brain tumors, especially among children, it is pertinent to explore the role of environmental toxins, including fluoride compounds, in the context of brain cancer. This study represents the first investigation into the influence of fluoride on mechanisms related to the invasiveness of human glioblastoma cells. We examined the effects of sodium fluoride (NaF) exposure on the migratory and invasive abilities of the U-87 human glioblastoma cell line, assessing levels of metalloproteinases MMP-2 and MMP-9 secreted by these cells. Additionally, the activation of metabolic pathways associated with invasiveness, including AKT and NF-κB, was analyzed. Our results suggest that the effects induced by NaF at physiologically high concentrations (0.1–10 µM) in U-87 glioblastoma cells may promote a pro-invasive phenotype. Full article
(This article belongs to the Special Issue Exploring Novel Molecular, Metabolic and Cellular Mechanisms for Developing New Therapeutic Targets Against Childhood Cancers, 2nd Edition)
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Review

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21 pages, 2210 KiB  
Review
EWSR1::ATF1 Translocation: A Common Tumor Driver of Distinct Human Neoplasms
by Julia Raffaella Bianco, YiJing Li, Agota Petranyi and Zsolt Fabian
Int. J. Mol. Sci. 2024, 25(24), 13693; https://doi.org/10.3390/ijms252413693 - 21 Dec 2024
Cited by 1 | Viewed by 1996
Abstract
Cancer is among the leading causes of mortality in developed countries due to limited available therapeutic modalities and high rate of morbidity. Although malignancies might show individual genetic landscapes, recurring aberrations in the neoplastic genome have been identified in the wide range of [...] Read more.
Cancer is among the leading causes of mortality in developed countries due to limited available therapeutic modalities and high rate of morbidity. Although malignancies might show individual genetic landscapes, recurring aberrations in the neoplastic genome have been identified in the wide range of transformed cells. These include translocations of frequently affected loci of the human genetic material like the Ewing sarcoma breakpoint region 1 (EWSR1) of chromosome 22 that results in malignancies with mesodermal origin. These cytogenetic defects frequently result in the genesis of fusion genes involving EWSR1 and a number of genes from partner loci. One of these chromosomal rearrangements is the reciprocal translocation between the q13 and q12 loci of chromosome 12 and 22, respectively, that is believed to initiate cancer formation by the genesis of a novel, chimeric transcription factor provoking dysregulated gene expression. Since soft-tissue neoplasms carrying t(12;22)(q13;q12) have very poor prognosis and clinical modalities specifically targeting t(12;22)(q13;q12)-harboring cells are not available to date, understanding this DNA aberration is not only timely but urgent. Here, we review our current knowledge of human malignancies carrying the specific subset of EWSR1 rearrangements that leads to the expression of the EWSR1::ATF1 tumor-driver chimeric protein. Full article
(This article belongs to the Special Issue Exploring Novel Molecular, Metabolic and Cellular Mechanisms for Developing New Therapeutic Targets Against Childhood Cancers, 2nd Edition)
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