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Cancers
Special Issues
Pediatric Cancer Research from Basic Biology to Experimental Therapy
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Pediatric Cancer Research from Basic Biology to Experimental Therapy

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

Deadline for manuscript submissions: 16 January 2026 | Viewed by 3528

Special Issue Editor

Prof. Dr. Atif Ahmed

E-Mail Website
Guest Editor
1. Department of Laboratory Medicine & Pathology, University of Washington, Seattle, WA 98195, USA
2. Department of Pathology, Seattle Children's Hospitals, Seattle, WA 98105, USA
Interests: pediatric tumors; pediatric cancer biology; protein expression in cancer; proteome profiling from histologic slides; microRNA expression
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Tumors in children are different from those in adults and can range from benign, intermediate, and malignant neoplasia. The incidence of pediatric tumors varies in different racial and ethnic groups and geographic regions, reflecting their diverse biology and environmental influence. A better understanding of pediatric cancer biology and genetics is needed to reflect its heterogeneity, clinical behavior, and response to therapy. Malignant tumors have a complex biology that is characterized by rapid proliferation, a spectrum of cellular differentiation, and an association with developmental genes. The pediatric cancer genetic profile is unique, featuring a high prevalence of specific structural variations (e.g., gene fusions and chromosomal rearrangements) and predisposing germline variants. The classification of pediatric tumors has recently evolved, now incorporating novel genetically defined entities and ancillary tests that have resulted in more precise tumor definition. This unique profile translates to unique biology, morphology, microenvironment, clinical behavior, and therapy response. Traditional and novel therapeutic regimens are burdened by therapy resistance and tumor progression. Basic and translation research, genetic sequencing, and epigenetic analysis have opened new opportunities for patients to be included in clinical trials. This Special Issue aims to highlight the recent advances in pediatric tumor research, including basic biology, tumor microenvironment, novel treatment, and cellular and genetic landscapes.

In this Special Issue, original research articles and reviews are welcome that may include (but are not limited to) the following:

  1. Developmental biology and cancer predisposition syndromes;
  2. Preclinical models of pediatric cancer and translational research;
  3. Genetics and epigenetics of different pediatric tumors including hematopoietic malignancies, solid cancers, and tumors of intermediate malignancy;
  4. Biologic basis of therapy and therapy resistance;
  5. Molecular diagnostic, prognostic, and predictive biomarkers.

We look forward to receiving your contributions

Prof. Dr. Atif Ahmed
Guest Editor

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

  • pediatric tumors
  • solid cancers
  • leukemias
  • cancer predisposition syndromes
  • genetics
  • omics
  • immunotherapy
  • therapy resistance

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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15 pages, 9911 KiB  
Article
Novel PP2A-Activating Compounds in Neuroblastoma
by Nazia Nazam, Laura V. Bownes, Janet R. Julson, Colin H. Quinn, Michael H. Erwin, Raoud Marayati, Hooper R. Markert, Sorina Shirley, Jerry E. Stewart, Karina J. Yoon, Jamie Aye, Michael Ohlmeyer and Elizabeth A. Beierle
Cancers 2024, 16(22), 3836; https://doi.org/10.3390/cancers16223836 - 15 Nov 2024
Viewed by 1017
Abstract
Background: Neuroblastoma (NB) remains one of the deadliest pediatric solid tumors. Recent advancements aimed at improving outcomes have been insufficient, and patients with high-risk NB continue to have a poor prognosis. Protein phosphatase 2A (PP2A) is a tumor suppressor protein downregulated in many [...] Read more.
Background: Neuroblastoma (NB) remains one of the deadliest pediatric solid tumors. Recent advancements aimed at improving outcomes have been insufficient, and patients with high-risk NB continue to have a poor prognosis. Protein phosphatase 2A (PP2A) is a tumor suppressor protein downregulated in many cancers, including NB. PP2A activation has been shown to affect the malignant phenotype in other solid tumors. The present studies aim to investigate the effects of two novel PP2A activators as a NB therapeutic. Methods: Four established NB cell lines and a patient-derived xenoline were utilized to study the effect on cell viability, proliferation, motility, and in vivo tumor growth using two novel tricyclic sulfonamide PP2A activators, ATUX-3364 and ATUX-8385. Results: ATUX-3364 and ATUX-8385 increased PP2A activity. These PP2A activators led to decreased viability, proliferation, and motility of NB cells. Treatment of animals bearing NB tumors with ATUX-3364 or ATUX-8385 resulted in decreased tumor growth in MYCN-amplified SK-N-BE(2) tumors. At the molecular level, PP2A-based reactivation led to dephosphorylation of MYCN-S62 and decreased MYCN protein expression. Conclusions: PP2A activators decreased NB cell viability, proliferation, and motility. In vivo experiments show that PP2A activators have more significant effects on tumorigenesis in MYCN-amplified tumors. Finally, phosphorylation of MYCN protein was decreased following treatment with novel sulfonamide PP2A activators. These data and mechanistic insights may be useful for developing new PP2A-based therapies that target MYCN for the treatment of NB. Full article
(This article belongs to the Special Issue Pediatric Cancer Research from Basic Biology to Experimental Therapy)
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Review

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18 pages, 1788 KiB  
Review
Updates in Diagnostic Techniques and Experimental Therapies for Diffuse Intrinsic Pontine Glioma
by Luke McVeigh, Tirth Patel, Madeline Miclea, Kallen Schwark, Diala Ajaero, Fareen Momen, Madison Clausen, Tiffany Adam, Rayan Aittaleb, Jack Wadden, Benison Lau, Andrea T. Franson, Carl Koschmann and Neena I. Marupudi
Cancers 2025, 17(6), 931; https://doi.org/10.3390/cancers17060931 - 10 Mar 2025
Viewed by 687
Abstract
Diffuse intrinsic pontine glioma (DIPG) is a rare but extremely malignant central nervous system tumor primarily affecting children that is almost universally fatal with a devastating prognosis of 8-to-12-month median survival time following diagnosis. Traditionally, DIPG has been diagnosed via MR imaging alone [...] Read more.
Diffuse intrinsic pontine glioma (DIPG) is a rare but extremely malignant central nervous system tumor primarily affecting children that is almost universally fatal with a devastating prognosis of 8-to-12-month median survival time following diagnosis. Traditionally, DIPG has been diagnosed via MR imaging alone and treated with palliative radiation therapy. While performing surgical biopsies for these patients has been controversial, in recent years, advancements have been made in the safety and efficacy of surgical biopsy techniques, utilizing stereotactic, robotics, and intraoperative cranial nerve monitoring as well as the development of liquid biopsies that identify tumor markers in either cerebrospinal fluid or serum. With more molecular data being collected from these tumors due to more frequent biopsies being performed, multiple treatment modalities including chemotherapy, radiation therapy, immunotherapy, and epigenetic modifying agents continue to be developed. Numerous recent clinical trials have been completed or are currently ongoing that have shown promise in extending survival for patients with DIPG. Focused ultrasound (FUS) has also emerged as an additional promising adjunct invention used to increase the effectiveness of therapeutic agents. In this review, we discuss the current evidence to date for these advancements in the diagnosis and treatment of DIPG. Full article
(This article belongs to the Special Issue Pediatric Cancer Research from Basic Biology to Experimental Therapy)
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31 pages, 5728 KiB  
Review
Progress Toward Epigenetic Targeted Therapies for Childhood Cancer
by Athanasia Liapodimitri, Ashley R. Tetens, Jordyn Craig-Schwartz, Kayleigh Lunsford, Kegan O. Skalitzky and Michael A. Koldobskiy
Cancers 2024, 16(24), 4149; https://doi.org/10.3390/cancers16244149 (registering DOI) - 12 Dec 2024
Viewed by 1361
Abstract
Among the most significant discoveries from cancer genomics efforts has been the critical role of epigenetic dysregulation in cancer development and progression. Studies across diverse cancer types have revealed frequent mutations in genes encoding epigenetic regulators, alterations in DNA methylation and histone modifications, [...] Read more.
Among the most significant discoveries from cancer genomics efforts has been the critical role of epigenetic dysregulation in cancer development and progression. Studies across diverse cancer types have revealed frequent mutations in genes encoding epigenetic regulators, alterations in DNA methylation and histone modifications, and a dramatic reorganization of chromatin structure. Epigenetic changes are especially relevant to pediatric cancers, which are often characterized by a low rate of genetic mutations. The inherent reversibility of epigenetic lesions has led to an intense interest in the development of epigenetic targeted therapies. Additionally, the recent appreciation of the interplay between the epigenome and immune regulation has sparked interest in combination therapies and synergistic immunotherapy approaches. Further, the recent appreciation of epigenetic variability as a driving force in cancer evolution has suggested new roles for epigenetic therapies in limiting plasticity and resistance. Here, we review recent progress and emerging directions in the development of epigenetic targeted therapeutics and their promise across the landscape of childhood cancers. Full article
(This article belongs to the Special Issue Pediatric Cancer Research from Basic Biology to Experimental Therapy)
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