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: 14 February 2025 | Viewed by 595

Special Issue Editor


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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
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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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Published Papers (1 paper)

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Research

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 361
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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