Special Issue "Neuroblastoma Pathogenesis and Therapy"

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 31 July 2022.

Special Issue Editor

Dr. Saurabh Agarwal
E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John’s University, 8000 Utopia Parkway, Queens, NY 11439, USA
Interests: pediatric cancers; neuroblastoma; cancer stem cells; metastasis; signaling pathways in cancer; immunotherapy; epigenetics; genetics; small molecule inhibitors; translational therapeutics; p53-myc interaction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroblastoma is an aggressive pediatric cancer that originates from neural crest tissues of the sympathetic nervous system. High-risk neuroblastoma accounts for almost 15% of all pediatric cancer-related deaths, with overall survival rates lower than 50%. This situation become murkier when the majority of neuroblastoma patients relapse with an aggressive, refractory, and metastatic disease, with an overall survival rate of only 10%. Therefore, understanding the causes of neuroblastoma pathogenesis, relapse, and developing novel therapeutic approaches is mandatory to effectively cure neuroblastoma.

Neuroblastoma is a highly heterogeneous tumor both from a clinical and a molecular perspective. The clinical impact and unique biology of neuroblastoma have made this aggressive solid tumor an interesting disease model for concerted translational research efforts. These efforts include novel insights into neuroblastoma tumor biology, molecular and epigenetic mechanisms, novel targeted therapeutic approaches including small molecule inhibitors, epigenetic, non-coding RNA, and cell-based immunologic therapies.

In this Special Issue, we invite authors to contribute articles focusing on different aspects of neuroblastoma tumor biology, pathogenesis, developmental therapeutics, and treatment approaches. The collected articles in this Special Issue will further enhance our knowledge and understanding of the complex neuroblastoma pathogenesis and drive the development of novel therapeutic strategies.

Dr. Saurabh Agarwal
Guest Editor

Manuscript Submission Information

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  • Neuroblastoma
  • Pediatric cancers
  • Neural crest
  • Pathogenesis
  • Metastasis
  • Epigenetics
  • Therapeutic approach
  • Tumorigenesis
  • Signaling mechanisms
  • Epithelial-to-mesenchymal transition

Published Papers (1 paper)

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In Vitro Assessment of the Role of p53 on Chemotherapy Treatments in Neuroblastoma Cell Lines
Pharmaceuticals 2021, 14(11), 1184; https://0-doi-org.brum.beds.ac.uk/10.3390/ph14111184 (registering DOI) - 19 Nov 2021
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Neuroblastoma is the most frequent malignant extracranial solid tumor of infancy. The overall objective of this work consists of determining the presence of alterations in the p53/MDM2/p14ARF signaling pathway in neuroblastoma cell lines and deciphering their possible relationship with resistance to known antineoplastic [...] Read more.
Neuroblastoma is the most frequent malignant extracranial solid tumor of infancy. The overall objective of this work consists of determining the presence of alterations in the p53/MDM2/p14ARF signaling pathway in neuroblastoma cell lines and deciphering their possible relationship with resistance to known antineoplastic drugs and to differentiation agents. Firstly, we characterized 10 neuroblastoma cell lines for alterations at the p53/MDM2/p14ARF signaling pathway by analysis of TP53 point mutations, MYCN and MDM2 amplification, and p14ARF methylation, homozygous deletions, and expression. Secondly, we chose SK-N-FI (mutated at TP53) and SK-N-Be(2) (wild-type TP53) cell lines, treated them with chemotherapeutic agents (doxorubicin, etoposide, cisplatin, and melphalan) and with two isomers of retinoic acid (RA): (9-cis and all-trans). Finally, we analyzed the distribution of the cell cycle, the induction of apoptosis, and the expression levels of p53, p21, and Bcl-2 in those two cell lines. P14ARF did not present promoter methylation, homozygous deletions, and protein expression in any of the 10 neuroblastoma cell lines. One TP53 point mutation was detected in the SK-N-FI cell line. MYCN amplification was frequent, while most cell lines did not present MDM2 amplification. Treatment of SK-N-FI and SK-N-Be(2) cells with doxorubicin, etoposide, cisplatin, and melphalan increased apoptosis and blocked the cycle in G2/M, while retinoic acid isomers induced apoptosis and decreased the percentage of cells in S phase in TP53 mutated SK-N-FI cells, but not in TP53 wild-type SK-N-Be(2) cells. Treatment with cisplatin, melphalan, or 9-cis RA decreased p53 expression levels in SK-N-FI cells but not in SK-N-Be (2). The expression of p21 was not modified in either of the two cell lines. Bcl-2 levels were reduced only in SK-N-FI cells after treatment with cisplatin. However, treatments with doxorubicin, etoposide, or 9-cis-RA did not modify the levels of this protein in either of the two cell lines. In conclusion, TP53 mutated SK-N-FI cells respond better to the retinoic isomers than TP53 wild-type SK-N-Be(2) cells. Although these are in vitro results, it seems that deciphering the molecular alterations of the p53/MDM2/p14ARF signaling pathway prior to treating patients of neuroblastoma might be useful for standardizing therapies with the aim of improving survival. Full article
(This article belongs to the Special Issue Neuroblastoma Pathogenesis and Therapy)
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