Signaling Pathway Regulation in Neuroblastoma Oncogenesis

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 1751

Special Issue Editor


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Guest Editor
Department of Pediatric Hemato-Oncology and Cell and Gene Therapy, IRCCS, Bambino Gesù Children's Hospital, Rome, Italy
Interests: pediatric oncology; neuroblastoma; basic tumor biology research and translational studies; cancer metastasis and in particular the crosstalk between tumor and its microenvironment via exosomes

Special Issue Information

Dear Colleagues,

Despite overall progress in the treatment of children with high-risk neuroblastoma, 5-year survival remains below 50%. Indeed, most of these patients present metastatic disease at diagnosis and have a high rate of relapse. Thus, a deeper understanding of the deregulated signaling pathways and complex networks of cellular interactions in the tumor microenvironment is needed if the community is to develop more effective therapeutic strategies to cure children with high-risk neuroblastoma.

The dynamic interaction between different tumor cell populations and the tumor microenvironments, together with stromal and immune system components, can be mediated by the bi-directional release and uptake of secreted factors. This can modulate tumor initiation, drug resistance and progression, sustaining the malignant features of the tumor.

In this context, we invite studies that investigate the various aspects of signaling pathways in neuroblastoma, the interactions with tumor microenvironment, metastasis, and targeted therapeutic strategies in this field. In this Topic, both original research articles and reviews are welcome.

Dr. Angela Di Giannatale
Guest Editor

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Keywords

  • neuroblastoma
  • signaling pathway
  • tumor microenvironment
  • crosstalk
  • exosomes
  • biomarkers
  • targeted therapy

Published Papers (1 paper)

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Research

20 pages, 1673 KiB  
Article
A Potential Prognostic Gene Signature Associated with p53-Dependent NTRK1 Activation and Increased Survival of Neuroblastoma Patients
by David Currie, Nicole Wong, Isabelle Zane, Tom Rix, Marios Vardakastanis, Amelia Claxton, Karine K. V. Ong, William Macmorland, Arthur Poivet, Anthony Brooks, Paola Niola, Derek Huntley and Ximena Montano
Cancers 2024, 16(4), 722; https://doi.org/10.3390/cancers16040722 - 8 Feb 2024
Viewed by 1489
Abstract
Neuroblastoma is the most common extracranial solid tumour in children, comprising close to 10% of childhood cancer-related deaths. We have demonstrated that activation of NTRK1 by TP53 repression of PTPN6 expression is significantly associated with favourable survival in neuroblastoma. The molecular mechanisms by [...] Read more.
Neuroblastoma is the most common extracranial solid tumour in children, comprising close to 10% of childhood cancer-related deaths. We have demonstrated that activation of NTRK1 by TP53 repression of PTPN6 expression is significantly associated with favourable survival in neuroblastoma. The molecular mechanisms by which this activation elicits cell molecular changes need to be determined. This is critical to identify dependable biomarkers for the early detection and prognosis of tumours, and for the development of personalised treatment. In this investigation we have identified and validated a gene signature for the prognosis of neuroblastoma using genes differentially expressed upon activation of the NTRK1-PTPN6-TP53 module. A random survival forest model was used to construct a gene signature, which was then assessed across validation datasets using Kaplan–Meier analysis and ROC curves. The analysis demonstrated that high BASP1, CD9, DLG2, FNBP1, FRMD3, IL11RA, ISGF10, IQCE, KCNQ3, and TOX2, and low BSG/CD147, CCDC125, GABRB3, GNB2L1/RACK1 HAPLN4, HEBP2, and HSD17B12 expression was significantly associated with favourable patient event-free survival (EFS). The gene signature was associated with favourable tumour histology and NTRK1-PTPN6-TP53 module activation. Importantly, all genes were significantly associated with favourable EFS in an independent manner. Six of the signature genes, BSG/CD147, GNB2L1/RACK1, TXNDC5, FNPB1, B3GAT1, and IGSF10, play a role in cell differentiation. Our findings strongly suggest that the identified gene signature is a potential prognostic biomarker and therapeutic target for neuroblastoma patients and that it is associated with neuroblastoma cell differentiation through the activation of the NTRK1-PTPN6-TP53 module. Full article
(This article belongs to the Special Issue Signaling Pathway Regulation in Neuroblastoma Oncogenesis)
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