Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.0
4.5
Journals
Cancers
Special Issues
Clinical and Translational Research in Pediatric Surgical Oncology
share announcement

Clinical and Translational Research in Pediatric Surgical Oncology

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (1 March 2022) | Viewed by 9837

Special Issue Editor

Dr. Sanjeev A. Vasudevan

E-Mail Website
Guest Editor
Division of Pediatric Surgery, Texas Children’s Hospital Department of Surgery, Michael E. DeBakey Department of Surgery, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX, USA
Interests: pediatric surgical oncology; hepatoblastoma; hepatocellular carcinoma; neuroblastoma; soft tissue sarcoma; cancer biology; drug targeting; patient-derived xenografts

Special Issue Information

Dear Colleagues,

Pediatric surgical oncology is a growing field in need of specialization and dedicated multidisciplinary care.  We perform very complex operations on children for resection of solid tumors from the brain, retroperitoneum, liver, lungs, and skeletal system. Surgeons offer a very unique perspective and understanding of tumor biology and clinical outcomes related to perioperative complications and impact on overall outcomes of these patients.  There is a growing need to highlight these perspectives and the translational research of pediatric surgical oncologists to help establish the specialty and lay the groundwork for awareness that specialized training and practice is needed to offer the best surgical care possible to our child patients with solid tumors.  I cordially invite you to submit translational basic research as well as clinical research manuscripts to this Special Issue to help accomplish this goal.

Dr. Sanjeev A. Vasudevan
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 surgical oncology
  • translational research
  • neuroblastoma
  • pediatric liver cancer
  • soft tissue sarcoma
  • Wilms tumor
  • rhabdomyosarcoma
  • Ewing’s sarcoma
  • osteosarcoma

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

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

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

22 pages, 3002 KiB  
Article
TERT Expression in Wilms Tumor Is Regulated by Promoter Mutation or Hypermethylation, WT1, and N-MYC
by Carolyn M. Jablonowski, Hyea Jin Gil, Emilia M. Pinto, Prahalathan Pichavaram, Andrew M. Fleming, Michael R. Clay, Dongli Hu, Christopher L. Morton, Shondra M. Pruett-Miller, Baranda S. Hansen, Xiang Chen, Karissa M. Dieseldorff Jones, Yanling Liu, Xiaotu Ma, Jun Yang, Andrew M. Davidoff, Gerard P. Zambetti and Andrew J. Murphy
Cancers 2022, 14(7), 1655; https://doi.org/10.3390/cancers14071655 - 25 Mar 2022
Cited by 6 | Viewed by 3437
Abstract
Increased TERT mRNA is associated with disease relapse in favorable histology Wilms tumor (WT). This study sought to understand the mechanism of increased TERT expression by determining the association between TERT and WT1 and N-MYC, two proteins important in Wilms tumor pathogenesis that [...] Read more.
Increased TERT mRNA is associated with disease relapse in favorable histology Wilms tumor (WT). This study sought to understand the mechanism of increased TERT expression by determining the association between TERT and WT1 and N-MYC, two proteins important in Wilms tumor pathogenesis that have been shown to regulate TERT expression. Three out of 45 (6.7%) WTs and the corresponding patient-derived xenografts harbored canonical gain-of-function mutations in the TERT promoter. This study identified near ubiquitous hypermethylation of the TERT promoter region in WT compared to normal kidney. WTs with biallelic inactivating mutations in WT1 (7/45, 15.6%) were found to have lower TERT expression by RNA-seq and qRT-PCR and lower telomerase activity determined by the telomerase repeat amplification protocol. Anaplastic histology and increased percentage of blastema were positively correlated with higher TERT expression and telomerase activity. In vitro shRNA knockdown of WT1 resulted in decreased expression of TERT, reduced colony formation, and decreased proliferation of WiT49, an anaplastic WT cell line with wild-type WT1. CRISPR-Cas9-mediated knockout of WT1 resulted in decreased expression of telomere-related gene pathways. However, an inducible Wt1-knockout mouse model showed no relationship between Wt1 knockout and Tert expression in normal murine nephrogenesis, suggesting that WT1 and TERT are coupled in transformed cells but not in normal kidney tissues. N-MYC overexpression resulted in increased TERT promoter activity and TERT transcription. Thus, multiple mechanisms of TERT activation are involved in WT and are associated with anaplastic histology and increased blastema. This study is novel because it identifies potential mechanisms of TERT activation in Wilms tumor that could be of therapeutic interests. Full article
(This article belongs to the Special Issue Clinical and Translational Research in Pediatric Surgical Oncology)
►▼ Show Figures

Figure 1

16 pages, 2109 KiB  
Article
Targeting High-Risk Neuroblastoma Patient-Derived Xenografts with Oncolytic Virotherapy
by Colin H. Quinn, Andee M. Beierle, Sara Claire Hutchins, Raoud Marayati, Laura V. Bownes, Jerry E. Stewart, Hooper R. Markert, Michael H. Erwin, Jamie M. Aye, Karina J. Yoon, Gregory K. Friedman, Christopher D. Willey, James M. Markert and Elizabeth A. Beierle
Cancers 2022, 14(3), 762; https://doi.org/10.3390/cancers14030762 - 1 Feb 2022
Cited by 9 | Viewed by 2869
Abstract
Cancer is the leading cause of death by disease in children, and over 15% of pediatric cancer-related mortalities are due to neuroblastoma. Current treatment options for neuroblastoma remain suboptimal as they often have significant toxicities, are associated with long-term side effects, and result [...] Read more.
Cancer is the leading cause of death by disease in children, and over 15% of pediatric cancer-related mortalities are due to neuroblastoma. Current treatment options for neuroblastoma remain suboptimal as they often have significant toxicities, are associated with long-term side effects, and result in disease relapse in over half of children with high-risk disease. There is a dire need for new therapies, and oncolytic viruses may represent an effective solution. Oncolytic viruses attack tumor cells in two ways: direct infection of tumor cells leading to cytolysis, and production of a debris field that stimulates an anti-tumor immune response. Our group has previously shown that M002, an oncolytic herpes simplex virus (oHSV), genetically engineered to express murine interleukin-12 (mIL-12), was effective at targeting and killing long term passage tumor cell lines. In the current study, we investigated M002 in three neuroblastoma patient-derived xenografts (PDXs). PDXs better recapitulate the human condition, and these studies were designed to gather robust data for translation to a clinical trial. We found that all three PDXs expressed viral entry receptors, and that the virus actively replicated in the cells. M002 caused significant tumor cell death in 2D culture and 3D bioprinted tumor models. Finally, the PDXs displayed variable susceptibility to M002, with a more profound effect on high-risk neuroblastoma PDXs compared to low-risk PDX. These findings validate the importance of incorporating PDXs for preclinical testing of oncolytic viral therapeutics and showcase a novel technique, 3D bioprinting, to test therapies in PDXs. Collectively, our data indicate that oHSVs effectively target high-risk neuroblastoma, and support the advancement of this therapy to the clinical setting. Full article
(This article belongs to the Special Issue Clinical and Translational Research in Pediatric Surgical Oncology)
►▼ Show Figures

Figure 1

12 pages, 1558 KiB  
Article
Expression of Immunomodulatory Checkpoint Molecules in Drug-Resistant Neuroblastoma: An Exploratory Study
by Nicholas J. Skertich, Fei Chu, Imad A. M. Tarhoni, Stephen Szajek, Jeffrey A. Borgia and Mary Beth Madonna
Cancers 2022, 14(3), 751; https://doi.org/10.3390/cancers14030751 - 31 Jan 2022
Cited by 5 | Viewed by 2634
Abstract
Neuroblastoma is a common childhood cancer with poor prognosis when at its advanced stage. Checkpoint molecule inhibition is successful in treating multiple advanced adult cancers. We investigated PD-L1 and other checkpoint molecule expression to determine their roles in drug resistance and usefulness as [...] Read more.
Neuroblastoma is a common childhood cancer with poor prognosis when at its advanced stage. Checkpoint molecule inhibition is successful in treating multiple advanced adult cancers. We investigated PD-L1 and other checkpoint molecule expression to determine their roles in drug resistance and usefulness as targets for drug therapy. We developed three doxorubicin-resistant (DoxR) cell lines from parental cell lines. Matrigel in vitro invasion assays were used to compare invasiveness. Western blot assays were used to compare PD-L1 expression. Immuno-oncology checkpoint protein panels were used to compare concentrations of 17 checkpoint molecules both cellular and soluble. PD-L1 and 12 other checkpoint molecules were present in all cell lysates of each cell line without significantly different levels. Three were solubilized in the media of each cell line. PD-L1 is expressed in all DoxR and parental neuroblastoma cells and may be a potential target for drug therapy although its role in drug resistance remains unclear. Benchmarking checkpoint molecules provides the basis for future studies identifying targets for directed therapy and biomarkers for cancer detection or prognosis. Full article
(This article belongs to the Special Issue Clinical and Translational Research in Pediatric Surgical Oncology)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop