Special Issue "Ewing Sarcoma"

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

Deadline for manuscript submissions: 31 March 2020.

Special Issue Editors

Prof. Kazutaka Kikuta
E-Mail Website
Guest Editor
Head of Department, Department of Musculoskeletal Oncology and Orthopaedic Surgery, Tochigi Cancer Center, 4-9-13, Yohnan Utsunomiya Tochigi 320-0824, Japan
Interests: Rare Cancer Researcn; Musculoskeletal oncological research; Orthopaedic Surgery; Proteomics
Prof. Tadashi Kondo
E-Mail Website
Guest Editor
Division of Pharmacoproteomics, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
Interests: Rare cancer research; sarcoma; proteogenomics; applications of patient-derived cancer model
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Special Issue Information

Dear Colleagues,

Ewing sarcoma is the most common sarcoma from childhood to adolescence. Treatment methods that have shown improvement in clinical outcomes of Ewing sarcoma include advanced chemotherapy, as well as multidisciplinary treatment that combines surgery and radiotherapy. Ewing sarcoma is classified into localized and metastatic types. While outcomes are good for patients with localized Ewing sarcoma, prognosis is poor for patients with metastatic Ewing sarcoma. Moreover, it remains challenging to optimize therapies for patients who have metastatic Ewing sarcoma.

Ewing sarcoma results from simple sarcoma-specific genetic alterations that produce TET/FET and ETS family member fusion proteins. Genomic analyses have been reported for Ewing sarcoma using whole exon sequencing; wide genome sequencing to identify drug targets has also been reported. The results have shown that Ewing sarcoma exhibits a low incidence of single nucleotide variation and that the frequency of mutations in the STAG2 gene, which exhibits the most frequent mutations other than ETS family member fusion genes, is only 8–17%. The frequency of p53 mutations in Ewing sarcoma is ≤10%, and many of the mutations are detected in tissue after treatment; this suggests that, in contrast to osteosarcoma, p53 mutations are extremely unlikely to be initial events in Ewing sarcoma. Clinically, overlapping STAG2 and TP53 mutations are associated with poor prognosis in patients with Ewing sarcoma. However, genome analysis studies have not revealed any factors that could serve as targets for new treatment for Ewing sarcoma, as it appears to be driven entirely by a fusion gene.

Multiple studies have been published regarding the fusion oncoprotein and the products of other genetic alterations that significantly impact Ewing sarcoma tumorigenesis; however, they are not yet utilized in clinical practice. This Special Issue, “Ewing Sarcoma” will highlight the diverse challenges encountered in understanding the pathogenesis of Ewing sarcoma, as well as in its clinical management. Invited articles will cover a wide range of topics, including but not restricted to the following: (1) update on the clinical management of Ewing sarcoma, focusing on therapies for patients with metastases; (2) applications of biomarkers related to therapeutic targets for patients with metastases; (3) update on the molecular tumorigenesis mechanism related to metastasis of Ewing sarcoma; and (4) role of personalized genomics in identifying therapeutic targets in metastatic Ewing sarcoma.

Prof. Kazutaka Kikuta
Prof. Tadashi Kondo
Guest Editors

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 papers will be 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 short 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 monthly 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 1800 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

  • Ewing Sarcoma
  • Fusion genes
  • Clinical management
  • Biomarkers
  • Molecular metastatic mechanism
  • Personalized genomics

Published Papers (1 paper)

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Research

Open AccessArticle
Sensitive and Specific Detection of Ewing Sarcoma Minimal Residual Disease in Ovarian and Testicular Tissues in an In Vitro Model
Cancers 2019, 11(11), 1807; https://doi.org/10.3390/cancers11111807 - 17 Nov 2019
Abstract
Ewing sarcoma (EWS) is a common pediatric solid tumor with high metastatic potential. Due to toxic effects of treatments on reproductive functions, the cryopreservation of ovarian tissue (OT) or testicular tissue (TT) is recommended to preserve fertility. However, the risk of reintroducing residual [...] Read more.
Ewing sarcoma (EWS) is a common pediatric solid tumor with high metastatic potential. Due to toxic effects of treatments on reproductive functions, the cryopreservation of ovarian tissue (OT) or testicular tissue (TT) is recommended to preserve fertility. However, the risk of reintroducing residual metastatic tumor cells should be evaluated before fertility restoration. Our goal was to validate a sensitive and specific approach for EWS minimal residual disease (MRD) detection in frozen germinal tissues. Thawed OT (n = 12) and TT (n = 14) were contaminated with tumor RD-ES cells (10, 100, and 1000 cells) and EWS-FLI1 tumor-specific transcript was quantified with RT-qPCR. All contaminated samples were found to be positive, with a strong correlation between RD-ES cell numbers and EWS-FLI1 levels in OT (r = 0.93) and TT (r = 0.96) (p < 0.001). No transcript was detected in uncontaminated control samples. The invasive potential of Ewing cells was evaluated using co-culture techniques. After co-culturing, tumor cells were detected in OT/TT with histology, FISH, and RT-qPCR. In addition, four OT and four TT samples from children with metastatic EWS were tested, and no MRD was found using RT-qPCR and histology. We demonstrated the high sensitivity and specificity of RT-qPCR to detect EWS MRD in OT/TT samples. Clinical trial: NCT 02400970. Full article
(This article belongs to the Special Issue Ewing Sarcoma)
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