Ewing Sarcoma
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: closed (31 March 2020) | Viewed by 36593
Special Issue Editors
Interests: sarcoma; rare cancer; biobank; patient derived cancer model
Special Issues, Collections and Topics in MDPI journals
Interests: rare cancer research; sarcoma; proteogenomics; applications of patient-derived cancer model
Special Issues, Collections and Topics in MDPI journals
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. Dr. Kazutaka Kikuta
Prof. Tadashi Kondo
Guest Editors
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Keywords
- Ewing Sarcoma
- Fusion genes
- Clinical management
- Biomarkers
- Molecular metastatic mechanism
- Personalized genomics
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