Document Type

Article

Publication Date

7-2020

Identifier

PMCID: PMC7346972

Abstract

Objectives: Ewing's sarcoma is an aggressive malignancy of bone and soft tissue in children and young adults. Despite advances in modern therapy, metastasis can occur and results in high mortality. The objective of this study was to identify whether the signaling transduction proteins, insulin growth factor receptor (IGF1R) and S6 kinase (S6K), can predict poor prognosis in Ewing's sarcoma.

Methods: After the Institutional Research Board approval, immunohistochemical experiments on tissue microarray slides containing 32 archived Ewing's sarcoma tumor samples were performed with antibodies against IGF1Rb and p-S6K. Immunohistochemical staining results were correlated with patients' clinical data including clinical stage and overall survival (OS).

Results: Patients had an age range of 12-72 years and 8 (25%) were ≤20 years. After a follow-up to 14 years, the OS ranged from 25 to 5065 days. High expression of IGF1Rb and p-S6K, defined as staining stronger than positive control, was identified in 25% and 68.75% of cases, respectively. Statistical analysis revealed that IGF1Rb high expression had a significant association with adverse outcome, shorter OS (P < 0.05), and near significant association with advanced stage tumors (P = 0.0534). Expression of S6K exhibited a trend toward shorter survival (P = 0.0934).

Conclusion: High expression or strong staining of IGF1Rb in Ewing's sarcoma may be more important than overall positive staining in identifying poor prognosis and aggressive cases to be selected for IGF1R inhibitory therapy. More definitive studies are needed to confirm the role of S6K in the prognosis in Ewing's sarcoma tumors.

Journal Title

Int J Health Sci (Qassim)

Volume

14

Issue

4

First Page

17

Last Page

21

Keywords

Ewing’s sarcoma; S6 kinase; immunohistochemistry; insulin growth factor 1Rb; tissue microarray

Comments

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Publisher's Link:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346972/

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