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Cytokeratin immunoreactivity in Ewing sarcoma/ primitive neuroectodermal tumour.

S H A Elbashier¹, A R Nazarina, L M Looi

¹University Malaya, Faculty of Medicine, Pathology Department, Jalan Universiti, 50603 Kuala Lumpur, Malaysia.

The Malaysian Journal of Pathology

|December 24, 2013

Summary

Cytokeratin expression is present in nearly 40% of Ewing sarcoma (ES)/primitive neuroectodermal tumors (PNET) in Malaysian patients. This finding supports epithelial differentiation and is crucial for diagnosing small round cell tumors.

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Area of Science:

Oncology
Pathology
Immunohistochemistry

Background:

Ewing sarcoma (ES)/primitive neuroectodermal tumor (PNET) is an aggressive small round cell tumor primarily affecting young individuals.
Cytokeratin expression in ES/PNET has been reported sporadically, necessitating further investigation.

Purpose of the Study:

To investigate the prevalence and patterns of cytokeratin expression in Malaysian patients diagnosed with ES/PNET.
To determine the association of cytokeratin expression with clinical and pathological parameters.

Main Methods:

Immunohistochemical staining for cytokeratin markers AE1/AE3 and MNF116 was performed on 43 ES/PNET cases.
Analysis of cytokeratin expression patterns (focal, intermediate, diffuse).
Correlation of cytokeratin immunoreactivity with patient age, sex, tumor location, stage, and treatment status.

Main Results:

Cytokeratin expression was observed in 17 out of 43 cases (39.5%) of ES/PNET.
No significant association was found between cytokeratin expression and patient demographics, tumor site, or disease status.
A significant association was demonstrated between cytokeratin expression and neuron-specific enolase (NSE) expression.

Conclusions:

The study provides evidence supporting epithelial differentiation in a subset of ES/PNET.
Cytokeratin expression should not exclude ES/PNET from the differential diagnosis of small round cell tumors.
Immunohistochemical findings aid in the diagnostic workup of challenging small round cell neoplasms.