Expression of TLE1, INI1, β-catenin, Claudin1, CK7, CK19, SS18 and calponin in synovial sarcoma

Abstract

Background and Objectives: Synovial sarcomas (SS) are enigmatic soft tissue tumors, which are yet to have a defined cell of origin. SS have a variety of differential diagnosis depending upon the age of the patient and the site of presentation. This makes diagnosis cumbersome unless the specific fusion SS18:SSX is identified by reverse transcription-polymerase chain reaction (RT-PCR) or fluorescence in situ hybridization (FISH). Immunohistochemistry is a useful tool in resource-poor settings in helping to narrow the differentials and help diagnose this tumor. This study set about assessing possible candidate immunohistochemical markers in their utility to recognize SS. Methods: Forty cases of SS, proven by FISH were included. A tissue microarray (TMA) was constructed, and immunohistochemistry was done using antibodies – TLE1 (OTI1F5), β-catenin (14), INI1 (MRQ-27), CK7 (OV-TL), CK19 (polyclonal), SS18 (polyclonal), calponin (CALP), and claudin1 (Polyclonal). The expression was analyzed to arrive at sensitivity and specificity. Results: TLE1 had a sensitivity of 92.5% and a specificity of 100%; β-Catenin had a sensitivity of 17.5% and specificity of 100%; Calponin had a sensitivity of 97.5% and a specificity of 81.25%; SS18 had a sensitivity of 95% and specificity of 100%; INI1 had a sensitivity of 95% and specificity of 100%; CK7 had a sensitivity of 90% and specificity of 87.5%; CK19 had a sensitivity of 90% and a specificity of 59.38%; and Claudin had a sensitivity of 85% and a specificity of 78.12%. Interpretation and Conclusions: The study showed both TLE1 and SS18 are robust diagnostic markers of synovial sarcoma with a sensitivity of 92% and 95%, respectively. INI1 can be used to discriminate SS from nonepithelioid and nonrhabdoid differentials. Calponin expression is helpful to differentiate poorly differentiated SS from its mimics. CK7 is a better marker than CK19 and can be used as a replacement for EMA in the initial screening panel. The use of claudin1 was restricted to delineating the epithelial component. β-Catenin had poor sensitivity, restricting its utility in SS.