摘要
Objective\ To study the origination and reality of Askin tumor. Methods\ Twenty two cases of these lesions have been studied by clinical pathologic observation, immunohistochemistry, electron microscopy, and cytogenics in this paper. Results\ The results revealed the positiveness of MIC2(CD99), NSE, Chromogranin A(CgA) by immunohistochemistry, neurosecretory granules by electron microscopy, and the specific genotypic translocation of t (11∶22) (q24∶q12) by cytogenetic analysis, which were identical to the malignant primitive neuroectodermal tumor (PNET). Conclusion\ We conclude that this lesion is actually the one member of the PNET/Ewing′s sarcoma family, except the special location. Differential diagnoses between this tumor and other small round cell sarcomas such as lymphoma, embryonal rhabdomyosarcoma, rhabdoid tumor, round cell liposarcoma and desmoplastic small round cell tumor were also discussed in this article.
Objective\ To study the origination and reality of Askin tumor. Methods\ Twenty two cases of these lesions have been studied by clinical pathologic observation, immunohistochemistry, electron microscopy, and cytogenics in this paper. Results\ The results revealed the positiveness of MIC2(CD99), NSE, Chromogranin A(CgA) by immunohistochemistry, neurosecretory granules by electron microscopy, and the specific genotypic translocation of t (11∶22) (q24∶q12) by cytogenetic analysis, which were identical to the malignant primitive neuroectodermal tumor (PNET). Conclusion\ We conclude that this lesion is actually the one member of the PNET/Ewing′s sarcoma family, except the special location. Differential diagnoses between this tumor and other small round cell sarcomas such as lymphoma, embryonal rhabdomyosarcoma, rhabdoid tumor, round cell liposarcoma and desmoplastic small round cell tumor were also discussed in this article.
