The Ewing family of tumors (EFT) is characterized by high MIC2/CD99 expression 
and specific EWS/ETS gene rearrangements, resulting in different chimeric 
transcripts. Further division into peripheral primitive neuroectodermal tumors 
and Ewing's sarcoma is still debated and, in the absence of distinct 
morphological parameters, has been based on the reactivity with neuroglial 
markers (NgM). We investigated 44 EFT in terms of a possible correlation between 
the type of EWS chimeric transcripts and reactivity with the following NgM: 
polyclonal and monoclonal neuron-specific enolase (NSE), S-100, chromogranin A, 
synaptophysin, Leu-7, glial fibrillary acid protein, and neurofilament. EWS/Fli1 
fusion type 1 was detected in 30 of 44 and type 2 in 11 of 44 tumors. Three 
tumors, presenting with an uncommon morphology, carried rare chimeric 
transcripts. Our results indicate an association of lack of NgM staining with 
type 1 EWS/Fli1 translocations, found in 16 of 18 tumors with no NgM expression 
as detectable by any of the antibodies we applied. Using the monoclonal NSE 
antibody, 21 of 26 tumors without NgM staining expressed type 1 EWS/FLI1chimeric 
RNA, whereas in the groups with 1 or more and 2 or more NgM, only 9 of 17 and 1 
of 5 tumors, respectively, carried type 1 EWS/Fli1 fusion transcripts. Despite 
this association of increased NgM expression with a non-type 1 EWS/Fli1 gene 
fusion, a strict correlation between the extent of NgM expression and certain 
EWS fusion types was not evident. This fortifies the concept to consider EFT as 
a spectrum of tumors and suggests the type of EWS fusion transcripts as one, but 
not the only parameter influencing the extent of differentiation.