In addition to functional alterations, our studies demonstrated PAX3-FKHR and PAX7-FKHR overexpression resulting from two distinct mechanisms, increased transcription of PAX3-FKHR by a copy number-independent mechanism, and gene amplification of PAX7-FKHR.     ///    "These differences extend to the phenotypic level, at which clinical differences have been found between the two ARMS subtypes: PAX7-FKHR tumors more often occur as localized lesions in the extremities of younger patients and are associated with longer event-free survival as compared to PAX3-FKHR tumors. "