that MAGE-A4, a member of a family of genes that encode for tumor antigens that can be recognized by tumor-specific cytolytic T lymphocytes derived from patients with malignant disease, is found in classic seminoma but not in anaplastic seminoma or NSGCT.6 It should be recalled that one of the features of classic seminoma is a lymphocytic infiltration, which theoretically could explain this phenomenon. Similarly, c-kit expression is found predominantly in seminoma rather than in NSGCT,7 as discussed below.

Thus, by morphologic and functional criteria, it appears most likely that the majority of testicular cancers, including the variants of seminoma and the NSGCTs, share a common origin from primordial germ cells, via the intermediary step of atypical germ cells or carcinoma in situ (CIS). The mechanism of this transition has been the subject of considerable pre-clinical and clinical investigation, as outlined below.

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