Lachman M F, Ricci A, Kosciol C
Yale University School of Medicine, New Haven, USA.
Conn Med. 1995 Mar;59(3):133-6.
Recent immunohistochemical and DNA ploidy analyses indicate that seminoma serves as a precursor to nonseminomatous germ cell tumors. It is believed that tumor progression from classical seminoma to nonseminoma is accompanied by inactivation and deletion of genetic material, and that these deletions are reflected in DNA ploidy. Twenty-three primary testicular germ cell tumors were studied by DNA flow cytometry to investigate whether a proposed histologic intermediate "atypical seminoma" (AS) could be separated from classical seminoma by ploidy analysis. The mean DNA indices (DI) for classical seminoma (N = 16), atypical seminoma (N = 5), and nonseminoma (N = 2; both embryonal carcinoma) were 1.53, 1.34, and 1.35, respectively. When a single "outlier" case of atypical seminoma was removed from consideration the mean DI for the AS rose to 1.45. This data is consistent with the interpretation of atypical seminoma as an intermediate between classical seminoma (CS) and embryonal carcinoma (ES). It suggests that genetic deletions characterizing progression from CS to nonseminoma may, in part, already be extant in atypical seminoma.
