BACKGROUND: No detailed data are available concerning the possible chromosomal heterogeneity within testicular germ cell tumors (TGCT) of adults. In addition, little is known about the chromosomal constitution of carcinoma in situ (CIS) of the human testis, the precursor of TGCTs, and the possible relation with the different histological tumor types (seminomas (SE), nonseminomatous (TGCTs (NS). EXPERIMENTAL DESIGN: Interphase cytogenetics in combination with immunohistochemistry was performed on tissue sections of SE, NS, and their adjacent CIS to study the numerical distributions of centromeric regions of chromosomes 1, 12, and 15. RESULTS: No differences in chromosomal constitution were found between CIS adjacent to SE and the invasive tumor itself. NS showed a significant lower number of copies of chromosome 15 than SE, which was also found for the adjacent CIS. In addition a significantly higher number of copies of chromosome 12 was found in CIS adjacent to SE compared with CIS adjacent to NS. Invasive NS showed a significantly higher chromosome 1 and 12 copy number compared with its adjacent CIS. CONCLUSIONS: Net loss of chromosomes during tumor evolution can explain the differences between SE and NS and also between their adjacent CIS. Based on these results, we hypothesize that CIS-S may progress not only into SE but also into CIS-NS. It is conceivable, therefore, that NS may evolve from SE or from CIS-NS.
BACKGROUND: No detailed data are available concerning the possible chromosomal heterogeneity within testicular germ cell tumors (TGCT) of adults. In addition, little is known about the chromosomal constitution of carcinoma in situ (CIS) of the human testis, the precursor of TGCTs, and the possible relation with the different histological tumor types (seminomas (SE), nonseminomatous (TGCTs (NS). EXPERIMENTAL DESIGN: Interphase cytogenetics in combination with immunohistochemistry was performed on tissue sections of SE, NS, and their adjacent CIS to study the numerical distributions of centromeric regions of chromosomes 1, 12, and 15. RESULTS: No differences in chromosomal constitution were found between CIS adjacent to SE and the invasive tumor itself. NS showed a significant lower number of copies of chromosome 15 than SE, which was also found for the adjacent CIS. In addition a significantly higher number of copies of chromosome 12 was found in CIS adjacent to SE compared with CIS adjacent to NS. Invasive NS showed a significantly higher chromosome 1 and 12 copy number compared with its adjacent CIS. CONCLUSIONS: Net loss of chromosomes during tumor evolution can explain the differences between SE and NS and also between their adjacent CIS. Based on these results, we hypothesize that CIS-S may progress not only into SE but also into CIS-NS. It is conceivable, therefore, that NS may evolve from SE or from CIS-NS.