TY - JOUR
T1 - Comparative genomic hybridization of microdissected samples from different stages in the development of a seminoma and a non-seminoma
AU - Looijenga, L H
AU - Rosenberg, C
AU - van Gurp, R J
AU - Geelen, E
AU - van Echten-Arends, J
AU - de Jong, B
AU - Mostert, M
AU - Wolter Oosterhuis, J
N1 - Copyright 2000 John Wiley & Sons, Ltd.
PY - 2000/6
Y1 - 2000/6
N2 - Human testicular germ cell tumours (TGCTs) of adolescents and adults, both seminomas and non-seminomas, originate from intratubular germ cell neoplasia (IGCN). Comparative genomic hybridization (CGH) was applied to microdissected samples from different stages of the development of a seminoma and a mixed non-seminoma, including IGCN of both. The different stages of the seminoma development, namely IGCN, intratubular and invasive seminoma, showed a very similar pattern of chromosomal imbalances, including gains of parts of 7, 8, 12,14, and X, and losses of parts of 3, 4, 5, 10, 11, 12q, 16, 18, 22, and Y. A more heterogeneous pattern was found for the non-seminoma. Some aberrations were present only in IGCN, or in IGCN and in all invasive components (gains of parts of 1q, 17, 19p, 20q, and 22, and losses of parts of 4, 5, 9p, 13, and 18q), while others were present in a less consistent pattern. These are the first reported CGH data from different stages in the development of TGCTs. Although only two cases were studied, the results suggest that particular numerical changes of (parts of) chromosomes are involved in the early development and progression of this cancer.
AB - Human testicular germ cell tumours (TGCTs) of adolescents and adults, both seminomas and non-seminomas, originate from intratubular germ cell neoplasia (IGCN). Comparative genomic hybridization (CGH) was applied to microdissected samples from different stages of the development of a seminoma and a mixed non-seminoma, including IGCN of both. The different stages of the seminoma development, namely IGCN, intratubular and invasive seminoma, showed a very similar pattern of chromosomal imbalances, including gains of parts of 7, 8, 12,14, and X, and losses of parts of 3, 4, 5, 10, 11, 12q, 16, 18, 22, and Y. A more heterogeneous pattern was found for the non-seminoma. Some aberrations were present only in IGCN, or in IGCN and in all invasive components (gains of parts of 1q, 17, 19p, 20q, and 22, and losses of parts of 4, 5, 9p, 13, and 18q), while others were present in a less consistent pattern. These are the first reported CGH data from different stages in the development of TGCTs. Although only two cases were studied, the results suggest that particular numerical changes of (parts of) chromosomes are involved in the early development and progression of this cancer.
KW - Adolescent
KW - Adult
KW - Aged
KW - Case-Control Studies
KW - Chromosome Aberrations
KW - Chromosomes, Human/genetics
KW - DNA/genetics
KW - Gene Amplification
KW - Humans
KW - Karyotyping
KW - Male
KW - Middle Aged
KW - Nucleic Acid Hybridization
KW - Seminoma/genetics
KW - Testicular Neoplasms/genetics
U2 - 10.1002/(SICI)1096-9896(200006)191:2<187::AID-PATH584>3.0.CO;2-T
DO - 10.1002/(SICI)1096-9896(200006)191:2<187::AID-PATH584>3.0.CO;2-T
M3 - Article
C2 - 10861580
SN - 0022-3417
VL - 191
SP - 187
EP - 192
JO - The Journal of pathology
JF - The Journal of pathology
IS - 2
ER -