Chromosomal aberrations in prostate cancer xenografts detected by comparative genomic hybridization

被引:38
作者
Laitinen, S
Karhu, R
Sawyers, CL
Vessella, RL
Visakorpi, T [1 ]
机构
[1] Univ Tampere, Inst Med Technol, Canc Genet Lab, FIN-33014 Tampere, Finland
[2] Tampere Univ Hosp, Tampere, Finland
[3] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA
[4] Univ Washington, Dept Urol, Seattle, WA 98195 USA
关键词
D O I
10.1002/gcc.10097
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
A major problem in studying prostate cancer has been the lack of model systems because of the difficulties in growing prostate cancer cells in vitro. Recently, however, several human prostate cancer xenografts, grown in immune-deficient mice, have been established. Here, we characterized 13 such xenografts (LuCap 23.8, 23.12, 35, 41. 49, 58, 69, 70. 73, LAPC-4AD, LAPC-4AI LAPC-9AD, and LAPC-9AI) as well as one prostate cancer cell line (22RvI) derived from a xenograft for chromosomal alterations by comparative genomic hybridization and a modification of multicolor fluorescence in situ hybridization. On average, the xenografts contained 13 (range 5-28) aberrations, 5 (1-13) gains, and 8 (1-15) losses, per case. The chromosome arms that most often contained losses were 2q, 5q, 6q, 8p, 13q, and 18q, and gains were 7q, 8q, and Xq. The same regions were previously shown to be often altered in advanced prostate carcinomas in patients. The androgen-dependent and corresponding androgen-independent sublines of LAPC-4 and LAPC-9 shared all genetic alterations, suggesting that the transition of the growth from androgen dependency to independence does not involve major chromosomal aberrations in these two models. In conclusion, the identified genetic aberrations lay the groundwork for further detailed genetic analyses of these xenografts. (C) 2002 Wiley-Liss, Inc.
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页码:66 / 73
页数:8
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