Model systems of prostate cancer: Uses and limitations

被引:74
作者
Navone, NM
Logothetis, CJ
von Eschenbach, AC
Troncoso, P
机构
[1] Univ Texas, MD Anderson Canc Ctr, Dept Genitourinary Med Oncol, Houston, TX 77030 USA
[2] Univ Texas, MD Anderson Canc Ctr, Dept Urol, Houston, TX 77030 USA
[3] Univ Texas, MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA
关键词
cell lines; xenografts; LNCaP; MDA PCa 2a; MDA PCa 2b; PC; 3;
D O I
10.1023/A:1006165017279
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
A valid experimental model system reflects the system under study and is reproducible. Model systems of prostate cancer that accurately reflect the different disease stages are necessary to ensure a proper experimental design aimed at increasing our understanding of the biology of the disease and such models are essential tools to accelerate development of new therapies for prostate cancer. Until recently, a limited number of experimental systems were available and more suitable models derived from human specimens have only recently been developed and become available for use. In addition, transgenic techniques have also permitted the development of unique mouse models. The difficulty in establishing model systems may reflect the complex requirements necessary for cancer progression and should lead us to interpret results from model systems with caution. It is unlikely that a single model system that faithfully reflects the whole process of cancer development and progression will be developed. However, thoughtful use of the available model systems will permit the study of a significant portion of prostate cancer progression. In this review we summarize the properties of the prostate cancer model systems in use and defined their utility and limitations. This review will guide the investigator seeking models with which to test specific hypotheses pertaining to prostate cancer.
引用
收藏
页码:361 / 371
页数:11
相关论文
共 76 条
  • [51] Pettaway CA, 1996, CLIN CANCER RES, V2, P1627
  • [52] XENOGRAFTS OF PRIMARY HUMAN PROSTATIC-CARCINOMA
    PRETLOW, TG
    WOLMAN, SR
    MICALE, MA
    PELLEY, RJ
    KURSH, ED
    RESNICK, MI
    BODNER, DR
    JACOBBERGER, JW
    DELMORO, CM
    GIACONIA, JM
    PRETLOW, TP
    [J]. JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1993, 85 (05) : 394 - 402
  • [53] PUGH TD, 1994, CANCER RES, V54, P5766
  • [54] QUARMBY VE, 1990, CANCER RES, V50, P735
  • [55] ROWLEY DR, 1992, IN VITRO CELL DEV-AN, V28A, P29
  • [56] HORMONE-REFRACTORY (D3) PROSTATE-CANCER - REFINING THE CONCEPT
    SCHER, HI
    STEINECK, G
    KELLY, WK
    [J]. UROLOGY, 1995, 46 (02) : 142 - 148
  • [57] Stapleton AMF, 1997, CLIN CANCER RES, V3, P1389
  • [58] METASTATIC MODEL FOR HUMAN PROSTATE-CANCER USING ORTHOTOPIC IMPLANTATION IN NUDE-MICE
    STEPHENSON, RA
    DINNEY, CPN
    GOHJI, K
    ORDONEZ, NG
    KILLION, JJ
    FIDLER, IJ
    [J]. JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1992, 84 (12) : 951 - 957
  • [59] ISOLATION OF A HUMAN PROSTATE CARCINOMA CELL LINE (DU 145)
    STONE, KR
    MICKEY, DD
    WUNDERLI, H
    MICKEY, GH
    PAULSON, DF
    [J]. INTERNATIONAL JOURNAL OF CANCER, 1978, 21 (03) : 274 - 281
  • [60] Dehydroepiandrosterone activates mutant androgen receptors expressed in the androgen-dependent human prostate cancer xenograft CWR22 and LNCaP cells
    Tan, J
    Sharief, Y
    Hamil, KG
    Gregory, CW
    Zang, DY
    Sar, M
    Gumerlock, PH
    White, RWD
    Pretlow, TG
    Harris, SE
    Wilson, EM
    Mohler, JL
    French, FS
    [J]. MOLECULAR ENDOCRINOLOGY, 1997, 11 (04) : 450 - 459