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
  • [41] PROSTATE AND MAMMARY ADENOCARCINOMA IN TRANSGENIC MICE CARRYING A RAT C3(1) SIMIAN-VIRUS-40 LARGE TUMOR-ANTIGEN FUSION GENE
    MAROULAKOU, IG
    ANVER, M
    GARRETT, L
    GREEN, JE
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (23) : 11236 - 11240
  • [42] McConkey DJ, 1996, CANCER RES, V56, P5594
  • [43] Nagabhushan M, 1996, CANCER RES, V56, P3042
  • [44] Suppression of caveolin expression induces androgen sensitivity in metastatic androgen-insensitive mouse prostate cancer cells
    Nasu, Y
    Timme, TL
    Yang, G
    Bangma, CH
    Li, LK
    Ren, CZ
    Park, SH
    DeLeon, M
    Wang, JX
    Thompson, TC
    [J]. NATURE MEDICINE, 1998, 4 (09) : 1062 - 1064
  • [45] P53 PROTEIN ACCUMULATION AND GENE MUTATION IN THE PROGRESSION OF HUMAN PROSTATE CARCINOMA
    NAVONE, NM
    TRONCOSO, P
    PISTERS, LL
    GOODROW, TL
    PALMER, JL
    NICHOLS, WW
    VONESCHENBACH, AC
    CONTI, CJ
    [J]. JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1993, 85 (20) : 1657 - 1669
  • [46] Navone NM, 1997, CLIN CANCER RES, V3, P2493
  • [47] p53 mutations in prostate cancer bone metastases suggest that selected p53 mutants in the primary site define foci with metastatic potential
    Navone, NM
    Labate, ME
    Troncoso, P
    Pisters, LL
    Conti, CJ
    Von Eschenbach, AC
    Logothetis, CJ
    [J]. JOURNAL OF UROLOGY, 1999, 161 (01) : 304 - 308
  • [48] Olumi AF, 1998, CANCER RES, V58, P4525
  • [49] STIMULATION OF HUMAN PROSTATIC-CARCINOMA TUMOR-GROWTH IN ATHYMIC MICE AND CONTROL OF MIGRATION IN CULTURE BY EXTRACELLULAR-MATRIX
    PASSANITI, A
    ISAACS, JT
    HANEY, JA
    ADLER, SW
    CUJDIK, TJ
    LONG, PV
    KLEINMAN, HK
    [J]. INTERNATIONAL JOURNAL OF CANCER, 1992, 51 (02) : 318 - 324
  • [50] MUTANT ANDROGEN RECEPTORS IN PROSTATIC TUMORS DISTINGUISH BETWEEN AMINO-ACID-SEQUENCE REQUIREMENTS FOR TRANSACTIVATION AND LIGAND-BINDING
    PETERZIEL, H
    CULIG, Z
    STOBER, J
    HOBISCH, A
    RADMAYR, C
    BARTSCH, G
    KLOCKER, H
    CATO, ACB
    [J]. INTERNATIONAL JOURNAL OF CANCER, 1995, 63 (04) : 544 - 550