Pretreatment p53 immunoreactivity does not infer radioresistance in prostate cancer patients

被引:18
作者
Stattin, P
Damber, JE
Modig, H
Bergh, A
机构
[1] UMEA UNIV,DEPT PATHOL,S-90185 UMEA,SWEDEN
[2] UMEA UNIV,DEPT UROL & ANDROL,S-90185 UMEA,SWEDEN
[3] UMEA UNIV,DEPT ONCOL,S-90185 UMEA,SWEDEN
来源
INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS | 1996年 / 35卷 / 05期
关键词
prostate cancer; transurethral resection; p53; immunohistochemistry; prognostic marker; radiation; survival;
D O I
10.1016/0360-3016(96)00134-4
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Purpose: To test, in a clinical context, the hypothesis that p53 aberrations, assessed by immunoreactivity, are related to radioresistance as suggested by several experimental studies. Methods and Materials: Sixty patients with prostate cancer who underwent transurethral resection of the prostate or biopsy prior to definitive external beam therapy were retrospectively identified. The endpoint in the study was cancer specific survival. The nuclear accumulation of the aberrant p53 protein was evaluated by immunohistochemistry with the pantropic, monoclonal Ab-6 anti-p53 antibody (clone DO-1) on pretreatment biopsies. Immunoreactivity was related to stage, grade, and cancer-specific survival. Results: There was a correlation between p53 immunoreactivity and low tumor stage (p < 0.001), but no relation between p53 status and grade was found. Moreover, no significant difference was found in cancer-specific survival between the p53 positive tumors (109 months) and the p53 negative tumors (99 months). Conclusions: No disadvantage regarding survival was seen for patients with p53 immunoreactive tumors, implicating that p53 immunoreactivity does not infer radioresistance in prostate cancer. This suggests that the p53 inactivation may be a less important determinant of tumor response to radiotherapy in some human cancers than in the previously studied experimental situations. Thus, other mechanisms may be more important in determining outcome after radiation. However, the series is small and data should be interpreted with caution.
引用
收藏
页码:885 / 889
页数:5
相关论文
共 34 条
  • [1] ASSOCIATION OF P53 PROTEIN EXPRESSION WITH TUMOR-CELL PROLIFERATION RATE AND CLINICAL OUTCOME IN NODE-NEGATIVE BREAST-CANCER
    ALLRED, DC
    CLARK, GM
    ELLEDGE, R
    FUQUA, SAW
    BROWN, RW
    CHAMNESS, GC
    OSBORNE, CK
    MCGUIRE, WL
    [J]. JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1993, 85 (03) : 200 - 206
  • [2] Campbell M. J., 1993, MED STAT
  • [3] THYMOCYTE APOPTOSIS INDUCED BY P53-DEPENDENT AND INDEPENDENT PATHWAYS
    CLARKE, AR
    PURDIE, CA
    HARRISON, DJ
    MORRIS, RG
    BIRD, CC
    HOOPER, ML
    WYLLIE, AH
    [J]. NATURE, 1993, 362 (6423) : 849 - 852
  • [4] FAN SJ, 1994, CANCER RES, V54, P5824
  • [5] GREENBLATT MS, 1994, CANCER RES, V54, P4855
  • [6] Grignon D., 1995, Journal of Urology, V153, p293A
  • [7] P53 IN TUMOR PATHOLOGY - CAN WE TRUST IMMUNOHISTOCHEMISTRY - REVISITED
    HALL, PA
    LANE, DP
    [J]. JOURNAL OF PATHOLOGY, 1994, 172 (01) : 1 - 4
  • [8] CLINICAL IMPLICATIONS OF THE P53 TUMOR-SUPPRESSOR GENE
    HARRIS, CC
    HOLLSTEIN, M
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1993, 329 (18) : 1318 - 1327
  • [9] CELL-CYCLE CONTROL AND CANCER
    HARTWELL, LH
    KASTAN, MB
    [J]. SCIENCE, 1994, 266 (5192) : 1821 - 1828
  • [10] JUNG M, 1992, CANCER RES, V52, P6390