Cell proliferation and apoptosis in BRCA-associated hereditary ovarian cancer

被引:29
作者
Levine, DA
Federici, MG
Reuter, VE
Boyd, J
机构
[1] Mem Sloan Kettering Canc Ctr, Dept Surg, Gynecol & Breast Res Lab, New York, NY 10021 USA
[2] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA
[3] Mem Sloan Kettering Canc Ctr, Dept Human Genet, New York, NY 10021 USA
关键词
ovarian cancer; hereditary; BRCA; cell proliferation; apoptosis;
D O I
10.1006/gyno.2002.6646
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Objective. The goal was to test the hypothesis that cellular growth properties differ between hereditary and sporadic ovarian cancers. Methods. Cell proliferation and apoptosis were assessed in 67 tumors associated with deleterious germline BRCA mutations (hereditary) and 69 tumors without BRCA mutations (sporadic). Cell proliferation was evaluated by immunohistochemical analysis of Ki-67 expression, and apoptosis was assessed using a TUNEL assay. Results. The mean number of Ki-67-immunopositive nuclei was significantly higher in ovarian cancers from the hereditary group compared with those from the sporadic group (P = 0.017). Cell proliferation did not differ significantly between BRCAl- and BRCA2-associated hereditary tumors, and apoptosis did not differ significantly between the hereditary and sporadic tumors. Conclusions. These data indicate that ovarian carcinomas associated with germline BRCA mutations have a significantly higher growth fraction than sporadic cancers. This property may contribute to an improved response to cytotoxic chemotherapy, partially accounting for the longer recurrence-free interval and overall survival observed in the hereditary group. (C) 2002 Elsevier Science (USA).
引用
收藏
页码:431 / 434
页数:4
相关论文
共 23 条
  • [1] Aida H, 1998, CLIN CANCER RES, V4, P235
  • [2] Barakat RR, 2000, CANCER, V89, P383, DOI 10.1002/1097-0142(20000715)89:2<383::AID-CNCR25>3.0.CO
  • [3] 2-T
  • [4] The breast cancer susceptibility gene BRCA1 is required for subnuclear assembly of Rad51 and survival following treatment with the DNA cross-linking agent cisplatin
    Bhattacharyya, A
    Ear, US
    Koller, BH
    Weichselbaum, RR
    Bishop, DK
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (31) : 23899 - 23903
  • [5] Clinicopathologic features of BRCA-linked and sporadic ovarian cancer
    Boyd, J
    Sonoda, Y
    Federici, MG
    Bogomolniy, F
    Rhei, E
    Maresco, DL
    Saigo, PE
    Almadrones, LA
    Barakat, RR
    Brown, CL
    Chi, DS
    Curtin, JP
    Poynor, EA
    Hoskins, WJ
    [J]. JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2000, 283 (17): : 2260 - 2265
  • [6] BOYD J, 2001, OVARIAN CANC, P3
  • [7] Garcia AA, 1998, SYNOPSIS GYNECOLOGIC, P391
  • [8] Husain A, 1998, CANCER RES, V58, P1120
  • [9] Tumour biological features of BRCA1-induced breast and ovarian cancer
    Johannsson, OT
    Idvall, I
    Anderson, C
    Borg, A
    Barkardottir, RB
    Egilsson, V
    Olsson, H
    [J]. EUROPEAN JOURNAL OF CANCER, 1997, 33 (03) : 362 - 371
  • [10] Multifactorial analysis of differences between sporadic breast cancers and cancers involving BRCA1 and BRCA2 mutations
    Lakhani, SR
    Jacquemier, J
    Sloane, JP
    Gusterson, BA
    Anderson, TJ
    van de Vijver, MJ
    Farid, LM
    Venter, D
    Antoniou, A
    Storfer-Isser, A
    Smyth, E
    Steel, CM
    Haites, N
    Scott, RJ
    Goldgar, D
    Neuhausen, S
    Daly, PA
    Ormiston, W
    McManus, R
    Scherneck, S
    Ponder, BAJ
    Ford, D
    Peto, J
    Stoppa-Lyonnet, D
    Bignon, YJ
    Struewing, JP
    Spurr, NK
    Bishop, DT
    Klijn, JGM
    Devilee, P
    Cornelisse, CJ
    Lasset, C
    Lenoir, G
    Barkardottir, RB
    Egilsson, V
    Hamann, U
    Chang-Claude, J
    Sobol, H
    Weber, B
    Stratton, MR
    Easton, DF
    [J]. JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1998, 90 (15): : 1138 - 1145