Hormonal suppressive therapy for endometriosis may not improve patient health

被引:37
作者
Blumenfeld, Z [1 ]
机构
[1] Technion Israel Inst Technol, Bruce Rappaport Fac Med, Rambam Med Ctr, Dept Obstet & Gynecol, IL-31096 Haifa, Israel
关键词
endometriosis; GnRH-a; Danazol; ovarian cancer; hormonal ablative treatment;
D O I
10.1016/j.fertnstert.2003.07.038
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objective: To critically examine the possible association between hormonal treatment of endometriosis and ovarian cancer. Result(s): The malignant potential of endometriosis has been suggested by several clinical studies. Although controversial, ovarian carcinoma of the endometrioid and clear cell subtypes has been associated with endometriosis, particularly among subjects with a longstanding disease. Furthermore, a significantly higher frequency of endometriosis has been found in patients undergoing surgery for endometrioid, clear cell, and mixed subtypes of ovarian carcinoma, as compared with the other subtypes. Changes in the genomic material in endometriotic implants were observed by many investigators in chromosomes 1, 5, 6, 7, 16, and 22 by several methods (fluorescent in situ hybridization, comparative genomic hybridization, and others). Because hormonal ablative treatments may suppress the normal, eukaryotic cells more than the aneuploid cells bearing chromosomal aberrations, it may increase the rate of dyskaryotic cells in the endometriotic implants, possibly augmenting the risk of malignant transformation. A recent published association between Danazol and ovarian cancer suggests that such a theoretical risk may occur. Conclusion(s): The hormonal ablative treatment of endometriosis may increase the risk of malignant transformation in the endometriotic implants by causing a negative selection and increasing the rate of dyskaryosis and loss of heterozygosity.
引用
收藏
页码:487 / 492
页数:6
相关论文
共 59 条
  • [1] OVARIAN ENDOMETRIOTIC CYSTS - AN ANALYSIS OF CYTOLOGIC ATYPIA AND DNA-PLOIDY PATTERNS
    BALLOUK, F
    ROSS, JS
    WOLF, BC
    [J]. AMERICAN JOURNAL OF CLINICAL PATHOLOGY, 1994, 102 (04) : 415 - 419
  • [2] Possible involvement of arylamine N-acetyltransferase 2, glutathione S-transferases M1 and T1 genes in the development of endometriosis
    Baranova, H
    Canis, M
    Ivaschenko, T
    Albuisson, E
    Bothorishvilli, R
    Baranov, V
    Malet, P
    Bruhat, MA
    [J]. MOLECULAR HUMAN REPRODUCTION, 1999, 5 (07) : 636 - 641
  • [3] GSTM1 null polymorphism and susceptibility to endometriosis and ovarian cancer
    Baxter, SW
    Thomas, EJ
    Campbell, IG
    [J]. CARCINOGENESIS, 2001, 22 (01) : 63 - 65
  • [4] Heritability and molecular genetic studies of endometriosis
    Bischoff, FZ
    Simpson, JL
    [J]. HUMAN REPRODUCTION UPDATE, 2000, 6 (01) : 37 - 44
  • [5] Somatic DNA alterations in endometriosis: high frequency of chromosome 17 and p53 loss in late-stage endometriosis
    Bischoff, FZ
    Heard, M
    Simpson, JL
    [J]. JOURNAL OF REPRODUCTIVE IMMUNOLOGY, 2002, 55 (1-2) : 49 - 64
  • [6] Recurrent DNA copy number changes in 1q, 4q, 6q, 9p, 13q, 14q and 22q detected by comparative genomic hybridization in malignant mesothelioma
    Bjorkqvist, AM
    Tammilehto, L
    Anttila, S
    Mattson, K
    Knuutila, S
    [J]. BRITISH JOURNAL OF CANCER, 1997, 75 (04) : 523 - 527
  • [7] Progestagenic effects of tibolone on human endometrial cancer cells
    Blok, LJ
    De Ruiter, PE
    Kühne, ECM
    Hanekamp, EE
    Grootegoed, JA
    Smid-Koopman, E
    Gielen, SCJP
    De Gooyer, ME
    Kloosterboer, HJ
    Burger, CW
    [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2003, 88 (05) : 2327 - 2334
  • [8] Cancer risk after a hospital discharge diagnosis of endometriosis
    Brinton, LA
    Gridley, G
    Persson, I
    Baron, J
    Bergqvist, A
    [J]. AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1997, 176 (03) : 572 - 579
  • [9] Bryan EJ, 1996, CANCER RES, V56, P719
  • [10] Endometriosis: candidate genes
    Campbell, IG
    Thomas, EJ
    [J]. HUMAN REPRODUCTION UPDATE, 2001, 7 (01) : 15 - 20