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). Recent studies have noted a small but significant increase in the incidence of endometrial cancer in postmenopausal women using hormonal replacement therapy ( Chlebowski et al. 2002 ), and there is also an increased risk of endometrial cancer
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First Department of Obstetrics and Gynecology, Section on Endocrinology and Genetics (SEGEN), Developmental Endocrinology Branch, Athens University Medical School, Alexandra Hospital, 115 28 Athens, Greece
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sporadic (not associated with CNC or any other familial tumor syndrome) lesions ( McDaid et al . 1999 , Sandrini et al . 2002 , Bertherat et al . 2003 ). Endometrial cancer is a hormone-dependent lesion. Although there have been no studies to date on
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. Because of the scope of published literature on these topics, this review is not a comprehensive analysis of lncRNAs and miRNAs in breast, prostate, endometrial and thyroid cancers. The reader is provided with citations to recent reviews and primary
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( Pan et al. 2017 ). TAM also has moderate (menopausal-like symptoms) to severe side effects (an increased risk of developing endometrial cancer) ( Bergman et al. 2000 , Jones et al. 2012 ) and compliance is variable with many patients not
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with amenorrhea and was treated at age 31 by transsphenoidal surgery, which was repeated 5 years later. Elevated plasma E 2 (>1840 pmol/l) and endometrial hyperplasia persisted after the second transsphenoidal surgery. At the age of 39, ovarian
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Oral contraceptive (OC) use significantly reduces the risk of endometrial and ovarian cancer, has only a minimal effect on breast cancer, but may increase the risk of cervical cancer. These effects can be readily explained in terms of the effects of OCs on cell proliferation in these tissues. This analysis suggests how a hormonal contraceptive based on a GnRH agonist plus low-dose add-back sex steroids could be made that would greatly reduce lifetime risk of breast and ovarian cancer. Such a hormonal contraceptive is also likely to significantly reduce the lifetime risk of cervical cancer. It is also likely to reduce the risk of endometrial cancer, although not to the same extent as OCs.
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It is very important to examine the influence of inhibition of in situ estrogen production on the pathobiology of human sex steroid-dependent tumors in order to understand the clinical effects of aromatase inhibitors. We have examined the biological changes before and after aromatase inhibitor treatment in vitro (endometrial and ovarian cancer) and in vivo (breast cancer). First, we analyzed these changes using histoculture of 15 human endometrial cancers and 9 ovarian cancers. Five of the fifteen endometrial cancers and four of the nine ovarian cancers demonstrated decreased [3H]thymidine uptake or Ki67 labeling index after 14alpha-hydroxy-4-androstene-3,6,17-trione (NKS01) treatment. In ovarian cancer cases, the responsive cases tended to be associated with higher aromatase and estrogen receptor alpha (ER) expression compared with the other cases but this was not seen in the endometrial cancer cases. There were no changes in ER and aromatase expression before and after NKS01 treatment in either ovarian or endometrial cancer cases. We then studied the same primary human breast tumors before and after aminoglutethimide (AMG, n=3) and 4-hydroxyandrostenedione (4-OHA, n=3) treatment. Tumor aromatase activity increased in 3 cases and decreased or was unchanged in 3 cases but aromatase immunoreactivity in stroma and adipocytes was unaltered in 5 cases. There were no changes in the ER labeling index before or after treatment. Five of the six cases including the responsive cases tended to be associated with decreased cell proliferation or Ki67 expression and increased apoptosis when examined by the TUNEL method. These results indicate that aromatase inhibitors may exert their effects on human breast and other cancers through decreasing proliferation and increasing apoptosis, possibly without altering ER status.
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The idea of breast cancer prevention by hormonal means stemmed from the results of treatment trials, many of them carried out by the National Surgical Adjuvant Breast and Bowel Project (NSABP). Over the years, a number of NSABP treatment studies demonstrated that breast cancer recurrence was reduced in women with the disease who were given tamoxifen, a selective estrogen receptor (ER) modulator (SERM). Five subsequent tamoxifen prevention trials with this agent have shown a 48% reduction in ER-positive cancers, but no effect for ER-negative cancers, and an increase in endometrial cancer and thromboembolic events. The drug raloxifene, another SERM, originally examined as an osteoporosis agent, has also shown promise for the prevention of breast cancer, although, as with tamoxifen, the drug carries a risk for thromboembolic events. There is recent evidence in a large treatment trial that the aromastase inhibitor anastrazole, a 'pure anti-estrogen', holds promise as a breast cancer preventive agent. Longer follow-up and the testing of additional agents is required before these drugs can be used widely for prevention. In addition, future research should focus on the identification of at-risk women who can perhaps be targeted for specific prevention agents.
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Abstract
Epidermal growth factor-receptor (EGF-R) expression was evaluated in the adenomyosis foci in comparison with its presence in endometrium and myometrium from the same patients. It was detected by an immunoperoxidase test, using a monoclonal antibody against EGF-R. EGF-R expression in adenomyosis foci as well as in endometrial and myometrial tissues was shown, but its expression and concentration were lower in the adenomyotic foci than in the endometrial tissue. EGF-R was detectable in glandular cells as well as in the stroma. The smooth muscle fibres directly surrounding the adenomyotic foci showed more intensive EGF-R expression in comparison with the unchanged myometrium. No significant dependence of EGF-R expression on the phase of the menstrual cycle was found.
Endocrine-Related Cancer (1996) 3 131-135
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Ovarian cancer accounts for 5% of all cancer deaths in Western countries and is the most frequent cause of gynaecologic cancer mortality. The incidence varies with age between 1% and 14% with a peak rate in the eighth decade, and in the majority of cases, the disease has already spread beyond the pelvic cavity at time of diagnosis. Although in the last decades the introduction of cisplatin-based chemotherapy resulted in an improvement of patient survival, the percentage of recurrent disease is high even in those patients who achieve a complete response to chemotherapy, so that more than 80% of patients with advanced stage of disease die within 5 years (Copeland & Gershenson 1986). At present the prognostic characterisation of ovarian cancer patients, based on clinico-pathological parameters, such as stage, histology, grade and residual tumour after surgery, seems to be inadequate, since patients with similar clinico- pathological characteristics often experienced different clinical outcome. Therefore, the identification of biological factors related to tumour aggressiveness could be relevant in order to identify patients with different prognosis and chance to respond to chemotherapy, thus allowing the selection, at time of initial diagnosis, of high risk patients needing more aggressive therapy or alternative treatment, and a closer follow-up. Among the biological parameters proposed as possible prognostic factors in ovarian cancer much attention has been focused on endocrine factors and especially on steroid hormones and their receptors. Although several epidemiological and in vitro evidences have demonstrated that, similarly to breast and endometrial cancer, ovarian cancer cell biology could be influenced by the biochemical pathways promoted by the interaction of estrogens and progesterone with their specific receptors (ER, PR) conflicting data have been reported about the possible clinical role of ER and PR in this neoplasm. This review is aimed: a) to summarise the informations about the influence of steroid hormones and their receptors in the biology of ovarian cancer in in vitro models as well as in primary tumours;b) to investigate the association of steroid hormone receptor expression with the clinico-pathological parameters and the clinical outcome in ovarian cancer patients.c) to report the data of the literature about the rationale and the results of endocrine therapy in ovarian cancer.
