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Endometrial cancer (EC) is the most frequent malignant tumor of the female genital tract. Increasing evidence suggests that at least two different types of EC exist. Type I is associated with an endocrine milieu of estrogen predominance. These tumors are of endometrioid histology and develop from endometrial hyperplasia. They have a good prognosis and are sensitive to endocrine manipulation. Type II EC is not associated with a history of unopposed estrogens and develops from the atrophic endometrium of elderly women. They are of serous histology, have a poor prognosis, and do not react to endocrine manipulation. Both types of EC probably differ markedly with regard to the molecular mechanisms of malignant transformation. This article reviews reproductive and lifestyle factors modifying the risk of developing type I EC, including the use of hormonal contraceptives, hormone replacement therapy and tamoxifen. The roles of established and novel therapies for precancerous lesions and for invasive EC in the adjuvant and palliative settings are discussed.
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Introduction Endometrial cancer development is strongly linked to lifestyle factors ( Kaaks et al. 2002 ). Excess weight is a major risk factor ( Kaaks et al. 2002 ) that is estimated to cause up to half of all endometrial cancer
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There is definitely a need for the development of new drugs for the treatment and cure of endometrial cancer. In addition there are various new drugs or phyto-remedies under development which are intended for use in the treatment and prevention of breast cancer, for the treatment of menopausal symptoms and for hormone replacement therapy. The efficacy of novel drugs targeting steroid receptors in endometrial cancers has to be evaluated and the safety of other endocrine measures on endometrial cancers or on endometrial carcinogenesis has to be assessed. For these experimental purposes five main classes of experimental models are available: spontaneous endometrial tumorigenesis models in inbred animals (Donryu rats, DA/Han rats, BDII/Han rats), inoculation tumors from chunks of tumors (rat EnDA-tumor, human EnCa 101 tumor) or from inoculated tumor cell lines (rat RUCA-I cells, human Ishikawa and ECC-1 cells), developmental estrogenic exposure or chemical carcinogen exposure of CD-1 and ICR mice, transgenic approaches such as mice heterozygous regarding the tumor suppressor gene PTEN (pten(+/-)-mice) and endometrial tumor cell lines cultured under conditions promoting in vivo-like morphology and functions e.g. cell culture on reconstituted basement membrane. Although the number of models is comparatively small, most aspects related to functions of estrogenic or gestagenic substances are assessable, particularly if various experimental models are combined. Whereas models based on human endometrial adenocarcinoma cells are widely used, the properties and advantages of animal-derived models have mainly been ignored so far.
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Abstract
The activity of estrone sulfatase (E1SF), which converts estrone sulfate to estrone, in uterine endometrial cancer tissue is remarkably high compared with endometrial tissues, and this is assumed to contribute to the growth of this tumor. Thus, in this study, in order to screen drugs for sulfatase inhibitor activity, the inhibitory effect of medroxyprogesterone acetate (MPA; which is widely used for advanced or recurrent endometrial cancer) on E1SF activity and steroid sulfatase (STS) gene expression in endometrial cancer cells was examined and compared with danazol (DZ).
MPA and DZ were shown to inhibit E1SF activity dose-dependently in the established endometrial cancer cell lines (Ishikawa and HEC-59 strains). These drugs (10−8 M) also inhibited the expression of STS mRNA, and this inhibition of STS gene expression is considered to partly explain their inhibitory actions against STS.
Endocrine-Related Cancer (1996) 3 337-340
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To clarify whether and how PTEN and the phosphatidylinositol 3-kinase/Akt pathway relates to endometrial cancer we examined the expression of these pathway-related proteins in patients with endometrial cancer. Of 103 endometrial cancers, 37 (36%) showed negative immunohistochemical staining for PTEN. Western blotting revealed that the level of phosphorylated Akt expression in PTEN-negative cases was significantly higher compared with that in positive cases. We found a significant inverse correlation between PTEN and phosphorylated Akt. The present study indicates the phosphorylation of Akt accompanied by the loss of PTEN in clinical specimens of endometrial cancers. In order to investigate the relationship between PTEN expression and prognosis in endometrial cancer, 98 patients with advanced endometrial cancer were newly enrolled. The survival rate for PTEN-positive patients was significantly higher than that for PTEN-negative or -heterogeneous staining patients. Of the 98 patients, 25 underwent radiation therapy, 62 received chemotherapy after surgery, and the remaining 11 did not have any postoperative treatment. When patients underwent chemotherapy, the survival rate for PTEN-positive cases was clearly higher than that for PTEN-negative or -heterogeneous cases (62.4 vs 11.8%). Subsequent multivariate analysis revealed that PTEN staining was an independent prognostic factor for patients undergoing chemotherapy. The current study demonstrates that PTEN-positive staining is a significant prognostic indicator of favorable survival for patients with advanced endometrial cancer who undergo postoperative chemotherapy.
Department of Disaster Obstetrics and Gynecology, Tohoku University Graduate School of Medicine, Sendai, Japan
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unknown. Therefore, we summarize the recent studies regarding the effects and/or actions of androgens in endometrial carcinoma in this review. Serum androgen and increased risk of developing endometrial cancer The great majority of endometrial
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among women rather than men, which suggests that there may be a predominant early effect mediated by reductions in circulating sex steroid hormone levels. Endometrial cancer The WCRF has estimated that 50% of incident endometrial cancer cases in the
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Introduction Endometrial cancer is the most common gynaecological malignancy in the developed world with the majority presenting as abnormal bleeding in post-menopausal women; the incidence of this cancer is increasing in parallel with
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Introduction Endometrial cancer (EC) is the most common gynecological malignancy worldwide, with an estimate of more than 288 000 women developing the cancer annually ( Jemal et al . 2011 ). Of significance, the incidence and mortality rates for EC
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Cancer Society, cancer of the reproductive tract will account for 12% of all female cancers (79 480 of 662 870 estimated cases) and ~15% of female cancer-related mortalities (28 910 of 275 000 estimated cases). Endometrial cancer is the most common
