Estrogen action in human ovarian cancer.

(PMID:9134308)

Abstract
Citations BioEntities Related Articles Clinton GM, Hua W Department of Biochemistry and Molecular Biology, Oregon Health Sciences University, Portland 97201-3098, USA. Critical Reviews in Oncology/hematology [1997, 25(1):1-9]

Type: Journal Article, Review

DOI: 10.1016/S1040-8428(96)00216-8 Abstract

Highlight Terms

Gene Ontology(1) Diseases(4) Genes/Proteins(1) Species(1) Chemicals(2) Evidence is accumulating for a facilitative role for estrogen in ovarian cancer. Although response to antiestrogen therapy has been poor, there is a distinct subset of patients that respond. Strategies for treatment of ovarian cancer would be improved by identification of patients likely to respond to hormonal therapy. Cell culture models that are responsive or resistant to estrogen and antiestrogen may be of value in finding markers that predict responsiveness to hormonal therapy. Several model cell lines have been generated that express ER and proliferate in response to estrogen in vitro. Further studies are needed to better characterize the response of these ER positive cells lines to estrogen in vivo in mouse xenograft models. Expression of many of the same genes are regulated by estrogen in breast and in ovarian cancer cell lines. One exception may be the HER-2/neu oncogene product, which is down-regulated by estrogen in responsive breast carcinoma cells but not in two ovarian carcinoma cell lines. Initial analyses of several estrogen responsive and one resistant cell model

suggests the potential value of progesterone receptor presence and low levels of HER-2/neu expression for predicting responsiveness to hormonal therapy. Additional cell models need to be investigated to determine the frequency with which these markers are associated with antiestrogen resistance.

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Estrogens and epithelial ovarian cancer.

(PMID:15262115) Abstract Citations BioEntities Related Articles Cunat S, Hoffmann P, Pujol P Laboratoire de Biologie Cellulaire, Centre Hospitalier Universitaire de Montpellier, Hpital Arnaud de Villeneuve, Montpellier Cedex 5, France. Gynecologic Oncology [2004, 94(1):25-32]

Type: Journal Article, Review, Research Support, Non-U.S. Gov't

DOI: 10.1016/j.ygyno.2004.03.026 Abstract No biological terms identified

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OBJECTIVE: Molecular mechanisms involved in ovarian carcinogenesis are still unclear, but
there is growing evidence that estrogens promote tumor progression in an epithelial ovarian cancer (EOC) subgroup.

METHODS: We reviewed current knowledge on the effects of estrogens in ovarian

carcinogenesis and new potential research focuses concerning hormonal therapy of EOC.

RESULTS: Experimentally, estrogen stimulates the growth of ovarian tumor cell lines
expressing estrogen receptors (ER). We and other authors have demonstrated differential expression of ERalpha or beta during ovarian carcinogenesis, with overexpression of ERalpha as compared to ERbeta in cancer. This differential expression in ER suggests that estrogen-induced proteins may act as ovarian tumor-promoting agents. Among these proteins, c-myc, fibulin-1, cathepsin-D, or several kallikreins may play a role, since high expression levels have been found in EOC. Consistently, recent prospective epidemiological studies have indicated that estrogen replacement therapy in postmenopausal women may increase ovarian cancer incidence and mortality.

CONCLUSION: Questions on the estrogen-sensitivity and potential benefits of new

hormone therapies in an EOC subgroup should be readdressed in the light of recent experimental and clinical data.

Read Article at ScienceDirect (Subscription required) Article at ScienceDirect (Subscription requPolycystic Ovarian Syndrome

Definition

Polycystic ovary disease is a condition in which there are many small cysts in the ovaries, which can affect a woman's ability to get pregnant.

Alternative Names

Polycystic ovaries; Polycystic ovarian syndrome (PCOS); Stein-Leventhal syndrome; Polyfollicular ovarian disease

Causes, incidence, and risk factors

Polycystic ovary disease affects hormone cycles. Hormones help regulate the normal development of eggs in the ovaries. It is not completely understood why or how hormone cycles are interrupted, although there are several ideas.

Follicles are sacs within the ovaries that contain eggs. In polycystic ovary disease, there are many poorly developed follicles in the ovaries. The eggs in these follicles do not mature and, therefore, cannot be released from the ovaries. Instead, they form cysts in the ovary.

This can contribute to infertility. The immature follicles and the inability to release an egg (ovulate) are likely caused by low levels of follicle stimulating hormone (FSH), and higher than normal levels of male hormones (androgens) produced in the ovary.

Women are usually diagnosed when in their 20s or 30s. Women with this disorder often have a mother or sister who has symptoms similar to polycystic ovary disease.

Symptoms

If you have polycystic ovary disease, you are likely to have some of the following symptoms: Abnormal, irregular, or very light or infrequent menstrual periods Absent periods, usually (but not always) after having one or more normal menstrual periods during puberty (secondary amenorrhea) Acne that gets worse Decreased breast size Development of male sex characteristics (virilization), such as increased body hair, facial hair, a deepening of the voice, male-pattern baldness, and enlargement of the clitoris Diabetes

Increased hair growth; body hair may be in a male pattern Infertility Poor response to the hormone, insulin (insulin resistance), leading to a build-up of insulin in the blood Weigh

The pattern of estradiol and progesterone differs in serum and tissue of benign and malignant ovarian tumors.
Lindgren PR, Bckstrm T, Cajander S, Damber MG, Mhlck CG, Zhu D, Olofsson JI. Source

Department of Clinical Sciences/Obstetrics and Gynecology, Umea University Hospital, S-901 85 Umea, Sweden. peter.lindgren@obgyn.umu.se

Abstract

Epidemiological studies have indicated a relationship between gonadal steroid hormones and ovarian cancer. A production of both estradiol and progesterone by ovarian cancers has been demonstrated. The local steroid concentrations and the putative relation to histopathological and clinical condition were investigated herein. Ovarian tissue, ovarian tumor cyst fluid, ovarian vein samples and peripheral serum concentrations of estradiol and progesterone in pre- and post-menopausal women, subdivided into groups with normal ovaries, benign, borderline and malignant ovarian tumors, were quantitatively assessed. Both ovarian tissue concentrations of estradiol and progesterone were more than 100-fold higher than in serum. Based on differences in concentrations between different ovarian tumor groups, the data is not coherent with the previously suggested increased production of estradiol and progesterone in ovarian cancer tissue, since post-menopausal women with ovarian cancer presented lower median tissue hormone levels, most pronounced between malignant and benign tumors; median (25 and 75 percentile) estradiol; 9.40 (6.67-15.50) vs 16.44 (12.49-23.20), p=0.02 and progesterone; 308 (240-575) vs 957 (553-1143) pmol/g wet weight, p<0.01, n=81. Lower concentrations of estradiol, but not progesterone, were found in ovarian cancer tissue, ovarian cyst fluid and peripheral serum in patients with FIGO stages 3 and 4 than in stages 1 and 2. The novel finding of a large ovarian tissue to serum difference of both estradiol and progesterone indicates an

important role of ovarian tissue concentrations in tumor biology and raises the question of adequate doses of anti-hormonal therapy in women with ovarian cancer. PMID: 12168103 [PubMed - indexed for MEDLINE]t gain, or obesityired)