Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2012 Nov 9;19(6):R255-79.
doi: 10.1530/ERC-12-0175. Print 2012 Dec.

Hormone response in ovarian cancer: time to reconsider as a clinical target?

Francesmary Modugno  1 , Robin Laskey, Ashlee L Smith, Courtney L Andersen, Paul Haluska, Steffi Oesterreich
Affiliations
Review

Hormone response in ovarian cancer: time to reconsider as a clinical target?

Francesmary Modugno et al. Endocr Relat Cancer. .

Abstract

Ovarian cancer is the sixth most common cancer worldwide among women in developed countries and the most lethal of all gynecologic malignancies. There is a critical need for the introduction of targeted therapies to improve outcome. Epidemiological evidence suggests a critical role for steroid hormones in ovarian tumorigenesis. There is also increasing evidence from in vitro studies that estrogen, progestin, and androgen regulate proliferation and invasion of epithelial ovarian cancer cells. Limited clinical trials have shown modest response rates; however, they have consistently identified a small subset of patients that respond very well to endocrine therapy with few side effects. We propose that it is timely to perform additional well-designed trials that should include biomarkers of response.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Steroid receptors as clinical targets in ovarian cancer. Estimates of % tumors expressing PR, ERα, or AR (without considering subtypes of ovarian cancer due to lack of information). Also listed are approved drugs or drugs used in previous or currently ongoing ovarian cancer trials.
See this image and copyright information in PMC

References

    1. Aabo K, Pedersen AG, Haid I, Dombernowsky P. High-dose medroxyprogesterone acetate (MPA) in advanced chemotherapy-resistant ovarian carcinoma: a phase II study. Cancer Treatment Reports. 1982;66:407–408. - PubMed
    1. Ahlgren JD, Ellison NM, Gottlieb RJ, Laluna F, Lokich JJ, Sinclair PR, Ueno W, Wampler GL, Yeung KY, Alt D, et al. Hormonal palliation of chemoresistant ovarian cancer: three consecutive phase II trials of the Mid-Atlantic Oncology Program. Journal of Clinical Oncology. 1993;11:1957–1968. - PubMed
    1. Akahira J, Suzuki T, Ito K, Kaneko C, Darnel AD, Moriya T, Okamura K, Yaegashi N, Sasano H. Differential expression of progesterone receptor isoforms A and B in the normal ovary, and in benign, borderline, and malignant ovarian tumors. Japanese Journal of Cancer Research. 2002;93:807–815. doi:10.1111/j.1349-7006.2002. tb01323.x. - PMC - PubMed
    1. Albanito L, Madeo A, Lappano R, Vivacqua A, Rago V, Carpino A, Oprea TI, Prossnitz ER, Musti AM, Andò S, et al. G protein-coupled receptor 30 (GPR30) mediates gene expression changes and growth response to 17β-estradiol and selective GPR30 ligand G-1 in ovarian cancer cells. Cancer Research. 2007;67:1859–1866. doi:10.1158/0008-5472.CAN-06-2909. - PubMed
    1. Anderson GL, Judd HL, Kaunitz AM, Barad DH, Beresford SA, Pettinger M, Liu J, McNeeley SG, Lopez AM, Women's Health Initiative Investigators Effects of estrogen plus progestin on gynecologic cancers and associated diagnostic procedures: the Women's Health Initiative randomized trial. Journal of the American Medical Association. 2003;290:1739–1748. doi:10.1001/jama.290.13.1739. - PubMed

Publication types

MeSH terms