Ovarian Cancer

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Questions to Ask Your Doctor about Ovarian Cancer
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Other Ovarian Cancer Therapies

Besides the ovarian cancer therapies that are currently in use—surgery, chemotherapy, radiotherapy—a number of treatment strategies are in development. Hundreds of clinical trials have been performed to evaluate the benefits, safety, and side effects of new techniques such as gene therapy and hormone therapy to treat ovarian cancer. The results of these studies are not yet conclusive.

Gene Therapy
Gene therapy eventually may provide some control over cancer susceptibility and its treatment. Ovarian cancer, like all cancers, is believed to result from a build-up of genetic defects within the cells. Genetic defects may be inherited, or they may be caused by exposures to environmental or other factors that damage the genes (see also What Causes Ovarian Cancer). Genetic engineers hope to correct such damage by transplanting copies of normal genes into cells with genetic defects. In addition, genetic manipulation may enable researchers to alter tumor cells so that they "commit suicide," are targeted by the immune system, or become more sensitive to chemotherapy. Investigators also have spent a lot of time trying to improve the resistance of bone marrow cells to chemotherapeutic agents, so that the doses of such drugs can be intensified.

The practical applications of gene therapy are still being refined. Yet, as more is learned about the genetic makeup of ovarian cancer and its biochemical pathways, the closer researchers come to developing workable methods of genetic therapy.

Hormone Therapy
Over the past few decades, there have been many reports of the potential benefits of hormone treatments in patients with ovarian cancer that does not respond to conventional therapy. For example, individuals with treatment-resistant (refractory) epithelial cancers have been treated with:

• progestins—crude forms of the female sex hormone progesterone; e.g., oral Provera® (medroxyprogesterone acetate, MPA), intramuscular Depo-Provera® (medroxyprogesterone acetate suspension), Megace® (megestrol acetate);
• estrogens—for example, diethylstilbestrol (DES);
• combination estrogen/progestin therapy;
• antiestrogens—for example, Nolvadex® (tamoxifen);
• androgens—male sex hormones for example, Halotestin® (fluoxymesterone); and
• gonadotropin-releasing hormone (GnRH)—a hormone of the hypothalamus that stimulates the release of ovary-related hormones from the pituitary gland.

Unfortunately, the responses to such therapies have been variable and not particularly effective in the management of this disease. Nevertheless, some researchers believe that hormone therapy with progestins eventually may play a role in the management of patients with sex cord-stromal tumors.

Experts guess that the patients most likely to respond to antiestrogen therapy (tamoxifen) are those who are estrogen receptor positive—that is, individuals who have receptors (molecules on/within a cell that recognize and bind with certain substances) for the female sex hormone estrogen (ER positive). Estrogen receptor-positive tumors may be biologically less malignant than receptor-negative tumors.

In addition, recent findings suggest that hormone replacement therapy (HRT) is not harmful to women who have been treated for epithelial ovarian cancer. But HRT therapy is controversial, since some physicians believe that the use of estrogen might increase the likelihood of cancer recurrence, for example in women with well-differentiated endometrioid carcinomas that may be hormone-sensitive.

As yet, there is no conclusive evidence that estrogen use in such patients is risky–or that it is safe.

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