Hormonal Therapy for Breast C... Video Transcript

Participants

, Cathy Conley , Paul Goss MD, PhD, F, Stephen E. Jones MD

Summary

Hormonal therapy has progressed steadily since it was introduced as treatment for breast cancer, and this year was no exception. At the 24th Annual San Antonio Breast Cancer Symposium, researchers presented information on the newest hormonal agents, and discussed new uses for existing drugs. Tune in to learn about the latest advances from top experts at the conference.

Webcast Transcript

CATHY CONLEY: Leading cancer specialists from around the world have gathered here at the San Antonio Breast Cancer Symposium to talk about the newest developments in breast cancer treatment. Today, I had an opportunity to talk to those experts about the exciting advances in hormonal therapy.

Set the stage for us, if you will. What has traditionally been the role of hormonal therapy in breast cancer?

PAUL E. GOSS, MD: Breast cancer doctors have understood that breast cancer is under female hormone control, particularly estrogen. Originated from the ovary in premenopausal women, and from skin, muscle and fat in postmenopausal women. And the body of evidence today is that estrogen causes breast cancer, promotes breast cancer growth.

STEPHEN E. JONES, MDThere's two areas. One is for patients who have recurrent breast cancer. And that was the original treatment for patients with recurrent breast cancer, which really dates back almost 100 years. I think what's interesting in current times is we have a lot better drugs that are more specific targeted types of hormonal treatment. And then the other setting is in prevention of early breast cancer, prevention of recurrence.

CATHY CONLEY: And what about hormonal treatments? What is standard practice today?

STEPHEN E. JONES, MD: If you're talking about recurrent breast cancer, there are a lot of different treatment options in the hormonal area. Including things like removing ovaries, which remove source of estrogen. A drug called "tamoxifen," which has been the gold standard for a long time. And a whole group of new drugs that really look, in some ways, like they might be better than tamoxifen.

As far as preventing recurrence for early breast cancer, the gold standard for 25 years has been a drug called "tamoxifen."

CATHY CONLEY: Anti-aromatase agents have been getting a lot of attention in the past and at these meetings. Can you explain what these drugs do, and how they're beneficial in breast cancer?

PAUL E. GOSS, MD: Aromatase enzyme is sitting there between androgens and estrogen. If you block the enzyme or you antagonize it with the so-called anti-aromatase drugs, they targeted at this enzyme and they shut off estrogen production.

We can divide anti-aromatase agents into aromatase inhibitors and aromatase inactivators. It's a bit technical, but it turns out to be important. What happens is the so-called "nonsteroidal" class of these drugs -- letrozole and anastrozole, or otherwise known as Femara and Arimidex --these two drugs, they inhibit the enzyme, they're competitive inhibitors.

So what they do is they compete with androgen for the enzyme site, and so they -- instead of the enzyme converting the androgen, they come into the way, they

push into the line. They occupy the line, and they can't be converted. So they inhibit the conversion of the natural androgens into the estrogen.

The anti-aromatase agent, Aromasin -- which is a aromatase inactivator -- is what we call a suicide substrate. It comes into the binding site and, instead of just competing with other members in the line to get through this gate, it actually just blows up the gate. It destroys the gate. So the enzyme site is destroyed and inactivated. And the body has to remake the enzyme site.

CATHY CONLEY: Dr. Jones, how do these drugs differ from tamoxifen and from each other?

STEPHEN E. JONES, MD: Well, tamoxifen is in a class of drugs called an "antiestrogen." It really binds to hormone receptor cells within breast cancer cells and stops the cells from dividing. These new class of drugs really shut down estrogen production in the body.