Prostate Cancer Update 2

Case 4

Tracks 1-8

DR MOUL: Prior to my evaluation of this 60-year-old man, the local physicians had started him on maximal androgen blockade (MAB). They started the bicalutamide 10 days before they started the LHRH to prevent a flare.

I believe this was reasonable in this case. When we saw him, his PSA level had dropped from 85 ng/mL to 9.6 ng/mL. His PSA level reached nadir at 0.9 ng/mL.

The new guidelines on hormonal therapy for advanced prostate cancer were published in the Journal of Clinical Oncology. ASCO now endorses complete hormonal therapy (Loblaw 2007; [1.4]), and I support this.

In the past, ASCO’s belief was that there was insufficient evidence to recommend complete hormonal therapy. Instead, they were suggesting an LHRH agonist alone, with oral antiandrogens simply for the flare.

Now with more data suggesting that bicalutamide is potentially a more potent oral antiandrogen, the new guidelines endorse complete hormonal therapy.

DR LOVE: Does that apply to any situation in which androgen deprivation is being used?

DR MOUL: For most situations in which a clinician would put a patient on traditional hormonal therapy for the first time with an LHRH agonist, they’re suggesting that an oral antiandrogen is beneficial.

DR LOVE: Has that had any impact on what you do? Or were you already using MAB?

DR MOUL: I was already using MAB. We all recognize that it was a controversial concept. The survival benefit associated with MAB traditionally has been modest. Even though I always tended to talk about it and recommend it, this made me feel more confident because I am practicing more in line with what the guidelines suggest.

1.4

By July 2006, this patient’s PSA level was up to 60 ng/mL. He was asymptomatic, but a follow-up bone scan in August of 2006 indicated bone progression in that he had some new lesions. At that point, we talked to him about chemotherapy. In August of 2006, our oncologists initiated docetaxel and prednisone. They were able to administer four cycles between August and October.

He had a nice PSA response — from 95 ng/mL down to 55 ng/mL within the four cycles — but then he developed pneumonia after his fourth cycle, which was probably not related to the chemotherapy, and we had to put the treatment on hold for a while.

In November of 2006, his PSA level crept back up to about 75 ng/mL. The pneumonia cleared and he was able to receive an additional six cycles of docetaxel and prednisone between November of 2006 and January of 2007. I believe that was important.

According to my medical oncology colleagues, the data seem to suggest that if you can administer 10 cycles to a patient, you have a better chance of having an impact on the disease. His PSA level has remained stable, varying from 50 to 60 ng/mL. Bone scans in January and June have continued to show stable disease.

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