IPCC Case-Based Discussion: How Should We Sequence Therapy?

Beth Fand Incollingo @fandincollingo
Published: Tuesday, Jun 12, 2012
A multidisciplinary audience gathered in New York City for the 5th Annual Interdisciplinary Prostate Cancer Congress. The meeting provided an opportunity for medical oncologists, radiation oncologists, and urologists to review the latest strategies and therapeutic agents available for patients with prostate cancer and fostered discussion to build consensus about best treatments.

Three case studies focused on how best to sequence therapy in prostate cancer were presented by Daniel P. Petrylak, MD, and discussed by a panel that included Robert Dreicer, MD, and Oliver Sartor, MD. The audience voted on the treatment options they would have chosen for the patients whose cases were presented.

Case 1

Petrylak: The patient is a 72-year-old man with a PSA score of 80. A biopsy of the prostate reveals Gleason score 10 adenocarcinoma with small-cell components. A bone scan demonstrates extensive metastatic disease, and a CT scan of the abdomen/pelvis demonstrates three hepatic metastases.

Which of the following treatment options would you recommend?
  1. Combined androgen blockade
  2. Combined androgen blockade with carboplatin/etoposide
  3. Carboplatin/etoposide alone
  4. Combined blockade with carboplatin/docetaxel

Case 1. Audience Response*

Case 1: Audience Response

*Totals may not equal 100%

Dreicer: When you see a patient like this, with hepatic metastases and a hint of small-cell pathology, you worry about a mixed lesion because that is more typical biologic behavior. So, clearly, androgen-deprivation therapy (ADT) is appropriate. Every once in a while, a patient will show up with liver metastases from the adenocarcinoma component, so I think it’s reasonable to start with ADT. I’d probably re-image the patient in eight to 10 weeks, assuming he is asymptomatic. Obviously, if there are symptoms, you’ll start systemic therapy.

Sartor: I’m thinking there are probably two components to the tumor. If small-cell is 80% on the biopsy, that pushes me a bit more toward combined androgen blockade with carboplatin/etoposide.

Petrylak: The patient was treated with combined blockade with six cycles of carboplatin and etoposide up front. His PSA normalized, and a CT scan of the adenocarcinoma showed that his liver metastases went away completely. He was maintained on combined blockade. After one year, his PSA rises to 40 and his liver metastases comes back. He also develops symptomatic bone pain.

Your next treatment choice is:

  1. Abiraterone acetate
  2. Carboplatin/etoposide
  3. Carboplatin/docetaxel
  4. Combined blockade with carboplatin and docetaxel
Petrylak: Fifty percent of the audience chose abiraterone acetate, and 39% selected carboplatin and docetaxel.

Sartor: To me, that PSA rise indicates that the androgen axis is still intact. So I feel that bringing an additional way to attack the androgen axis, like the abiraterone, is very reasonable. We don’t have a lot of data in this sort of setting—in fact, we have almost none—and I wouldn’t fault anybody who would go with the carboplatin/ docetaxel.

Dreicer: It still may be that what we’ve seen here is just mostly adenocarcinoma, so if at this juncture he’s symptomatic, I think abiraterone is a very reasonable choice. I probably would again give him four weeks of therapy and see whether or not there’s any clinical response.

Petrylak: The patient was treated with abiraterone/prednisone. On that treatment, his PSA dropped from 120 to 30, but a CT scan shows continued progression of the disease in his liver. Do you think the patient has a small-cell component at this point? Do you think he has an adenocarcinoma?

Your next treatment options are:

  1. Carboplatin/docetaxel
  2. Oral etoposide
  3. Carboplatin/etoposide
  4. Irinotecan-based therapy
Petrylak: Approximately 67% of the audience said they’d treat with carboplatin/docetaxel, 17% said carboplatin/etoposide, 10% said irinotecan, and 7% said oral etoposide.

Sartor: Is there a role for measuring chromogranin A or neuronspecific enolase? Would that help determine whether to do a re-biopsy at that point?

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