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Identifying and Managing Nonmetastatic Prostate Cancer

Insights From: Evan Yu, MD, University of Washington; Ulka Vaishampayan, MD, Barbara Ann Karmanos Cancer Institute ; Neeraj Agarwal, MD, Huntsman Cancer Institute
Published: Wednesday, Nov 28, 2018



Transcript:

Evan Yu, MD:
When you’re making a diagnosis of metastatic prostate cancer, that’s really a key event in the life of any patient. If you really think about it, there are 2 key events for someone with prostate cancer. One is when they first are diagnosed with metastatic disease on scans, and another is when they develop castration resistance. That means their testosterone level is low and their PSA [prostate-specific antigen] is rising. But the first event that I mentioned, the diagnosis of metastatic disease on scans, actually points towards the standard imaging that we use, which is with CT [computed tomography] scans and bone scans. If you look at clinical trials with the new therapeutic agents that are out there, that’s what they use: CT scans and bone scans. Certainly, there are newer imaging modalities out there—fluciclovine, PET [positron emission tomography]/CT, the PMSA [prostrate-specific membrane antigen] PET/CT—but those, at this point in time, are not utilized for diagnosis of metastatic disease in clinical trials.

The clinical trials that led to the approval of enzalutamide and apalutamide in the M0 castration resistant prostate cancer setting, or the nonmetastatic castration resistant prostate cancer setting, accrued a specific subset of high-risk patients for the development of metastatic disease. Those patients had a PSA doubling time of less than 10 months prior to enrollment in the trial, and they used standard CT scans and bone scans for imaging the metastatic disease.

The patients who I would consider eligible for use of enzalutamide or apalutamide would be patients who fit those criteria. Basically, you image them with standard imaging to ensure there is no metastatic disease identified on those imaging studies, and they must have those short PSA doubling times. Keep in mind the fact that 75% of the patients in those studies actually had a PSA doubling time of less than 6 months, which really portends an even worse prognosis.

Ulka Vaishampayan, MD: Nonmetastatic prostate cancer therapy is relatively new in the arena of prostate cancer treatment in general. The treatments that are currently FDA approved are 2 different medications. One is called apalutamide and the other is called enzalutamide. Both of these are antigen-receptor access targeted agents that have shown efficacy in terms of delaying metastatic-free survival in nonmetastatic prostate cancer. Both of these are indicated in patients with rapidly progressing disease, which is typically defined by the PSA doubling time.

The clear rationale for using these after ADT [androgen deprivation therapy] is that there are data to suggest that in prostate cancer, as it evolves and becomes castrate resistant, there is typically an increase in the tumor microenvironment testosterone levels. Inhibiting those becomes a priority in treatment. The other mechanism is that there is an increased density of androgen receptor, and because of that it is also important to try and block androgen receptor access in nonmetastatic castrate resistant disease.

Transcript Edited for Clarity 
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Transcript:

Evan Yu, MD:
When you’re making a diagnosis of metastatic prostate cancer, that’s really a key event in the life of any patient. If you really think about it, there are 2 key events for someone with prostate cancer. One is when they first are diagnosed with metastatic disease on scans, and another is when they develop castration resistance. That means their testosterone level is low and their PSA [prostate-specific antigen] is rising. But the first event that I mentioned, the diagnosis of metastatic disease on scans, actually points towards the standard imaging that we use, which is with CT [computed tomography] scans and bone scans. If you look at clinical trials with the new therapeutic agents that are out there, that’s what they use: CT scans and bone scans. Certainly, there are newer imaging modalities out there—fluciclovine, PET [positron emission tomography]/CT, the PMSA [prostrate-specific membrane antigen] PET/CT—but those, at this point in time, are not utilized for diagnosis of metastatic disease in clinical trials.

The clinical trials that led to the approval of enzalutamide and apalutamide in the M0 castration resistant prostate cancer setting, or the nonmetastatic castration resistant prostate cancer setting, accrued a specific subset of high-risk patients for the development of metastatic disease. Those patients had a PSA doubling time of less than 10 months prior to enrollment in the trial, and they used standard CT scans and bone scans for imaging the metastatic disease.

The patients who I would consider eligible for use of enzalutamide or apalutamide would be patients who fit those criteria. Basically, you image them with standard imaging to ensure there is no metastatic disease identified on those imaging studies, and they must have those short PSA doubling times. Keep in mind the fact that 75% of the patients in those studies actually had a PSA doubling time of less than 6 months, which really portends an even worse prognosis.

Ulka Vaishampayan, MD: Nonmetastatic prostate cancer therapy is relatively new in the arena of prostate cancer treatment in general. The treatments that are currently FDA approved are 2 different medications. One is called apalutamide and the other is called enzalutamide. Both of these are antigen-receptor access targeted agents that have shown efficacy in terms of delaying metastatic-free survival in nonmetastatic prostate cancer. Both of these are indicated in patients with rapidly progressing disease, which is typically defined by the PSA doubling time.

The clear rationale for using these after ADT [androgen deprivation therapy] is that there are data to suggest that in prostate cancer, as it evolves and becomes castrate resistant, there is typically an increase in the tumor microenvironment testosterone levels. Inhibiting those becomes a priority in treatment. The other mechanism is that there is an increased density of androgen receptor, and because of that it is also important to try and block androgen receptor access in nonmetastatic castrate resistant disease.

Transcript Edited for Clarity 
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