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Merel Nissenberg On Non-Metastatic Castrate-Resistant Prostate Cancer

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Non-metastatic castrate-resistant prostate cancer (nmCRPC) is a clinical state in which a patient on androgen-deprivation therapy (ADT) has a rising PSA but there are no radiological findings of metastases on CT or bone scan. Management of nmCRPC is evolving quickly, but it is a field in which there have been recent drug approvals amid a strong and growing interest in keeping patients metastasis-free for as long as possible. About 10-20% of prostate cancer cases are castrate-resistant, but nearly 16% of those castrate-resistant patients have no evidence of metastatic disease at the time their castrate-resistance is diagnosed.

Not all nmCRPC disease is the same. For some patients, observation is a viable option; for other patients—especially those with a PSA doubling time of less than or equal to 10 months—randomized Phase III clinical trials have shown a benefit and an increase in metastasis-free survival with the use of Xtandi (enzalutamide) or Erleada (apalutamide). New imaging techniques on the horizon may also be very helpful in assessing nmCRPC patients.

In February 2018, the FDA approved Erleada (apalutamide) for nmCRPC patients and was the first such FDA-approved treatment for this subset of patients—i.e. those who are no longer responding to ADT but who have no radiological evidence of metastasis. The Erleada (apalutamide) approval followed the release of the results of SPARTAN, a randomized clinical trial of 1,207 patients in which patients received either Erleada (apalutamide) or placebo, discussed at the American Society of Clinical Oncology Genitourinary (ASCO GU) Meeting in February of this year. All of the patients who were enrolled also received hormone therapy. The exciting results showed that the median metastasis-free survival for patients in the Erleada (apalutamide) arm was 40.5 months versus 16.2 months for the placebo group. Both applications received priority review from the FDA due to the exciting results with clear benefit for nmCRPC patients.

The results of another trial known as the PROSPER Trial were also first presented at the 2018 ASCO GU Meeting. In PROSPER, with 1,401 participants, men with nonmetastatic castrate-resistant prostate cancer (nmCRPC) were given either Xtandi (enzalutamide) or placebo; these were men in whom the PSA doubling time was 10 months or less, but, again, there was no evidence of disease seen by CT or bone scan or by MRI. Those nmCRPC patients receiving Xtandi (enzalutamide) had delayed time to metastatic disease or death (whichever occurred first) by a median of 21.9 months, versus placebo (36.6 months compared to 14.7 months), signifying a 71% reduction of the risk for metastasis or death. Another result: Xtandi (enzalutamide) delayed the time until men needed additional cancer treatment, compared to placebo (a median of 39.6 months compared to 17.7 months). On July 13, 2018 the FDA approved Xtandi (enzalutamide) for the treatment of nmCRPC patients.

This means that men with nonmetastatic castrate-resistant prostate cancer now have two choices that they did not have before, when they would simply be continued on ADT. We still do not know, however, if the added Xtandi (enzalutamide) or Erleada (apalutamide) will increase overall survival for these patients.

[This article deals only with nonmetastatic CRPC. There have also been various trials conducted in the metastatic space, and there are other trials currently underway or planned involving anti-androgens such as Zytiga (abiraterone), including some in combinations with other types of therapy, dealing with metastatic disease (mCRPC patients). One of the trials looking at the metastatic disease space is the PEACE1 Trial, which is looking at the benefit of Taxotere (docetaxel) plus ADT, with or without Zytiga (abiraterone) and prednisone, and with or without radiotherapy. This trial is expected to conclude in October 2018 and may help answer the question of whether it is of benefit to patients to add Zytiga (abiraterone acetate) to Taxotere (docetaxel) in metastatic disease that is still castrate-sensitive. The Phase III STAMPEDE Trial showed that adding Zytiga (abiraterone/ prednisone) to standard ADT lowered the relative risk of death by 37% and improved progression-free survival by 71%, versus ADT alone. The CHAARTED Trial looked at Taxotere (docetaxel) plus ADT or ADT alone in patients with metastatic, castrate-sensitive disease, resulting in a greater median survival in the ADT + Taxotere (docetaxel) arm (57.6 months versus 44.0 months with ADT alone).]

Learn more details about these drugs by viewing the Evidence Report from Institute for Clinical and Economic Review (ICER). ICER also held a public hearing on the topic on September 13, 2018 in Chicago.

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Switching from One Chemo Drug to Another

Dr. Emmanuel Antonarakis is an Associate Professor of Oncology and Urology at the Johns Hopkins University Sidney Kimmel Comprehensive Cancer Center.

Prostatepedia spoke with him recently about his work on the benefit of switching men from Taxotere (docetaxel) to Jevtana (cabazitaxel)— or vice versa—if his PSA doesn’t go down by 30% in the first twelve weeks of treatment.

You’ve published a paper on switching patients from Taxotere (docetaxel) to Jevtana (cabazitaxel) and vice versa. What is the thinking behind switching chemotherapeutic agents? Why would you want to switch agents earlier as opposed to when the first chemotherapy drug stops working?

Dr. Emmanuel Antonarakis: The motivation behind this paper was that the FDA-approved recommended dosing schedule for both Taxotere (docetaxel) and Jevtana (cabazitaxel) is a course of ten doses, given three weeks apart. When patients begin FDA-approved Taxotere (docetaxel) or FDA approved Jevtana (cabazitaxel), they’re often told by their oncologists that they should expect to receive this chemotherapy once every three weeks for up to ten doses. A patient may not receive ten doses or might stop the therapy before he reaches ten doses because he cannot tolerate the therapy and has unmanageable side effects, or his cancer begins to progress before he ever get to dose number ten. If his PSA begins to increase again at dose six or seven or the tumors begin to grow again, his oncologist might ask him to stop chemotherapy.

We then wondered whether the ten doses was a reasonable time to wait or whether there could be an early indicator, or an early sign, of therapy resistance or therapy futility without having to go through six, seven, eight, nine or ten doses.

The idea that we had was to test an early intermediate marker of sensitivity or resistance to the chemotherapy. The best marker of early sensitivity or resistance that we could think of was whether or not a patient had a 30% PSA drop within the first four cycles of therapy. As you recall, if the therapy is given once every three weeks, four cycles basically means 12 weeks, which roughly equates to about three months.

The decision to use this intermediate endpoint was not arbitrary; it was based on some large retrospective meta-analyses that have shown that the strongest predictor of overall survival in patients receiving both Taxotere (docetaxel) and also separately Jevtana (cabazitaxel) was whether or not patients had a 30% PSA reduction after 12 weeks.

Patients who do achieve at least a 30% or greater reduction in the first 12 weeks have a survival that’s longer than patients who don’t achieve that endpoint. We thought, well if this endpoint is strongly correlated to survival, perhaps we can use it as a decision point. If after four doses of therapy or 12 weeks of therapy a patient don’t achieve a 30% reduction in PSA perhaps we should switch him to the other chemotherapy, rather than sticking with it and just waiting for either the toxicity to develop or the PSA or the radiographic disease to progress. That was the hypothesis.

We designed a relatively small study of about 63 patients. We used a 2:1 randomization so they were twice as likely to get Taxotere (docetaxel) compared to Jevtana (cabazitaxel). Approximately 41 patients got Taxotere (docetaxel) first. The other 22 patients, got Jevtana (cabazitaxel) first. Irrespective of which arm they were randomized to, they received the first four doses of chemotherapy in 12 weeks. We checked their PSA every three weeks.

At the end of the fourth dose, if the PSA level had dropped by 30% or more, the patients would continue on the same therapy on which they started. However, if patients did not achieve a 30% reduction or more, they would be switched to the other chemotherapeutic agent.

If a patient had a 25% reduction, we would switch him to the other agent because we thought that was not good enough. If someone received Taxotere (docetaxel), and their PSA dropped by 25%, even though it dropped by 25%, it did not meet that 30% threshold so they would then switch for the fifth dose to receive Jevtana (cabazitaxel) for the remainder of their chemotherapy. The inverse was also true. If the patient received Jevtana (cabazitaxel) first and also did not get a 30% reduction by week 12, in other words four doses, they would also switch to receive Taxotere (docetaxel). The interesting thing that we found in both treatment arms was that the chance that a patient had a favorable PSA response, which was defined as a 50% or more decrease, was higher than we had seen in historical trials using each drug by itself without switching. To put some numbers on that, we found that there was about a 54% chance that patients would have a 50% reduction in PSA if they had to the opportunity to switch from one chemotherapy to the other, compared to about a 45% chance of PSA reduction in the historical data where patients did not switch.

Did it matter if they got Jevtana (cabazitaxel) first or Taxotere (docetaxel) first?

Dr. Antonarakis: What we found out is a bit of a paradox: people could benefit from the switch in both down over time and the availability of non-chemotherapy agents is going up. A lot of these patients who may not have a 30% PSA reduction with one chemotherapy, might choose to do another hormone therapy, a radiopharmaceutical drug like Xofigo (radium-223), immunotherapy like Provenge (sipuleucel-T), or even a PD-1 inhibitor, or potentially a PARP inhibitor.

It might be difficult to convince a patient who has just failed one chemotherapy after four doses to go immediately to a second chemotherapy. I’m not 100% sure what the future will hold. I also don’t think this is a trial that we could have conducted today.

What would you say to a man reading it? That this is worth talking to his oncologist about or is this just something interesting for him to know about?

Dr. Antonarakis: Patients who are beginning their first chemotherapy should discuss this trial with their oncologist, and together with the oncologist decide in a joint fashion whether switching from one chemotherapy agent to another after four doses might be right for him, especially if he’s tolerating the chemotherapy well. If he tolerates the drug and his PSA has not dropped by 30% or is continuing to increase, then in my opinion rather than continue with the potentially futile therapy, a patient and his oncologist may wish to consider using this trial to guide or justify their choice of switching drugs earlier rather than later. directions. That was fascinating to us because, as we all know

Jevtana (cabazitaxel) was specifically approved by the FDA as a second-line curative therapy only indicated in men who have failed Taxotere (docetaxel) first. Based on that reasoning, one might expect Jevtana (cabazitaxel) to work better after Taxotere (docetaxel) but not Taxotere (docetaxel) after Jevtana (cabazitaxel).

This is not what we found.

We found that in both directions, both from the Taxotere (docetaxel) to Jevtana (cabazitaxel) switch, but also in the Jevtana (cabazitaxel) to Taxotere (docetaxel) switch, there was a significant amount of patients, approximately half, who were salvaged by the crossover therapy. By salvaged, I mean those who did not achieve a 30% PSA reduction with the first drug but did achieve a PSA reduction of 50% or more after crossing over to the second drug.

As I mentioned before, this occurred in both directions, both in patients receiving Jevtana (cabazitaxel) after Taxotere (docetaxel) and Taxotere (docetaxel) after Jevtana (cabazitaxel).

Are the side effects of Jevtana (cabazitaxel) a little bit easier to take than the side effects of Taxotere (docetaxel)?

Dr. Antonarakis: Interestingly, the side effects of Jevtana (cabazitaxel) in the published literature indeed appear to be slightly better. In this particular trial, which was very small obviously, they seemed comparable. In other words, we did not see any appreciable difference between the Taxotere (docetaxel) and the Jevtana (cabazitaxel) overall in terms of side effects. Taxotere (docetaxel) had a little bit more neuropathy nerve damage, which Jevtana (cabazitaxel) did not do. On the other hand, Jevtana (cabazitaxel) had a little bit more neutropenia, while the Taxotere (docetaxel) did not.

I would say that when patients receive these agents in a first-line setting, in other words, when they had not received another chemotherapy previously, their side effects were fairly comparable. I don’t think there was a clear signal in terms of one drug being clearly safer than the other.

Does it matter which you get first?

Dr. Antonarakis: From a side effect perspective, they’re both fairly equivalent in terms of tolerability, with slight differences in neutropenia, which is worse with Jevtana (cabazitaxel) and neuropathy, which is worse with Taxotere (docetaxel).

What is the next step? Are you going to run a similar trial with more patients?

Dr. Antonarakis: One question that arises is if this small randomized trial is enough to change practice. Should a community oncologist or urologist give Taxotere (docetaxel) for four doses and wait to see if the patient’s PSA drops by 30% or more? If it doesn’t drop to 30% or more, should he to switch to Jevtana (cabazitaxel)?

I have to admit that this is something that I have done in my practice a few times, but I really don’t believe that this is ready for clinical practice yet. Yes, in this trial, we showed that the PSA response rates could potentially be improved by this switch strategy. What we did not demonstrate was whether this improves overall survival.

The ultimate question is does switching chemotherapy agents after four doses improve survival, compared to just waiting until we see radiographic or clinical progression to switch agents. That would, as you mentioned, require a larger Phase III randomized study. The idea of study design would be to randomize patients to the switch strategy versus no-switch. We would randomize one group of patients to receive chemotherapy and switch if their PSA did not drop by 30%. The second group of patients would start chemotherapy but would not be given the opportunity to switch, even if their PSA did not drop by 30% or more. The randomization would not necessarily be the randomization to the chemotherapy, but would be randomization to a switch strategy versus a stick-with the first-chemotherapy strategy.

Sanofi, which makes both Jevtana (cabazitaxel) and Taxotere (docetaxel), have not been eager eager to respond to such a study because of financial considerations and also because the patent life of Taxotere (docetaxel) is over and the patent life of Jevtana (cabazitaxel) will be expiring soon.

Unfortunately, we might be left with a Phase II study that may, potentially, not translate into a Phase III study. I think individual patients and individual oncologists may look at these data and might be convinced that some patients might potentially benefit from a switch strategy, especially those who did not have any degree of PSA reduction after four cycles.

An added complexity is that the popularity of chemotherapy is going down over time and the availability of non-chemotherapy agents is going up. A lot of these patients who may not have a 30% PSA reduction with one chemotherapy, might choose to do another hormone therapy, a radiopharmaceutical drug like Xofigo (radium-223), immunotherapy like Provenge (sipuleucel-T), or even a PD-1 inhibitor, or potentially a PARP inhibitor.

It might be difficult to convince a patient who has just failed one chemotherapy after four doses to go immediately to a second chemotherapy. I’m not 100% sure what the future will hold. I also don’t think this is a trial that we could have conducted today.

What would you say to a man reading it? That this is worth talking to his oncologist about or is this just something interesting for him to know about?

Dr. Antonarakis: Patients who are beginning their first chemotherapy should discuss this trial with their oncologist, and together with the oncologist decide in a joint fashion whether switching from one chemotherapy agent to another after four doses might be right for him, especially if he’s tolerating the chemotherapy well. If he tolerates the drug and his PSA has not dropped by 30% or is continuing to increase, then in my opinion rather than continue with the potentially futile therapy, a patient and his oncologist may wish to consider using this trial to guide or justify their choice of switching drugs earlier rather than later.

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Radiation Therapy + The Abscopal Effect

Dr. Charles G. Drake of New York Presbyterian/Columbia University Medical Center, discusses the rare but intriguing abscopal effect.

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Dr. Charles Drake says: There was an article in the New England Journal of Medicine showing an abscopal response with Yervoy (ipilimumab) anti-CTLA-4 in a patient with melanoma. It was a beautifully done paper with nice immunological correlates. After that got published, we found that radiation oncologists and medical oncologists were giving people a combination of immunotherapy and radiation and were telling patients they would get abscopal responses. But that’s a bit overly ambitious. In the clinic, it’s not that easy. It’s going to be a while before we understand what’s needed therapeutically to be able to induce abscopal responses in the majority of patients. It’s going to take a little more work before we can have that happen broadly. On the other hand, if we can make it work, it’ll be fantastic. Dr. Hammers’ trial combining anti- PD-1, anti-CTLA-4, and radiation in kidney cancer is perhaps a more clever approach. That may be what we need to do.

In other words, abscopal responses do happen, but we don’t exactly know why or how and can’t reproduce it?

Dr. Drake: Exactly. And it doesn’t happen nearly as often as we’d like.

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Prostate Cancer Clinical Trials

Dr. Charles Myers frames our May conversations about prostate cancer clinical trials:

Over the past ten years, the management of prostate cancer has been revolutionized by the appearance of new drugs and new concepts using established drugs as well as surgery and radiation. Every one of these advances only exists because of clinical trials. This is the only path forward. This month, we discuss many of the issues patients face when they consider entering a clinical trial.

The fact that most large clinical trials include a randomization to a control arm is often a major source of patient concern, especially if the control arm uses a placebo. When the control arm involves an active treatment, that treatment will typically represent current state-of-art care that you might receive if you do not enter a clinical trial. However, the cost to you will be less because the clinical trial sponsor will commonly cover the cost of care. The financial benefit to you could easily reach thousands of dollars.

What if the trial includes a placebo arm? First, the existence of a placebo arm commonly indicates that no existing treatment has proven to be of benefit. As a patient, you should do your due diligence on this point. Second, there are strict rules in place to protect patients on the placebo arm. You should know these rules and make sure you are comfortable with them.

Patients on a trial’s placebo arm commonly do better than similar untreated patients not on a clinical trial. There is actually a large literature on why the Placebo Effect exists.

One explanation offered is that patients on the placebo typically get better standard care, and I think this is a major factor. It may also be that patients on placebo do better for psychological reasons or a mind-body effect. The latter might be particularly relevant for the treatment of nausea, pain, anxiety, or depression.

Finally, many patients enter clinical trials for altruistic reasons. By entering a well-designed clinical trial, you will help answer questions that will benefit future patients. The progress we have made over the past decade only happened because patients who came before you chose to enter clinical trials.

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Patients Speak: I Had Genomic Testing

Steve S. talks to Prostatepedia about how genomic testing gave him confidence that active surveillance was a safe choice for him.

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How did you find out that you had prostate cancer?

Steve: I don’t remember exactly, but I think I went to the urologist on the recommendation of a doctor who said I should have some PSA tests. I went to the urologist. The urologist ran some PSA tests and said, “They’re a little elevated. Maybe we need to run a biopsy,” which they did. That was about ten years ago. The biopsy came back with three or four cores indicating cancer with a Gleason score of 6 (3+3), which has remained the same over the last ten years. I think that’s what happened.

What kinds of genomic tests did you have and when?

Steve: That happened about five years later. I went to a support group and I heard about genomic testing. My doctor at the time hadn’t mentioned anything about genomic testing to me. I said to him that I didn’t see any downside in having genomic testing. Why couldn’t I have it? He said that he didn’t think it would be covered by my insurance and it’s not something they had done. I felt like a little bit of a pioneer.

I actually got on the phone with the people at Genomic Health in California and asked how much the test would cost. They mentioned a figure of about $500. I asked, “So that’s what I’m going to be charged?” They said, “Probably.” They weren’t really clear about it. In the end I was never charged.

They sent three results to my physician after a few weeks. Because my physician had never given them instructions as to what risk category he felt that I was in, they sent back three results based on different risk profiles. To this moment, I still don’t know exactly which risk profile I fit into.

All three results looked somewhat encouraging to my layperson’s eyes. I discussed the results with the doctor at the time and he said, “I think this confirms what we’re doing at the moment is right. You can continue on active surveillance, but of course it’s your choice.” They will always say that….

The results definitely changed your treatment path?

Steve: I was already on active surveillance, although in the first two or three years, I was thinking about some form of radiation therapy.

We talked about seeds. We talked about beams. I even talked to a friend a few years older than me who had gone through proton beam therapy and he was very encouraged by his results. My insurance at the time did not cover that, so proton beam therapy came off the table. I was not thinking about surgery. I was turned off by the idea of surgery, even though they had a DaVinci robot.

Then I got the OncoTypeDX test. I looked at the results with my physician and decided to proceed. It confirmed what I was already inclined towards.

Do you feel like it gave you more confidence in your decision?

Steve: Yes. I think so. I think that’s fair to say.

Would you recommend that other men take these tests?

Steve: Everybody has a very different psychological makeup. For example, I’ve got a brother-in-law who doesn’t have prostate cancer, but is very educated on medical matters. He’s a smart guy, and so I talked to him about it. He said, “God, if it was me, I would take care of it right away. I’d have that prostate out of there and have peace of mind.” I responded with: “I’ve lost very little sleep over the years about it.” That’s just my makeup. It doesn’t bother me. I’ve got other things to think about, other things I care about. Health is very, very important.

I’m not a complete passenger in this process. That’s why it’s called active surveillance. I’m very careful about going to my doctor’s appointments, following up, trying to keep myself educated, and so forth. Would I recommend it to somebody else? Somebody else who has the same psychological makeup that I do? Absolutely. Somebody who is a nervous person, a Type A person, somebody who is likely to lose sleep? Perhaps not. I don’t see any possible downside to the testing, though. It’s another tool for you and your doctor to use to help you make your decisions.

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Can Decipher Change Your Prostate Cancer Treatment Plan?

Dr. John Gore is a clinician, surgeon, researcher, and educator specializing in urologic oncology and general urology at the University of Washington.

Prostatepedia spoke with him about how Decipher changes the way doctors treat men with prostate cancer.

What is Decipher?

Dr. Gore: Decipher is from a family of genomic tests. In general, it tries to look at some of the alterations in people’s genes associated with cancer or its progression. Decipher attempts to create a panel of genes associated with the likelihood of a cancer coming back. It takes that panel of genes and integrates it with clinical information to calculate the risk of developing spread of cancer to sites that could be detected clinically, like the bones or the lymph nodes, within five years after prostate cancer surgery.

When is a man likely to encounter this test? After that initial biopsy when he is first diagnosed? After his prostatectomy?

Dr. Gore: The most common scenario would be after surgery. If a man has his prostate removed and the pathology shows that he has a cancer that by all accounts seems to have been successfully treated with the surgery, Decipher may not be the right test for him.

If he has some high-risk features— his cancer is potentially encroaching on the shell of his prostate, he has a positive surgical margin, or there is involvement of the seminal vesicles that sit behind the prostate—then he might benefit from Decipher.

That way we can ask if—in addition to knowing that he had some high-risk pathology features—he appears genomically to have a high-risk cancer?

What do the results look like? Do they change how a man is going to be treated post-surgery? How?

Dr. Gore: The actual report that a patient or doctor gets tells them the probability, or percent risk, that he will have clinical metastases within five years of having his prostate removed for prostate cancer. In general, those numbers tend to be in the single digits to low teens. It’s not a common event.

For most people, prostate cancer surgery successfully treats their cancer. That is why this is best used on higher-risk individuals.

In our study, we looked at a cadre of patients who were either found to have high-risk features at the time of their prostate cancer surgery, or now their PSA is subtly rising after going to zero after surgery. Those patients should potentially have more aggressive treatment.

We showed that if a patient had the Decipher test, physicians’ recommendations changed. If your Decipher results showed a lower risk score, your doctor was more likely to recommend observation.

Patients with a higher risk Decipher score were more aggressively treated. They were recommended to go ahead and get additional radiation to the area where their prostate was removed, rather than just active surveillance.

The bottom line is that Decipher changes how men are treated?

Dr. Gore: Yes. We have some follow-up data we just presented at the American Society of Clinical Oncology, Genitourinary meeting in February that showed that those treatment recommendations were actually followed 80% of the time.

You said only men who are high-risk should really be tested. Not everyone getting prostate cancer surgery needs a Decipher Test?

Dr. Gore: That’s right.

Is Decipher widely accepted in the medical community? If a man in rural Minnesota goes to his local urologist or local community oncologist, will he likely be offered the Decipher Test? If not, should he ask his doctor to order it?

Dr. Gore: I think it’s definitely worth requesting it. One thing that has come up is insurance payer coverage, not just for the Decipher Test, but also for other tests like it. The bar that some of these companies have to cross to get their test approved is fairly high.

Some insurance companies are asking if the test not only changes treatment for patients. The trial they’re looking for will compare patients who got the Decipher Test with patients who didn’t to see if the decisions that were made impacted cancer outcomes. If, for example, your Decipher results say you’re high-risk, and you get radiation based on that information, was that the correct decision? The challenge is that prostate cancer is immensely slow-growing. Even when it’s high-risk, even when it’s aggressive, we’re talking about clinical outcomes that take years and years to manifest. It imposes an irrationally onerous burden to prove that these tests are the right thing.

You could wait 10 years to find out if the treatment decisions were correct. Meanwhile, time is passing and these men need to make choices…

Dr. Gore: Absolutely.

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Dr. John Gore: Why Medicine?

Dr. John Gore is a clinician, surgeon, researcher, and educator specializing in urologic oncology and general urology at the University of Washington.

Prostatepedia spoke with him about how Decipher changes the way doctors treat men with prostate cancer.

Why did you become a doctor?

Dr. John Gore: My initial vision for my life was that I was going to be a lawyer. Then I found that I really enjoyed my experiences while interning at the hospital. That brought about an application to medical school. I think being a doctor offers a chance to have a daily meaningful impact, which is a unique part of the job.

How did you end up working in urology?

Dr. Gore: Urology is a specialty that very few people enter medical school thinking that they want to do. In part, most people are like I was and don’t even know about the specialty. I don’t have any doctors in my family. The only doctor I knew was my own pediatrician. I just assumed I was going to be a pediatrician.

But I really enjoyed surgery. I enjoyed being in the operating room. I just really enjoy the generic construct that someone has a problem and I have the tools to fix it.

Urology is an interesting hybrid. Most surgeries have a homolog in internal medicine. For example, there’s cardiothoracic surgery and cardiology. There’s colorectal surgery and gastroenterology. We don’t really have that in urology. We do a lot of chronic disease management. We do a lot of long-term follow-up of our own patients. It is, in many ways, a hybrid of internal medicine and surgery, which is really cool.

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